i

Myofascial Release of the Pectoral : Effect on Posture, Pectoral Length, Muscle Activity, and Movement Performance

by:

Sarah Bohunicky

A Thesis submitted to the Faculty of Graduate Studies of The University of Manitoba in partial fulfillment of the requirements of the degree of

MASTER OF SCIENCE

Faculty of Kinesiology and Recreation Management University of Manitoba Winnipeg

June 23rd, 2021

Copyright © 2021 by Sarah Bohunicky ii

Abstract

Context: Neck-shoulder pain is among the most common health care problems, especially in office workers and females. Forward shoulder posture (FSP) is a common postural deviation and known risk factor for the development of neck-shoulder pain and pathology. Common approaches for reducing FSP include stretching and performing manual techniques to increase the length and extensibility of the scapular protractors and strengthening the scapular retractors. Myofascial release (MFR) is a group of manual techniques that elongate and soften restricted fascia, however, the effects of myofascial release to the pectorals on FSP are currently unknown. Objective: To determine the impact of 4-minutes of MFR on: 1) FSP, 2) pectoral length, 3) muscle activity of the upper, middle, and lower and , 4) scapular retractor to protractor ratio of activity, and 4) movement performance compared to a soft-touch control. Participants: Eighteen females (27 years ± 10) with FSP but otherwise healthy . Interventions: One 4-minute MFR treatment and one 4-minute soft-touch control (CON) treatment. Main Outcome Measures: FSP, pectoral length, muscle activity of upper, middle, and lower trapezius (UT, MT, LT) and pectoralis major (PEC), scapular retractor-protractor ratio of activity (R/P), and movement performance (reaction time [RT], movement time [MvT], end-point accuracy [constant and variable error]). Statistical Analysis: Two-way (treatment [MFR or CON] by time [PRE and POST]) repeated measures analysis of variance (ANOVA) was conducted on all dependent variables. Results: There was a statistically significant decrease in FSP, F(1, 17) = 6.66, p = .019, partial η2= .282. The means (millimetres) and standard deviations were as follows: PRE-MFR 124 (15), POST-MFR 118 (14), PRE-CON 124 (15), POST-CON 122 (15). There were no statistically significant changes in pectoral length, muscle activity, or movement performance. Conclusion: A 4-minute MFR to the pectoral fascia is effective at reducing FSP, but does not impact pectoral length, muscle activity, or movement performance. However, the study sample was well underpowered, thus possibly impacting the results of the other outcome variables. It is unclear if this reduction in FSP is considered clinically significant in reducing the risk for development of neck-shoulder pain or pathology.

iii

Acknowledgements

When I made the decision to return to school to complete my Master of Science degree, I do not think I ever could have anticipated the road that lied ahead. The ebbs and flows of graduate studies are more challenging, frustrating, and exhausting than I ever imagined, yet rewarding, exciting, and fulfilling all at once. The tremendous support I have received from family, friends, lab mates, colleagues, professors, and supervisors is truly humbling and overwhelming and has helped get me through this seemingly endless degree (thanks to COVID-19). I am proud of my work thus far in graduate studies and cannot wait to see where my academic pursuits take me. I have overcome many barriers, some of which were unprescendented, and for that, I thank you all for pushing me when I didn’t want to push myself.

First and foremost, I want to thank my supervisor, Dr. Trisha Scribbans. In January 2018, when we first discussed me pusuing graduate studies under your supervision, I never would have imagined our working relationship to be as seamless and enjoyable as it now is. I have never had another person outside my family wanting to see me as wildly successful as you do. Your personal, academic, and professional support, mentorship, and guidance is truly astounding and words cannot express my gratitude for you enough. I am very much looking forward to the many years we have left working together.

Secondly, I would like to thank my other committee members Dr. Cheryl Glazebrook and Dr. Joanne Parsons for their valuable support, input, and expertise on the project. In particular, I would like to thank Dr. Glazebrook for the numerous hours she spent advising and guiding me through the use of E-Prime and scripting letters of reference.

Thirdly, I would like to thank my lab mates in the Integrative Musculoskeletal Research Lab for their knowledge, patience, and support throughout my degree. I could not have asked for a better group of grad students-turned-friends to go through this experience with. Thank you for your help with piloting, listening to my 3MT about 50 times, and fueling me with coffee, high- fives, and laughs, even on the darkest of grad school days. I would especially like to thank Zach for his non-judgemental help with research, ethics, analysis, and all things stats related. I thoroughly enjoyed learning from you and participating in “tea-time.”

Lastly, but certainly not least, I would like to thank my parents, Bernie and Diane. “Thank-you” doesn’t seem like enough for your endless emotional, personal, and yes, financial support. You two have and will always be my rock, and I am forever grateful to have such supportive, loving, and compassionate parents. Thank-you for always supporting my endeavors and encouraging me in ways I would not be able to do for myself. Thank-you for being my shoulders to cry on, my personal bartenders and chefs, the ones who make me laugh (even when I don’t want to), the ones to jump up and down in celebration with, and my persistent force to do the absolute best I can. Without you, I would not be where I am or who I am today.

“This is an investment in your future”- my Dad

This project was supported by the Massage Therapy Research Foundation, College of Massage Therapists of Ontario, and Massage Therapy Association of Manitoba iv

Table of Contents Abstract ...... ii Acknowledgements ...... iii List of Tables ...... vii List of Figures ...... viii 1. Introduction ...... 10 2. Review of the Literature ...... 13 2.1 Shoulder Complex Applied Anatomy Review ...... 13 2.1.1 Sternoclavicular, Glenohumeral, and Acromioclavicular Joints ...... 13 2.1.2 Scapulothoracic Joint ...... 14 2.1.3 Scapular Protractors ...... 15 2.1.4 Scapular Retractors ...... 16 2.1.5 Fascia ...... 17 2.1.6 Pectoral Fascia ...... 17 2.1.7 Fascial Adhesions and Trigger Points ...... 18 2.1.8 Implications of Fascial Adhesions and Trigger Points ...... 19 2.2 Posture ...... 20 2.3 Reciprocal Inhibition ...... 22 2.4 Movement Performance ...... 23 2.4.1 Speed-Accuracy Trade Off (aka Fitts’ Law) ...... 23 2.4.2 Schema Theory ...... 24 2.4.3 Applicability to Whole-Limb Real Movements ...... 25 2.5 MSK Disorders ...... 26 2.5.1 Work-Related Musculoskeletal Disorders ...... 27 2.5.2 MSK Disorders in Office Jobs ...... 28 2.5.3 Changes in Muscle Activity Due to MSK Disorders ...... 29 2.5.4 MSK Disorder Risk Factors ...... 30 2.5.4a Sex Differences ...... 30 2.6 Forward Shoulder Posture (FSP) ...... 31 2.6.1 Does Posture Really Matter? ...... 33 2.7 Management of FSP ...... 35 2.7.1 Strengthening of Scapular Retractors ...... 36 2.7.2 Increasing the Length and Extensibility of the Scapular Protractors and Connective Tissue ...... 36 2.7.2a Stretching ...... 36 2.7.2b Manual Techniques ...... 38 2.7.2c Myofascial Release ...... 39 2.7.2d Combined Approaches ...... 41 v

3. Purpose ...... 42 4. Objectives ...... 43 5. Hypotheses ...... 43 6. Experimental Methods ...... 43 6.1 Experimental Method ...... 43 6.2 Participants ...... 44 6.3 Experimental Sessions ...... 48 6.3.1 Forward Shoulder Posture (FSP) Measurement ...... 48 6.3.2 Pectoral Muscle Length ...... 50 6.3.3 Muscle Activity - Surface Electromyography (sEMG) ...... 51 6.3.3a Maximum Voluntary Isometric Contractions (MVICs) ...... 53 6.3.4 Reaching Task ...... 54 6.4 Treatment Conditions ...... 57 6.4.1 Myofascial Release (MFR) ...... 57 6.4.2 Soft-touch Control (CON) ...... 58 6.5 Blinding ...... 59 6.6 Data Processing ...... 60 6.6.1 Electromyography (EMG) ...... 60 6.6.2 Movement Performance ...... 61 6.7 Statistical Analysis ...... 62 7.0 Results ...... 64 7.1 Forward Shoulder Posture ...... 67 7.2 Pectoral Length ...... 68 7.3 Muscle Activity ...... 69 7.3.1 Upper Trapezius (UT) ...... 69 7.3.2 Middle Trapezius (MT) ...... 71 7.3.3 Lower Trapezius (LT) ...... 71 7.3.4 Pectoralis Major ...... 72 7.3.5 Scapular Retractor-Protractor Ratio of Activity (R/P) ...... 73 7.4 Movement Performance ...... 74 7.4.1 Reaction Time (RT) ...... 74 7.4.2 Movement Time (MvT) ...... 76 7.4.3 End Point Accuracy ...... 77 7.4.3a Constant Error X-Axis Left Targets (CEL) ...... 77 7.4.3b Constant Error X-Axis Right Targets (CER) ...... 78 7.4.3c Constant Error Y-Axis Top Targets (CET) ...... 79 7.4.3d Constant Error Y-Axis Bottom Targets (CEB) ...... 79 7.4.3e Variable Error X-Axis (VEX) ...... 80 7.4.3f Variable Error Y Axis (VEY) ...... 81 7.5 Reliability ...... 83 vi

8. Discussion ...... 83 8.1 Forward Shoulder Posture (FSP) ...... 84 8.2 Pectoral Length ...... 87 8.3 Muscle Activity ...... 90 8.3.1 Upper Trapezius (UT) ...... 91 8.3.2 Middle Trapezius ...... 92 8.3.3 Lower Trapezius ...... 93 8.3.4 Pectoralis Major (PEC) ...... 95 8.3.5 Scapular Retractor to Protractor Ratio of Activity (R/P) ...... 96 8.4 Movement Performance ...... 98 8.4.1 Reaction Time (RT) ...... 98 8.4.2 Movement Time (MvT) ...... 98 8.4.3 End-Point Accuracy ...... 98 8.4.3a Constant Error X-Axis Left and Right Targets (CEL & CER) ...... 98 8.4.3b Constant Error Y-Axis Top and Bottom Targets (CET & CEB) ...... 99 8.4.3c Variable Error X- and Y- Axis (VEX & VEY) ...... 99 9. Limitations and Future Directions ...... 101 10. Conclusion ...... 104 References ...... 105 Appendices ...... 129 Appendix A- Participant Intake Medical Form ...... 129 Appendix B- Research Ethics Board Approval ...... 131 Appendix C- Individual Trial Number Outliers for RT, MvT, End-Point Accuracy and EMG Variables During the Reaching Task ...... 132 Appendix D- Paired T-test Results ...... 135 Appendix E- Post-hoc a priori sample size calculation to reach 80% power ...... 136 Appendix F- Individual Participant Dependent Variable Means ...... 137 Appendix G- Registered Massage Therapist Notes on Treatment Condition ...... 145

vii

List of Tables

TABLE 1: BIPOLAR ELECTRODE PLACEMENT FOR UPPER, MIDDLE, AND LOWER TRAPEZIUS, AND PECTORALIS MAJOR...... 52 TABLE 2: TARGET CENTRE COORDINATES AND CALCULATION OF CONSTANT ERROR...... 61 TABLE 3: MEAN AND STANDARD DEVIATIONS OF PRE- AND POST- MFR AND CON CONDITIONS ...... 65 TABLE 4: PERCENT CHANGE FROM PRE TO POST MFR AND CON OF INDIVIDUAL PARTICIPANT MEANS...... 67 TABLE 5: ACHIEVED POWER AND EFFECT SIZES ...... 82 TABLE 6: INTRACLASS CORRELATIONS OF FSP, PECTORAL LENGTH, AND MAXIMAL VOLUNTARY ISOMETRIC CONTRACTIONS (MVICS)...... 83 TABLE 7: POST-HOC A PRIORI CALCULATED SAMPLE SIZE...... 101

viii

List of Figures FIGURE 1: SCAPULAR COORDINATE SYSTEM AND MOVEMENTS OF THE SCAPULOTHORACIC JOINT. 14 FIGURE 2: MUSCLES THAT ACT ON THE SCAPULA TO PRODUCE PROTRACTION. 15 FIGURE 3: MUSCLES THAT ACT ON THE SCAPULA TO PRODUCE RETRACTION. 16 FIGURE 4: SUPERFICIAL AND DEEP PECTORAL FASCIAL LAYERS. 18 FIGURE 5: LATERAL PLUMB LINE TO ASSESS POSTURE 22 FIGURE 6: SCHEMATIC REPRESENTATION OF THE EXPERIMENTAL PROTOCOL. 45 FIGURE 7: CONSORT DIAGRAM OF PARTICIPANT RECRUITMENT AND EXPERIMENTAL PROTOCOL 47 FIGURE 8: DOUBLE-SQUARE METHOD FOR FORWARD SHOULDER POSTURE MEASUREMENT. 49 FIGURE 9: PECTORAL LENGTH MEASUREMENT. 50 FIGURE 10: SEMG BIPOLAR ELECTRODE SETUP FOR PECTORALIS MAJOR, UPPER, MIDDLE, AND LOWER TRAPEZIUS IN REACHING TASK. 52 FIGURE 11: REACHING TASK SETUP. 55 FIGURE 12: COMPLETE TARGET SETUP FOR REACHING TASK. 56 FIGURE 13: TREATMENT CONDITION SETUP 58 FIGURE 14: FSP BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 68 FIGURE 15: PECTORAL LENGTH BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 69 FIGURE 16: UPPER (UT), MIDDLE (MT), AND LOWER TRAPEZIUS (LT) ACTIVITY BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 70 FIGURE 17: PECTORALIS MAJOR ACTIVITY BEFORE (PRE) AND AFTER (POST) 4- MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 73 FIGURE 18: SCAPULAR RETRACTOR TO PROTRACTOR RATIO OF ACTIVITY BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 74 FIGURE 19: REACTION TIME BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 75 FIGURE 20: MOVEMENT TIME BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT (INDIVIDUAL AND GROUP MEANS). 77 FIGURE 21: X-AXIS CONSTANT ERROR BEFORE (PRE) AND AFTER (POST) 4- MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT FOR THE LEFT AND RIGHT TARGETS (INDIVIDUAL AND GROUP MEANS). 78 ix

FIGURE 22:Y-AXIS CONSTANT ERROR BEFORE (PRE) AND AFTER (POST) 4- MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT FOR THE TOP AND BOTTOM TARGETS (INDIVIDUAL AND GROUP MEANS). 79 FIGURE 23: VARIABLE ERROR BEFORE (PRE) AND AFTER (POST) 4-MINUTES OF MYOFASCIAL RELEASE (MFR) OR SOFT-TOUCH CONTROL (CON) TREATMENT FOR X- AND Y- AXES (INDIVIDUAL AND GROUP MEANS). 81

x

List of Abbreviations

AC–– acromioclavicular joint CEB –– constant error bottom targets CEL –– constant error left targets CER–– constant error right targets CET–– constant error top targets EMG –– electromyography FSP –– forward shoulder posture GH–– glenohumeral joint LT –– lower trapezius MT –– middle trapezius MV–– Millivolts MvT –– movement time MVIC –– maximal voluntary isometric contraction PEC–– pectoralis major R/P –– scapular retractor to protractor ratio of activity RT–– reaction time SA –– serratus anterior SC –– sternal clavicular joint ST –– scapulothoracic joint UT –– upper trapezius VEX –– variable error x-axis VEY –– variable error y-axis

10

1. Introduction Musculoskeletal (MSK) disorders cost the Canadian healthcare system over $26 billion annually1 with those affecting the shoulder, upper back, and neck being amongst the most common2–6. These disorders are responsible for 40-50% of all work-related disease costs7, and while the etiology responsible for the development of these work-related disorders is known to be multifactorial, work posture is one risk factor for the development of neck-shoulder pain8. Occupations considered at a heightened risk for the development of MSK disorders involve highly repetitive work, and office jobs typically have workers engage in prolonged static and awkward postures such as working at a computer for several hours at a time9,10. While computer use in the workplace has revolutionized the way we work, it has also shifted many physically active jobs to more sedentary ones11. These types of jobs have demonstrated a high prevalence of MSK disorders2,12, as computer work is associated with many upper extremity disorders11,13,14 and is considered a risk factor for the development of neck-shoulder pain15–17. Interestingly, biological sex is also considered a risk factor for the development of neck- shoulder pain18. While females tend to have better posture than males19 and use computers less20, they report increased rates of neck-shoulder pain and MSK disorders21,22. It is theorized that these discrepancies may be due to differences in tissue composition, structure, muscular strength, motor control, or fatigue between the sexes23. For example, females have more type I muscle fibres in comparison to males24, which are associated with increased muscular endurance and are traditionally weaker than type II fibres25. Individuals with shoulder pathology demonstrate altered muscle activity and kinematics compared to individuals who have healthy shoulders. Generally, shoulder pain is accompanied with increased upper trapezius (UT) activity, and decreased serratus anterior (SA)26–30, middle (MT) and lower trapezius (LT)28,31,32 activity, as well as altered onset of activation between these muscles33. Forward shoulder posture (FSP) is a common postural deviation where the shoulder complex is in an anterior position that affects up to 73% of the healthy population34. Increased rates of computer usage is a risk factor for the development of FSP, as it often requires the maintenance of awkward static positions where the shoulders are internally rotated, flexed and abducted for prolonged periods10,35. Forward shoulder posture is characterized by adaptive shortening of the shoulder protractors (e.g. pectorals) and adaptive lengthening of the scapular 11 retractors (e.g. trapezius, rhomboids)36. Additionally, FSP alters scapular position and motion37, demonstrating increased muscular activity in the upper trapezius, levator scapulae, and pectoralis major, and decreased activity of SA and MT28,38–40. The shortened are associated with anteriorly tilted, downwardly rotated, protracted, and depressed scapula36,41–43 which alter the kinematics of the shoulder joint43. Collectively, it is theorized that FSP alters the muscle activity and the ratio of activation within the scapular protractors and retractors44, and over time, movement produces pain as a response to the altered movement and subjects individuals to shoulder pathologies45. Musculoskeletal therapists (i.e. massage, physical, or athletic therapists) are routinely taught to correct FSP by utilizing different techniques such as stretching or manual therapy to lengthen the pectoral muscle group to reduce the anterior position of the shoulder complex46. Further, it is believed that these strategies not only increase pectoral length, but that the increase in pectoral length results in a concomitant increase in activity of the pectoral muscle’s antagonists, the scapular retractors44, though no research has examined this. It is theorized that when is adaptively shortened it is hypertonic and overactive, leading to a reciprocal inhibition (i.e. reduced activation) of the antagonist44. This theory aligns with reciprocal inhibition, which states that when an agonist muscle contracts (i.e. increased activation), the antagonist muscle is inhibited (i.e. decreased activation)47. A shortened muscle produces changes in the sarcomeres of a muscle48, demonstrating a proportional relationship between decreases in adaptive muscle length and sarcomere number49. Different rehabilitation strategies such as stretching and manual techniques aim to lengthen and increase the extensibility of muscles and their connective tissue components50,51, further attempting to decrease the level of activity by decreasing the amount of active actin-myosin cross-bridges52. Indeed, increasing the length of the scapular protractors using manual techniques (e.g. myofascial release) to facilitate an increase in activation within the scapular retractors in individuals with FSP is an extremely common therapeutic approach used by musculoskeletal therapists. While several studies have demonstrated the ability of lengthening the pectorals and additionally strengthening the retractors to reduce FSP53–58, research seldomly quantifies the impact these approaches have on changes in muscle activity or movement performance. Movement performance is the study of motor control and learning and is quantified through four fundamental measures: error, time and speed, magnitude, and performance on 12 secondary tasks59. Fitts’ Law defines the relationship between speed and accuracy, stating that target-oriented, discrete movements observe an inverse relationship- as speed increases, accuracy decreases and vice-versa60. Fitts’ tasks are often used not only in research, but in real life, as humans are required to interact with their environment using parts of their body to complete simple, goal-directed movements such as pointing61. Fitts’ tasks have been used in research looking at aircraft navigation62, chiropractic spinal adjustments63,64, older adults65, autistic individuals66, and healthy individuals67, and are resistant to learning and have a varying degree of difficulty68. Myofascial release is a form of manual therapy that requires a practitioner to apply a mechanical pressure to fascia until deformation occurs which elongates and softens restricted fascia69. Previous research has demonstrated that treatment time of only 3.3 minutes of MFR is required to observe a change in fascial mobility70. However, despite MFRs routine use, it is not currently known if a 4-minute MFR to the scapular protractors alters FSP, pectoral length, muscle activity within the scapular protractors and retractors, or movement performance. The following work aimed to address these gaps by examining the impact of one 4- minute MFR treatment to the pectoral fascia on FSP, pectoral length, muscle activity of the scapular protractors (pectoralis major) and retractors (upper, middle, and lower trapezius), as well as the ratio of activity between the scapular retractors and protractors, and movement performance during a reaching task in individuals with FSP. Movement performance will be quantified through analysis of reaction time, movement time, and end-point accuracy. The following document will begin with a thorough review of current literature regarding work- related musculoskeletal disorders of the shoulder, upper back and neck, a review of pertinent anatomy of the shoulder complex, FSP, and current treatment strategies for FSP including MFR. Methodological details will then be presented, followed by statistical analysis, results, discussion, limitations, and conclusions. References and appendices will be included following the conclusion.

13

2. Review of the Literature The musculoskeletal (MSK) system is comprised of the bony skeleton and associated tissues such as muscles, joints, tendons, ligaments, connective tissue, peripheral nerves and supporting blood vessels9,71,72. The viscera of the body are protected and supported by the skeleton and it is through the actions of attached skeletal muscles that movement of joints is permitted71,73. 2.1 Shoulder Complex Applied Anatomy Review The following anatomical review of the shoulder complex is cited from Gray’s Anatomy71. The shoulder complex consists of a total of four joints: three of which (sternoclavicular, glenohumeral, acromioclavicular) connect the upper extremity to the trunk through bony articulations, while the scapulothoracic joint articulates with the trunk through muscular attachments. These four joints work in tandem to produce a wide range of movements such as flexion, extension, rotation, abduction, and adduction, and allow for more freedom of movement than any other joint in the body71. Many muscles act directly or indirectly on the shoulder girdle itself, including the axio-appendicular muscles (indirect) that attach the trunk to the appendages, and scapulohumeral muscles (direct) that attach from the scapula to the humerus. For example, the pectoral muscles, trapezius, and rhomboids act indirectly (axio- appendicular), while rotator cuff, deltoid, and teres minor (scapulohumeral) act directly on the shoulder girdle. 2.1.1 Sternoclavicular, Glenohumeral, and Acromioclavicular Joints The sternoclavicular joint is stable in nature, and voluntary movements do not specifically occur at the joint but accommodate for the mobility of the by rotating and gliding the joint anteriorly/posteriorly and superiorly/inferiorly. The glenohumeral joint (GH) is relatively unstable due to the shallow nature of the glenoid cavity. It is capable of a wide range of movement: flexion/extension, abduction/adduction, horizontal abduction/adduction, and internal/external rotation. The acromioclavicular joint (AC) articulates the scapula with the clavicle and exhibits movements that are passive or involuntary; it is with movements of the scapula and humerus that cause rotational movement and anterior/posterior and superior/inferior glides at the AC joint. 14

2.1.2 Scapulothoracic Joint Though not considered a “true” joint due to its absence of bony articulations, the scapulothoracic joint plays an integral role in the functioning of the shoulder complex74. The joint consists of the scapula and musculature that attach to the posterior that act on the scapula to produce movements. The scapula serves as an attachment point for several muscles that act on the glenohumeral joint (e.g. rotator cuff; supraspinatus, infraspinatus, teres major, and subscapularis), which makes its stability essential for glenohumeral stability and function. Thus, it is essential that the muscular forces acting on the scapulothoracic joint remain balanced to ensure proper scapular position, and therefore stabilization of the shoulder girdle. The specific movements that occur at the scapulothoracic joint include scapular protraction/retraction and elevation/depression, along with rotation throughout humeral movement (Figure 1).

Figure 1: Scapular Coordinate System and Movements of the Scapulothoracic Joint. (A) Scapular coordinate system respective to the acromioclavicular joint where X, Y, and Z 75 planes are relative to the scapula, where YC is the local axis for the clavicle coordinate system . (B) Movements about the different scapular axes located at the acromioclavicular axes: abduction/adduction (protraction/retraction) about the Y-axis, elevation/ depression about the X- axis, and scapular tilt (anterior/posterior) about the Z-axis. Regarding the axes originating at the centre of the scapula (blue), internal rotation about the Y-axis will produce scapular winging, where upward/downward rotation of the scapula will occur about the Z-axis76.

15

These four joints combined allow the glenohumeral joint to achieve a larger range of motion than any other joint and is primarily stabilized dynamically by the surrounding soft tissues (i.e. muscles, tendons, and fascia). 2.1.3 Scapular Protractors The scapular protractors include the pectoralis major, , and serratus anterior (Figure 2). Collectively, these muscles act to protract (or abduct) the scapula anteriorly on the ribcage. The pectoralis major consists of two heads: the clavicular head (attaches to anterior surface of medial half of clavicle) and sternal head (attaches to anterior surface of the , superior six costal cartilages, and aponeurosis of external oblique). They attach at the intertubercular sulcus of the humerus. Together, the two heads of the pectoralis major protract the scapula and medially rotate the humerus. The pectoralis minor attaches proximally on the 3rd- 5th costal cartilages and distally to the coracoid process of the scapula, protracting the scapula by pulling it anteriorly and inferiorly. The serratus anterior is the only muscle of the three to additionally hold the scapula against the thoracic wall through rotation71. It sits on the external surfaces of the lateral 1st to 8th ribs and attaches to the medial border of the scapula.

Figure 2: Muscles that act on the Scapula to Produce Protraction. (A) Sternal and clavicular heads of pectoralis major (left). https://commons.wikimedia.org/wiki/Commons:GNU_Free_Documentation_License,_version_1.2 (B) Pectoralis minor (deep to pectoralis major). http://lifesciencedb.jp/bp3d/info/userGuide/faq/credit.html (C) Serratus anterior. http://lifesciencedb.jp/bp3d/info/userGuide/faq/credit.html

16

2.1.4 Scapular Retractors The scapular retractors consist of the trapezius and rhomboids (minor and major) (Figure 3). The rhomboids attach proximally to the spinous processes of C7-T1 (minor) and T2-T5 (major) and run distally to the medial border of the scapula. Both muscles retract the scapula71. The trapezius is a flat, triangular muscle extending over the upper back and neck, playing a large role in neck, shoulder, and thoracic movement. The proximal attachment of the trapezius is the medial third of superior nuchal line, external occipital protuberance, and spinous processes of C7-T12, and its distal attachment is the lateral third of the clavicle, acromion and spine of the scapula. It is divided into three primary fiber directions, each assisting with a separate action. The superior fibres consist of fibres that descend and produce elevation of the scapula. The middle fibres run horizontally and help with retraction of the scapula. Finally, the lower fibres of the trapezius ascend and depress the scapula downwards. Collectively, the three sections of the trapezius retract the scapula and collaborate with other muscles to control and stabilize the scapula, especially during movements of the arm78.

Figure 3: Muscles that act on the Scapula to Produce Retraction. (A) The upper (orange), middle (red), and lower (pink) trapezius. http://lifesciencedb.jp/bp3d/info/userGuide/faq/credit.html (B) Rhomboid minor (light red) and major (dark red) that run deep to the trapezius. http://lifesciencedb.jp/bp3d/info/userGuide/faq/credit.html

17

2.1.5 Fascia Fascia is web-like connective tissue that is large enough to be visible to the naked eye69. It provides passive and active support from head to toe, encapsulating skeletal muscles, joints, organs, nerves, and vascular properties79. Fascia serves many purposes such as providing structural support and stability69, and allowing for the transmission of mechanical forces between muscles80. Fascia is comprised of collagen, elastin and ground substance where collagen provides support, shape and stability; elastin provides dynamic flexibility; and ground substance provides cushion69. Fascia is typically divided into superficial and deep types71,80. Superficial fascia, also known as subcutaneous tissue, is made up of variable thicknesses of loose connective tissue that amalgamates with the deep layers of the dermis71. Its structure tends to be highly variable with interlaced collagen fibres that do not appear in a parallel orientation as seen in tendons or muscles71. Superficial fascia allows for increased mobility of the skin and contains adipose tissue, allowing for thermal regulation and energy storage71. Deep fascia, on the other hand, is mainly composed of compact collagen fibres that are often identical to aponeurotic tissue surrounding musculature71,73. In certain areas, the deep fascia compartmentalizes contained muscles and attaches to the periosteum of bone71,73. 2.1.6 Pectoral Fascia The fascia that surrounds the pectoral region is a thin lamina, attaching medially to the sternum, superiorly to the clavicle, and is continuous inferolateral with the fascia of the shoulder, , and thorax (Figure 4A). The fascia covers pectoralis major superiorly and laterally ascends to cover the entire muscle, emerging as a new fascial layer called the , which encloses the subclavius and pectoralis minor71,81. The pectoral fascia is unique as it acts as a secondary insertion point for the pectoralis major muscle, with continuity between the muscle fibres and fascia often observed (Figure 4B)82. 18

Figure 4: Superficial and Deep Pectoral Fascial Layers. (A) The superficial layer of the pectoral fascia passes over the sternum (S) and continues with the superficial layer of the clavipectoral fascia (PM). (B) The superficial layer of fascia is removed to show the deep pectoral fascia that is adhered to the pectoralis major muscle81.

2.1.7 Fascial Adhesions and Trigger Points A fixed connection between different fascial layers where sliding or gliding would normally occur, impacting the range of motion of the tissues, is considered an adhesion83. This, in part, may be due to changes in the normally lubricating hyaluronic acid that is present in healthy tissue. Hyaluronic acid is a straight chain carbohydrate polymer that is present in fascial layers that largely contributes to ease of fascial glide over surrounding musculature84,85. However, hyaluronic acid often becomes adhesive rather than lubricating, which alters the distribution of lines of force within the fascia85. Stecco et al. (2013)85 speculate this contributes to the formation of adhesions as the tissue becomes dense. Densification is a term often used to describe the changes in collagen in fascia and can be easily identified through imaging such as magnetic resonance imaging (MRI), computerized axial tomography (CAT scans), and ultrasonography85. Similarly, myofascial trigger points are defined as areas within hypertonic muscles or fascia that may refer pain and lead to motor dysfunction86. They are associated with a 19 hypersensitive, palpable band which may refer pain, tenderness, and motor dysfunction when compressed, stretched, overloaded or contracted86,87. Trigger points may develop after injury to muscle fibres or in reaction to microtrauma or stress, including chronic fatigue86,88,89 and may be classified as active or latent90. Active trigger points are generally symptomatic causing pain and dysfunction within the muscle and into referral zones91. Alternatively, latent trigger points do not cause pain but have been shown to alter normal muscle function92 in seemingly healthy individuals with no pre-existing pain90. Despite longstanding research and treatment, trigger points and adhesions are a controversial topic as there has been a lack of consensuses among researchers and clinicians regarding diagnostic criteria93. In addition, current literature has reported unreliable and invalid means of identifying trigger points through these criteria94,95. These findings and conclusions have lead some researchers to doubt their existence96,97. Simons, a once contributing author of a 1983 trigger point manual86, has since called the phenomenon an ‘enigma,’ stating trigger points are complex and lack not only a diagnostic gold standard, but also a generally recognized etiology86. Simons calls for further research using advanced technology such as ultrasound or MRI to further identify and quantify the presence of trigger points. However, a critical evaluation of trigger point phenomenon by Quinter et al. in 2015 proposed that sufficient research has been completed to discard the notion of trigger points, stating that the diagnosis is unreliable and treatment of trigger points does not differ from placebo treatments97. This article was contested by Rathbone et al. (2015), claiming diagnosis of a trigger point needs to have more quantitative parameters that previous literature had not incorporated, allowing for inconclusive and unreliable findings98. It seems recent advancement of ultrasonic technology has allowed for this to happen, as suggested by Simons. In 2016, Chen et al. demonstrated the presence of taut bands of tissue parallel to muscle fibres via magnetic resonance elastography, claiming trigger points do exist99. In fact, it has been shown that these trigger points may be up to 50% stiffer than surrounding musculature that is not considered taut100. 2.1.8 Implications of Fascial Adhesions and Trigger Points Interestingly, research has suggested that fascia becomes tighter and more restrictive following trauma, surgery, or overuse, changing the sliding that occurs between the fascia and surrounding musculature85,101. It is suggested that changes in fascial flexibility may contribute to postural deviation which may affect biomechanics101, range of motion102, and motor control103. 20

Specifically, latent myofascial trigger points cause localized tenderness with and without radiating pain only when mechanically stimulated104, and are associated with muscle cramps105,106, decreased range of motion86, altered muscle activity via motor unit cycling107, increased intramuscular activity90, variability in recruitment patters and latencies108, and accelerated development of muscle fatigue109. In addition, subjects with chronic low back pain demonstrated ~25% increased thickness of the compared to controls without back pain110, and shear strain was reduced by ~20% during a passive flexion test allowing for less deformation of the tissue111. Identifying changes in connective tissue structure and shear strain may be utilized as biomarkers that predispose individuals to pain or pathology111,112.

2.2 Posture

Posture is a term that is used to describe the position of the different segments of the body relative to another74. “Good” posture consists of a balance between minimizing the load on the spine and individual joints while minimizing the muscle work required71. “Faulty” posture is any static position that increases stress to the joints, potentially leading to a more cumulative and chronic effect of microtrauma, such as excessive wearing of articular surfaces and weakened or traumatized soft tissue74. It is these chronic stresses that can lead to the same consequences as seen with sudden or acute injuries within the body74 and potentially result in MSK disorders. Clinically, posture is assessed through ideal lines of gravity, or plumb lines, using anatomical landmarks from the anterior, posterior and lateral sides of the body74. The plumb line most pertinent in recognizing characteristic neck and shoulder faulty postures such as forward shoulder posture is the lateral plumb line, as it assesses the positioning of the head and shoulders relative to the centre line of the body in the sagittal plane (Figure 5). The anatomical landmarks used to identify the lateral plumb line are the ear lobe, the tip of the acromion, the high point of the iliac crest, the greater trochanter of the femur, the head of the fibula, and the lateral malleolus of the fibula.

From the lateral side and through observation of the plumb line, other conclusions can be drawn such as: protracted shoulders (i.e. forward shoulder posture), excessive curvatures of each of the spinal segments (i.e. lumbar and cervical lordosis, thoracic kyphosis), pelvic angle and 21 balance between the ASIS and PSIS, forward head posture with the chin poking forward, and knee alignment such as flexion or hyperextension. “Faulty” posture is often identified as the deviation of these landmarks from their identified position according to the plumb line, such as the head being held forward relative to the trunk or rounded shoulders113. The most common cause of postural deviations from this ideal plumb line manifests from poor personal maintenance in correct posture, especially in those who stand or sit for long periods of time, leading to slouching74. These types of positions may lead to various muscular imbalances74, altering the relationship and balance between paired muscle groups that are prone to either inhibition/weakness or facilitation/shortness114, such as those seen with FSP. Shortened, tight musculature is thought to be neurally facilitated, whereas lengthened and weak muscles exhibit a pattern of neural inhibition, leading to delayed response time and often resulting in global firing patterns that are uncoordinated43. The development of these faulty postures and muscular imbalances are the first steps towards developing musculoskeletal disorders. In fact, research has clearly demonstrated a relationship between resting scapular position and abnormal scapular motion with a variety of shoulder pathologies28,37,45,115–118. 22

Figure 5: Lateral Plumb Line to Assess Posture

Visual of lateral plumb line with anatomical landmarks identified relative to the line: external auditory meatus (in line), AC joint (in line), high point of the iliac crest (anterior), greater trochanter (in line), head of the fibula (posterior), and lateral malleolus (posterior)74.

2.3 Reciprocal Inhibition Reciprocal inhibition is a reflex that causes antagonist muscle(s) to relax as an agonist contracts47. When an agonist receives an impulse to contract, an inhibitory impulse is also sent to the antagonist119,90, resulting in simultaneous excitatory activity in an agonist and inhibitory relaxation in an antagonist47. This is demonstrated empirically via comparisons of the amplitude of electrical activity within a force-couple (i.e. agonist and antagonist) while conducting a voluntary contraction120. As a muscle contraction is initiated and maintained, its opposite muscle experiences a proportional, inhibitory, or relaxation response121. While reciprocal inhibition has been commonly studied in the lower leg122,123 and forearm119,124, little research has been completed on the musculature of the shoulder. McClelland, 23

Miller, and Eyre (2001) demonstrated the inhibitory reflex in force-couples such as the biceps/triceps and pectoralis major/posterior deltoid in contractions of these muscle groups125. Interestingly, Ibarra et al. (2011) reported greater muscle activity in the posterior deltoid muscle with myofascial trigger points in comparison to those without myofascial trigger points, both at rest and during shoulder flexion90. This demonstrates that myofascial trigger points in antagonist muscles have increased levels of activity during an agonist contraction, suggesting a reduced efficiency of reciprocal inhibition in a voluntary movement40.

2.4 Movement Performance

Human movement is an essential aspect of life, and the study of motor control and learning has various applications that relate to nearly every aspect of daily living59. Quantification of motor behaviour outcomes can be achieved through four fundamental measures: 1) error, 2) time and speed, 3) movement magnitude, and 4) performance on secondary tasks59. Error may be quantified through several measurements such as constant error (average error; amplitude and directional bias) and variable error (consistency). Time and speed are often measured via reaction time (RT; the time from arrival of stimulus to beginning of response) and movement time (MvT; time from RT to completion of the movement). Reaction time represents the time it takes a subject to process the stimulus, make a decision, and determine motor programming. 2.4.1 Speed-Accuracy Trade Off (aka Fitts’ Law) The relationship between speed and accuracy during discrete, target-oriented movement is defined by Fitts’ Law, which states as either speed or accuracy increases, there is a corresponding decrease in the other60. Fitts’ Law encompasses the relationship between the distance (D) of a movement, the target width (W), and the resulting average movement time (MT)59, demonstrating a “trade-off” between speed and accuracy, as both cannot be increased simultaneously. The movement is required to be performed as quickly as possible in order to observe this trade-off126. The combination of target D and W create an associated index of difficulty (ID; bits) which portrays the level of difficulty of the movement task in relation to the distance and narrowness of each target59. As ID increases (i.e. increased difficulty), the speed at which the task is performed will increase (i.e. longer), forming a linear relationship between ID and MT60,59. In traditional Fitts’ tasks, using a stylus, participants reciprocally tap two targets 24 across a one-dimensional plane60,127. Fitts and Peterson (1964)128 went on to later create a discrete version of this task that followed the same trade-off. However, an additional factor to completing a pointing Fitts’ task is the subjectivity of the participant in terms of target utilization and precision129. The participant may choose speed over precision, resulting in over-utilization of the target area, or alternatively choose precision over speed, resulting in under-utilization of the target area and slower movement times. Instructing a participant to move as quickly and accurately as possible towards the target is considered ambiguous and participant interpretation may bias or emphasize one component over another, either speed or accuracy130. This subjective performance of the task leads to inconsistencies between the nominal task precision and the actual precision of the participants’ performance, defined by index of target utilization, and is not consistent in pointing tasks with ambiguous instruction129. Effective target width is considered the actual precision, or range of input, of the participants’ movement behaviour around a target127, and reflects the actual distribution of hits rather than the target width (W), or what the participants were expected to do131. This is calculated using the x- and y- coordinates of the participants response around the target to determine the ID, rather than using W131. Interestingly, amplitude variation, or y-axis dispersion, has been shown to be less variable than directional variation, or x- axis dispersion131. 2.4.2 Schema Theory There are four components to a goal-oriented movement that an individual will store: 1) the initial conditions; 2) the response specifications of the motor program; 3) the sensory consequence of the movement produced; and 4) the outcome of the movement132. The initial conditions gather information of the pre-response of the muscular system and environment, such as proprioceptive or visual and auditory information which are then stored after the movement as conditions to plan said movement. The response specifications include variations in speed or force that change movements from general muscle commands into specific produced movements. Sensory consequences are the response-produced sensory information, such as visual, auditory, or proprioceptive information, as a result of the movement. Finally, the response outcome is the resulting response which is compared to the desired response; for example, being short of the target centre as opposed to hitting the centre. Together, these four response outcomes are stored after the movement is produced and strengthen their relationship and accuracy with one another as successive movements are completed. 25

Ultimately, these conditions create the motor program which is comprised of specifications of which muscles must contract, what order they must contract in, the forces in which they are to contract, and the phasing of said contractions133. Uno et al.’s (1989)134 proposed model for voluntary movement involves three processes: first, determination of desired trajectory from a finite number of possible paths; second, transformation of visual coordinates of desired trajectory to body coordinates; and third, generation of motor commands, or torques, to execute desired trajectory. These components of the motor program may be altered by application of different parameters, allowing an individual to produce a similar on a different occasion at a different amplitude133. For example, completing one reaching movement at one distance, and a second, similar movement at twice the distance of the first. The same general motor program would be selected, but forces generated would increase, allowing the limb to travel twice the distance in the same time59. However, there exists a linear relationship between force and force variability over a wide range of forces59,133. As such, greater muscular force results in a proportional increase in variability, or rather, less accuracy. Collectively, this demonstrates how simple pointing tasks may be related to larger-scale movements using the same motor program. 2.4.3 Applicability to Whole-Limb Real Movements More recently, modified Fitts’ tasks have been implemented in limb reaching tasks looking at human arm dynamics and use models consistent with Fitts’ Law equations135. Using feedforward and feedback control, the participant selects and plans the movement to successfully execute the required task which includes determining desired trajectory135. The trajectory determines the torque necessary to complete the movement, and in combination with torque noise, can predict variability in movement and endpoint error (i.e. accuracy). In other words, muscular forces produce movements and variability in those forces produces variability in movement59. Humans are required to interact with their environment by using parts of their body to complete simple goal-directed movements, such as pointing, that contribute to more large-scale movements61. The experimental use of Fitts’ Law in discrete pointing tasks provides a framework for the evaluation and prediction of human performance in practical environments136, providing a link between perception and movement control61. Moreover, application of Fitts’ Law has been demonstrated to hold true for 3D reaching tasks, even though higher forces are required to complete the movement due to greater limb involvement137. Fitts’ tasks have also 26 been used in research looking at aircraft navigation62, chiropractic spinal adjustments63,64, older adults65, autistic individuals66, and healthy individuals67, and are resistant to learning and have a varying degree of difficulty68. The use of a modified Fitts’ task assesses the participant’s ability to complete small-scale, discrete movements that are constituent to larger movements, and have the ability to assess component parts of movement performance such as reaction time, movement time, and precision. This gives us the ability to assess how manual treatments effect changes in motor control.

2.5 MSK Disorders

Approximately 15% of Canadians experience a change in normal functioning of the MSK system annually through injuries that negatively affect their activities of daily life138. These injuries cost the Canadian healthcare system over $26 billion annually1 and in Manitoba, Workers Compensation Board claims totaled over $186 million in 2018139. The definitions of MSK injuries and disorders are inconsistent across the literature. MSK injuries can be defined as one-time events associated with trauma9 and are recognized as a leading health care problem140. Alternatively, MSK disorders can often be chronic and recurrent in nature, often developing over time with variability in frequency, severity and impact, leading to intermittent and episodic presentation of symptoms9,72,141. However, some sources use MSK disorders as an umbrella term in which acute and chronic injuries of the MSK system are categorized within142, while others simply define injuries as acute or chronic and do not define MSK disorders143. This lack of uniformity has made it difficult for researchers to define and categorize different types of injuries. Thus, for the sake of this review, MSK disorders will refer to both acute and chronic injuries. More than 150 different diagnoses are considered MSK disorders; all of which can limit mobility and function, further reducing ability to work and participate in social roles144. The onset of symptoms varies as they may be associated with activity or have an insidious or gradual onset141. The most common signs and symptoms include pain, inflammation, alterations in nerve conduction or other alterations of MSK structures145 such as restricted mobility144, altered posture146, muscle activity and recruitment147, and biomechanics and kinematics148. Examples of MSK disorders involving the neck-shoulder complex include, but are not limited to, myalgia (muscle pain), inflammatory conditions (e.g. rotator cuff tendinopathy, 27 subacromial bursitis, adhesive capsulitis, some of which may or may not be inflammatory), nerve damage or compression disorders (e.g. shoulder impingement), vascular compromise (e.g. thoracic outlet syndrome), repetitive chronic strain injuries (e.g. glenohumeral osteoarthritis, tension neck syndrome), and chronic spine disorders such as degenerative disc disease or spinal stenosis9,72,143 2.5.1 Work-Related Musculoskeletal Disorders The World Health Organization (WHO) reported that up to 33% of the world’s population are living with a painful MSK disorder, while other report as high as one in every two adults is living with a MSK disorder149. Musculoskeletal disorders are reported by more than 30% of working populations72, accounting for approximately one-third of all compensation claims9,10. Though the impact of MSK disorders is widespread, accurate data on the incidence and prevalence are often difficult to obtain72, perhaps due to discrepancies in reporting. However, as high as two-thirds of work-related disorders are reported to be MSK150,151. MSK disorders account for more worker absenteeism and disability than any other group of diseases72. Work-related musculoskeletal disorders can be induced or exaggerated by one’s job152. In 2018, more than 264 000 lost time claims were reported to the Association of Workers’ Compensation Boards of Canada (AWCBC), almost 230 000 of which were traumatic injuries or disorders153. According to the AWCBC, approximately 60 000 of those were neck or upper extremity injuries153. While some research demonstrates work-related musculoskeletal disorders affecting the shoulder, upper back, and neck as being the most common2, in 2019, the Workers Compensation Board of Ontario reported 5% of lost-time claims were due to shoulder injuries, 13% were low back, 11% were cranial, and 15% were multiple body parts154. Interestingly, claims by females were higher in the shoulder, cranial region, and multiple body parts, where more claims for men were in the low back and legs. A report by Statistics Canada in 2007 claimed hand and low back work- related injuries were the most common, representing 28% and 16%, respectively155. Many factors increase the risk of developing a musculoskeletal disorder, and though not solely caused by work, ergonomic work factors play a large role9,72. The WHO recognizes the impact of the work environment in work-related diseases and identifies it as a predominant and essential factor in their development156. High risk occupations have reported rates for MSK disorders three or four times that of other sectors72. These high-risk occupations involve highly 28 repetitive work, rapid changes in direction, forceful gripping, forceful or awkward movements, insufficient rest or recovery time, heavy or frequent lifting, and use of vibration tools9,10. Office jobs, where workers engage in highly repetitive tasks in prolonged static and awkward postures (e.g. using a computer for several hours), are one example of a high-risk occupation for the development of MSK disorders, particularly in the upper limb9,10. The consequences MSK disorders have on individuals are devastating. An inverse relationship between the severity of pain of work-related MSK disorders and concentration or focus has been demonstrated, which negatively effects productivity levels7. Additionally, work- related MSK disorders negatively impact rationality/mood, mobility, and stamina157, resulting in employees who are more likely to lose working days, retire early, or lose employment7,158. These outcomes have a detrimental impact on social and economic wellbeing for not only the affected individuals, but also their families72. 2.5.2 MSK Disorders in Office Jobs Work-related MSK neck-shoulder disorders are among the most commonly reported health problems in office workers2, as they are responsible for 40-50% of all work-related diseases costs159. More than 50% of Canadians experience neck pain within a 6-month period160, with more than five percent experiencing a new episode that is considered disabling and only one-third reporting complete resolution of their condition161. In fact, the annual prevalence rate of neck-shoulder pain is up to 72% of the general population, and up to 85% of those who experience pain will report neck pain again between the next one to five years162. The use of computers in the workplace has revolutionized the way work is completed, allowing employees to carry out multiple activities at a faster rate than ever before11. Over the last 50 years, this paradigm shift from more physically active jobs to more sedentary ones has had various health implications, including increased risk for the development of many diseases such as obesity, high cholesterol, osteoporosis, and cardiovascular disease163,164. Furthermore, office workers are among those who have a high prevalence of musculoskeletal disorders 2,12, as increased computer work is associated with many upper body disorders11,13,14. Prolonged computer work often allows for the adoption of awkward or non-neutral postures in the upper limb and neck (e.g. FSP), leading to increased rates of neck-shoulder MSK disorders as greater tissue loads are generated in this area10,35. In fact, computer use has been shown to be a risk factor for the development of neck-shoulder pain in office workers15–17. Neck 29 and shoulder posture are altered during computer use and may possibly influence posture outside of computer work165. Straker et al. (2007) found that even small variations in computer use posture, such as flexion in head, neck and thoracic spine (i.e. slumped posture) might lead to more permanent changes in habitual postures in both seated and standing positions through adaptive neuromusculoskeletal changes165. 2.5.3 Changes in Muscle Activity Due to MSK Disorders Numerous studies have looked at scapular stabilizer activity in uninjured versus injured or painful shoulders and determined the level of muscle activity change in the presence of shoulder pain or pathology. Generally, the literature agrees that individuals who experience shoulder pain or pathology have increased UT activity26,28–32,166,167, and decreased serratus anterior activity26–30 and MT and LT activity28,31,32. Interestingly, increased UT activity has also been demonstrated in those with FSP40 and greater UT activity and lesser LT activity is correlated with greater scapular posterior tipping and elevation32. However, conflicting reports exist regarding altered muscle activity in the MT and LT, as other literature has reported no difference in activity amongst injured shoulders168–170 while one study observed greater LT activity in those with shoulder impingement28. A study by Cools et al. (2004) observed significantly decreased LT activity in participants with injured shoulders compared to their non- injured side in a retraction movement171. In those with shoulder impingement, MT and LT demonstrated latent activation compared to healthy shoulders33. The authors noted that delayed LT activation may cause the UT hyperactivity, causing the overactivation to contribute more to scapular elevation rather than upward rotation. Moraes et al. (2008) found late recruitment of all scapular muscles (UT, MT, LT and SA) in those with impingement syndrome169. Several studies have examined the ratios of activity between the different regions of the trapezius and serratus anterior. In those with pathology, disruptions in these ratios have been reported, noting higher UT/LT and lower LT/SA ratios during arm elevation compared to healthy controls. The higher UT/LT ratio indicated greater UT activity relative to LT activity. The lower LT/SA ratio was dependent on ascending and descending phase, demonstrating the LT was more active than the SA during the descending phase but less active during the ascending phase in those with pathology172. Michener et al. (2016) discussed the deficiencies of the LT in these two ratios in individuals with subacromial pain syndrome, noting that it is possible that the LT is 30 intended to contract in coordination with other scapular muscles in order to produce normal shoulder motion that is pain-free172. While current literature has seldomly examined the scapular protractor to retractor ratio of activation, some research has examined a similar ratio but in power output instead of muscular activity. Cools et al (2004) observed a significantly lower protraction to retraction force ratio on injured shoulders compared to non-injured shoulders171. Similarly, Morales et al. (2008) examined the work ratio of concentric and eccentric muscle forces in the shoulder rotators during internal and external rotation169. Their results demonstrated no significant differences between injured vs. non-injured shoulders. 2.5.4 MSK Disorder Risk Factors While the etiology responsible for the development of neck-shoulder pain is known to be multifactorial, sustained work posture is one risk factor in the development of neck-shoulder pain7,8,173. Additionally, repetitive motion within daily tasks is consistently reported to contribute to the development of neck-shoulder pain173,174. Office work requires extended periods of time performing a repetitive motion (e.g. typing) in a work posture that requires little variability requiring the shoulder muscles to contract for prolonged periods of time16,175. Further, while sustained work posture and repetitive motion are two major risk factors in the development of neck-shoulder pain7,173,174, increased durations of computer work are a risk factor in the development of neck-shoulder pain13,15–17,176. 2.5.4a Sex Differences While computer use is a risk factor for the development of neck-shoulder pain15–17,176, being female is also a risk factor for neck-shoulder pain18. Interestingly, females hold a more upright seated position than males19 and spend less time using the computer20, yet report higher rates of neck-shoulder pain and musculoskeletal disorders21,22. Many sex differences have been noted in regard to anthropometrics such as body/tissue composition, structure, muscular strength, power and endurance, as well as other areas such as motor control, fatigue, stress reactions and pain23. Females have shown greater trapezius activity than males in identical repetitive work tasks relative to muscular capacity despite having similar postures, meanwhile reporting a higher prevalence of upper-body musculoskeletal disorders177. These variances in muscular activity and strength may be explained by the composition of female muscle tissue, as they tend to have more type I muscle fibres in general muscle 31 composition and the trapezius in comparison to males, making females more fatigue resistant than males24,178. These fibres are associated with smaller motor units25 and smaller cross- sectional area of muscle fibres18,178. Thus, in combination with type I fibres being traditionally weaker25, these muscles are required to increase muscular activity to perform similar tasks as males25, possibly indicating a lower functional capacity18,178 and prolonged activation periods that lead to injury23. Furthermore, low-load work demand primarily recruits and sustains activation of type I fibres and their low-threshold motor units25. It is hypothesized that muscular injury will occur due to the overload of these fibers and possible damage179. Collectively, these factors may explain the prevalence and mechanism of neck-shoulder pain in females25.

2.6 Forward Shoulder Posture (FSP)

FSP is one of the most common postural deviations with up to 73% of the healthy population demonstrating anterior translation of the shoulder complex from the lateral midline of the body34. It is characterized as abduction of the scapula and anterior deviation of the acromion process that alters the rotational axis of the glenoid fossa, causing an internal and upward rotation, and anterior tilt of the scapula37,180. Several factors may contribute to the development of FSP including static posture, muscle imbalances, soft tissue damage, or repetitive motion181– 187. Degree of FSP has been strongly negatively correlated to pectoralis minor resting length188 and those with FSP have demonstrated significantly greater pectoralis major muscle activity40. Individuals with FSP have increased electromyographic activity of UT and pectoralis major, and decreased serratus anterior and MT compared to those without FSP28,40. This suggests that the reduced activity within the serratus anterior and MT is offset by the increased activity within the upper trapezius28,189 which also acts to assist in stabilizing the head of the humerus due to altered scapular position38,39. Combined, these imbalances alter movement patterns within the glenohumeral joint, leading to decreased stability of the scapula38,114 and internally rotating the glenohumeral joint190. Furthermore, a protracted shoulder is suggested to result in excess strain of the anterior band of the inferior glenohumeral ligament, which results in glenohumeral joint instability in cadavers191. Interestingly, a study by Karagiannakis et al. (2018) assessed female volleyball players with resting scapular asymmetry and found no differences in SA, UT and MT electromyographic activity levels during a closed chain exercise in their dominant, protracted side compared to their non-dominant side192. 32

Shortened scapular protractors is the most common indication of the presence of FSP193. In theory, the adoption of static, non-neutral postural changes allow soft tissue on one side of the joint to adaptively lengthen, while the soft tissue on the opposite side will adaptively shorten36,37. In regards to FSP, the pectorals are adaptively shortened due to prolonged approximation of the muscle’s insertion points36,37,43, while the retractors (i.e. trapezius and rhomboids) experience adaptive lengthening36. Given the pectoralis minor’s attachments to the scapula and thorax, when adaptively shortened, it limits normal scapulothoracic motion and alters scapular position37,193, and may augment conditions that lead to the development of neck-shoulder pain193. This position predisposes the pectoral muscles to shortening37,194, and individuals with a tightened pectoralis minor tend to have an anteriorly tilted, downwardly rotated, protracted, and depressed scapula36,41–43. This position associated with a shortened pectoralis minor is projected to elongate and weaken its antagonist, the trapezius, and lead to the development of pain and pathology41,43,148,195,196. Sahrman (2002) proposed that the efficiency of muscular performance is dependent on their resting length, theorizing a mid-length positioning demonstrates the greatest efficiency for a muscle and its antagonist. When an agonist/antagonist relationship becomes imbalanced, such as in the pectorals and scapular stabilizers, theoretically, muscle performance is decreased43. Shortening of the scapular protractors is speculated to cause a reciprocal, inhibitory weakness of the scapular retractors44. Furthermore, comparison of isometric shoulder flexion strength was measured in a protracted, neutral, and retracted scapular position, determining that a protracted scapula had significantly reduced strength than either a neutral or retracted scapula197. The authors hypothesized this resulted from the protracted scapular (i.e. FSP) altering the length- tension relationship of the pectorals and scapular stabilizers, which affected other muscle function in the shoulder complex. This suggests that changes in scapular position observed with FSP alters activation within the scapular protractors and retractors that can impact muscle function of the upper limb. However, research has yet to explore this relationship188. Collectively, these changes lead to an altered scapulohumeral rhythm and kinematics, which impacts the body’s biomechanical system ability to efficiently produce movement43. Over time, exposure to monotonous tasks can produce pain as a response, predisposing individuals to shoulder pathologies such as glenohumeral joint instability, adhesive capsulitis, subacromial impingement syndrome, and rotator cuff pathology45. 33

A variety of techniques exist for clinicians and researchers to measure the presence of forward shoulder posture, including radiographic, goniometry, and photographic and digitization methods198 in addition to other methods requiring specific tools such as Baylor Square, Double- Square, and the Sahrmann Techniques199. However, the most commonly used and clinically relevant technique is the assessment of the lateral plumbline through visual observation198. While these techniques are able to detect the presence of FSP, the classification of degree of FSP is arbitrary. A study by Roddey, Olson, and Grant (2002) distinguished between mild and moderate FSP by determining the deviation of the acromion from the external auditory meatus, where <1cm was considered mild and >1cm was considered moderate46. Other techniques for quantifying FSP include measuring distance of the thoracic spine vertebrae to the medial border of the scapula180, or calculating a ratio between bony landmarks of the spine, acromion, and sternum37. Given the protractors’ length plays a fundamental role in FSP, it is indeed essential to measure the length of the pectorals. A variety of techniques exist in the current literature, many of which focus solely on measuring pectoralis minor. The pectoralis minor may be measured by landmarking the coracoid process and the edge of the fourth rib (the attachment points of the muscle) and measuring the distance with a soft measuring tape or caliper (often referred to as the pectoralis minor index)188,200. Another measurement described by Sahrmann (2002)43 is proposed to indirectly measure the pectoralis minor by measuring the distance of the acromion to the table while laying supine with and without pressure on the coracoid process. This test may possibly provide information regarding pectoralis minor extensibility, as applying pressure to the coracoid process has been shown to elongate the muscle similarly to 150° of shoulder flexion (Muraki 2009). While this measurement demonstrated excellent inter-rater reliability, it lacked validity and was not recommended to be used clinically as it may not distinguish between a normal and shortened pectoralis minor201. 2.6.1 Does Posture Really Matter? Despite the allegations of the role postural deviation plays in development pain and pathology, current literature still questions this association due to lack of hard evidence in high- quality, controlled studies. In addition, clinical researchers are now questioning the role posture 34 has in injury development more than ever, stating support for posture or movement screening as a primary prevention of pain in the workplace is unsubstantiated202. The ideal postural alignment as described previously74 is uncommon, and considered unrealistic by some34,203,204. Griegel-Morris et al. (1992) found that up to 73% of healthy subjects had rounded shoulders, and rounded shoulders were associated with interscapular pain but not shoulder pain34. Interestingly, subjects who were considered to have more severe postural abnormalities experienced a greater incidence of pain, but not necessarily frequency or severity of pain. Further, their research demonstrated many individuals with ‘normal’ posture had significant pain, yet some individuals with ‘severe’ postural deviations had minimal pain. Several studies have attempted to demonstrate the relationship between numerous postural variables and found no association, and great individual variability, between postural variables related to head position, thoracic spine, and forward shoulder posture113,205,206. Specifically, some research has evaluated FSP between symptomatic and healthy controls as equivocal206–208, and women have been found to have more rounded shoulders than men209. It is argued that neither asymptomatic nor symptomatic participants demonstrated postural habits that aligned with the ideal norm, and the discrepancy in the research regarding postural factors of pathological shoulders may be a result of, rather than predisposition to, pathology210. It has been proposed that rather than linking postural deviations to impairment, the focus should be on the relationship between postural deviations and movement dysfunction, where movement dysfunction may subsequently result in impairment43. Borstad (2006)37 investigated this posture-impairment connection, finding a connection between scapular malalignment (i.e. posture) and anatomical structure of the pectoralis minor. In participants with a shortened pectoralis minor resting length, increased scapular internal rotation and decreased scapular posterior tilting was found compared to those with longer resting lengths37; kinematics that are consistent with those who suffer shoulder pathology28,45,117,118. However, the author concludes that even though these findings are correlated, it cannot indicate a cause-and-effect relationship. Collectively, these findings beg the question: is the ideal postural alignment as recommended by Magee74 or Kendall36 feasible? What is considered a ‘clinical’ deviation from these plumb lines? Further, what degree of FSP, or deviation from this plumb line, is required for an individual to experience the kinematic changes that are consistent with shoulder pathology? To date, little research has investigated clinical degrees of forward shoulder posture, 35 and varying measurements are used to define what is considered true FSP. For example, Roddey et al. (2002)46 classified mild FSP as one centimeter or less of anterior deviation of the acromion from the plumb line, and moderate FSP as more than one centimetre. Using this same method, Lynch et al (2010)211 included participants with any anterior deviation from this plumb line. On the other hand, Sahrmann (2002)43 recommended a supine measurement of FSP which measures the distance from the posterior acromion to the table on which the participant lays, and a minimum measurement of 2.5 centimeters was required for the participant to be classified as having FSP. This method has been used by multiple researchers56,208. Various other measurements of FSP include standing acromion measurement to wall212, scapular abduction ratio54, and lateral photography assessment of anatomical landmarks, where forward shoulder angle is greater than 52°190,213. The lack of a uniform assessment and measurement of FSP contributes to skepticism of the impact of postural deviations from the recommended plumb line. It is suggested that both static and dynamic observation of scapular positioning be assessed in order to effectively evaluate shoulder function116, and that, when it comes to posture, one size does not fit all202. Lewis et al. (2005)210 discuss the clinical limitations of assessing shoulder posture in the sagittal plane, stating that an individual may have ‘faulty posture’ but be able to complete movements that are pain free and non-predisposing to pathology. While more research is needed to define the clinical degree of FSP, there is accumulating scientific evidence that supports the role faulty scapular posture has in shoulder pathology28,37,45,116–118.

2.7 Management of FSP

Traditional approaches to managing FSP include strategies aimed at restoring the balance of muscle activation and length between the scapular protractors and retractors to return the shoulder (anterior tip of the acromion) to a neutral position42,210. It is believed that this will result in a decreased risk of developing neck-shoulder pain by correcting the associated scapular position and movement dysfunctions. In general, this is thought to be accomplished by: strengthening inhibited, lengthened musculature (i.e. scapular retractors), and lengthening the shortened, hypertonic musculature (i.e. scapular protractors) and surrounding connective tissue (i.e. fascia)46,180. 36

2.7.1 Strengthening of Scapular Retractors The purpose of scapular retractor strengthening is to re-educate and condition the muscles that control and stabilize the scapula during movement, further improving scapular mechanics and force couples acting on the scapula214. This is done via specific exercises that target the scapular retractors, traditionally focusing on the lower and middle trapezius, serratus anterior, and rhomboids211. Exercises that target these muscles have been shown to not only activate and strengthen the musculature but establish scapular control in both symptomatic and asymptomatic populations215. Exercises such as shoulder external rotation, rows, D2 patterns (combination of shoulder flexion, horizontal abduction, and external rotation) and serratus punches have demonstrated a decrease in FSP in as little as six-weeks216. However, a review by Goodman and Hrysomallis (2001)217 question the use of resistance training alone of antagonist musculature to elicit adaptive shortening of muscle and postural changes. 2.7.2 Increasing the Length and Extensibility of the Scapular Protractors and Connective Tissue Methods used to address the length and extensibility of the scapular protractors and associated connective tissue include stretching and manual techniques. These techniques are thought to help to restore normal shoulder positioning by increasing the length and extensibility of muscles and their surrounding connective tissue through changes of viscoelasticity and structural properties such as actin-myosin cross-bridges. 2.7.2a Stretching One common method of lengthening the scapular protractors to reduce FSP is stretching36,42, including static, dynamic, ballistic, and proprioceptive neuromuscular facilitation218,219. These interventions are applied to increase the extensibility of the soft tissue crossing a joint by applying a tension50. Stretching results in direct or indirect changes in muscle stiffness: direct changes to the viscoelastic properties within the muscle or indirect, reflexive changes through muscle inhibition by decreasing actin-myosin cross-bridges52. Direct changes can also affect the tendons and connective tissues of the stretched area52. Studies have demonstrated the significant impact stretching the scapular protractors has on the degree of FSP46,220,221. Stretching scapular protractors once daily for two weeks has shown significant decreases in the degree of FSP in those with a moderate level of FSP46. A study by Viriyatharakij et al. (2017)220 demonstrated the effects of a combination of active scapular 37 retraction and a pectoralis minor stretch at 60° of scaption on pectoralis minor length and forward shoulder posture, as measured by supine acromial distance from a table in healthy participants. Their results indicated that those in the experimental group demonstrated greater increases and decreases in pectoral length and FSP, respectively, than the control group who sat in a chair instead of stretched220. Additionally, proprioceptive neuromuscular facilitation (PNF) style stretching has demonstrated decreased FSP following 3 consecutive weeks of 3 PNF sessions per week219. Williams, Laudner, and McLoda (2013)221 had 29 NCAA swimmers with asymptomatic shoulders complete either a focused stretch, gross stretch, or serve as controls. The focused stretch required a clinician to lift the pectoralis minor away from the thorax, while the gross stretch had the clinician horizontally abduct the participants arm and apply an overpressure. Significant immediate changes in pectoralis minor length were observed only with the gross stretch. In a cadaveric study, researchers tested the effect of three different stretches on pectoralis minor length222. Each cadaver had all three stretches performed three times in random order where each stretch was maintained for a minimum of 10-seconds until no increase or decrease in lengthening was observed. Change in pectoralis minor length was determined using displacement sensors mounted within the muscle fibres that detected lengthening or shortening of the muscle. One of the stretches applied was similar to the MFR intervention performed in the current study, as a posterior pressure was placed on the anterior shoulder at 0° of shoulder abduction. The other two stretches involved a posterosuperior force in 30° of shoulder flexion, and a posterior force to the proximal humerus while in 90° of shoulder abduction. The results demonstrated a significant difference in lengthening of pectoralis minor for all three stretches, though the first stretch that was the most similar to the current study’s technique observed significantly less lengthening as to the other two stretches by approximately 50%. Stretching has also demonstrated changes in muscle activity within an agonist/antagonist force couple. Blazevich et al. (2012) found that chronic stretching of the calf musculature (i.e. soleus and gastrocnemius) reduced peak amplitudes of muscle activity in those muscles during a voluntary dorsiflexion movement120. Furthermore, Janda, Frank, and Liebenson (1996) suggest that stretching a hypertonic muscle will increase muscular activity of an inhibited antagonist muscle. A study by Sandberg, Wagner, Willardson, and Smith (2012) investigated the effects of static stretching of antagonist musculature on multiple agonist strength and power measurements 38 in 16 men who consistently resistance train223. Participants stretched their hamstrings, hip flexors, and dorsiflexor muscle groups during the experimental visit prior to having knee extensor peak torque and vertical jump tests completed. Each participant completed a control visit one to three days later where they did not stretch prior to the same measurements being taken. The results indicated significantly greater torque in the knee extensors at 300°, and significant improvement in vertical jump height and power on days where the stretching was completed in comparison to the days where stretching was not completed. However, EMG muscle activity of the knee extensors showed no significant difference between stretching and non-stretching groups. Stretching the scapular protractors uses end ranges of motion of horizontal abduction in the shoulder to lengthen the tissues218,224; however, it is argued that this gross stretch technique puts unwanted stress on the anterior capsule and other lengthening techniques should be incorporated when possible225. 2.7.2b Manual Techniques A secondary strategy used by practitioners to address the length and extensibility of the scapular protractors in those with FSP is manual techniques. Manual therapy involves the application of pressure to a shortened muscle and its connective tissue to promote changes within the myofascial components, encouraging elongation of these structures51. A variety of manual techniques have been shown to increase range of motion226–228, and perhaps be more effective than traditional stretching229. Manual therapy is thought to change the resting length of tissues through plastic deformation and improves mobility by breaking up adhesions and restoring interstitial fluid content230. A study done by Hopper et al. (2005) evaluated the effectiveness of two different manual techniques on the hamstring length in female field hockey players with hamstring tightness. A total of 35 participants received either a classic massage intervention or dynamic soft tissue mobilization intervention. Both groups exhibited an increase in passive hamstring range of motion through straight leg raise and knee extension immediately following the treatment, though the authors note that these results were no longer present after 24 hours. Similar results were found by Crosman, Chateauvert, and Weisberg (1984) in females who were randomized to receive a massage therapy intervention in one leg while the other leg acted as the control. Range 39 of motion measurements were taken on both legs and they found significantly greater range of motion in the leg that received the intervention in comparison to the control leg. Massage techniques have additionally been shown to decrease muscle activity within the same muscle for the duration of a three or six-minute treatment231,232. However, this reduced muscle activity returned to baseline levels upon termination of treatment and demonstrated no facilitative or inhibitory effects during a five-minute post-treatment recovery period231. 2.7.2c Myofascial Release In response to micro-trauma (i.e. chronic strain), some believe that the fascial system experiences tightening, becoming restricted and less pliable, leading to poor biomechanics, altered structural alignment, and decrements in motor performance69. It is the connective tissue surrounding the muscle that is responsible for the mechanical properties of relaxed muscle48. Furthermore, fascial restrictions can allow the shortening of the surrounding muscle through the development of trigger points233, further limiting its functional length and generating malalignment of the joints which it attaches to69. The elastic properties of fascia allow it to experience lengthening. Myofascial release (MFR) is a group of manual therapy techniques widely practiced by musculoskeletal therapists where mechanical pressure is applied to fascia until deformation occurs, inducing elongation and softening of restricted fascia69. In addition, MFR increases the tissue temperature, which changes the viscosity of hyaluronic acid present in the fascia from an adhesive to lubricating quality85. In turn, these mechanisms reduce adhesions within the fascia and optimize fascial slide by reducing viscosity in order to improve function in corresponding muscles85, 234. This sustained pressure treatment can be performed by a therapist directly or indirectly, with tools, or by the person themselves (i.e. self-myofascial release)235. In general, MFR involves slower movement than classic massage, providing deeper pressure to a more concentrated area of tension236. Ercole et al. (2010) analyzed the required time for a MFR treatment to be applied in order to observe a change in fascial fibrosis (i.e. an increase in tissue mobility)as measured subjectively by the therapist70. Interestingly, they found that the increase in tissue mobility occurred at relatively the same time as the patient perceived a reduction of pain, which was at approximately 3.3 minutes70. Literature is inconsistent at demonstrating MFR’s effectiveness of both quality of research and results of a treatment235,237,238, though demonstrate encouraging results, especially 40 as an evolving treatment strategy238. Furthermore, little research demonstrating the acute effects of myofascial release within the upper body, specifically the shoulder joint, has been published239. Forms of MFR date back to Ancient Chinese Medicine where Gua Sha was used as a traditional healing technique for illnesses such as colds, fevers, and respiratory problems240. John Barnes, a leading pioneer in MFR, began teaching MFR seminars to other manual therapists in the 1970s241, and in the 1980s, the term “myofascial trigger point” first started being used by Dr. Travell104. Self-MFR (SMFR) is completed using the same principles, but often in combination with equipment such as a tool, foam rollers, myofascial stick, or sports ball (i.e. tennis, golf, or lacrosse ball)236. SMFR techniques to the pectoralis muscles have been shown to improve anterior scapular tilting242, while both practitioner and SMFR pectoral techniques have resulted in increased shoulder range of motion243. Furthermore, SMFR in combination with stretching infraspinatus exhibited significant improvements in shoulder internal rotation, external rotation strength, ratio of agonist (infraspinatus) to antagonist (pectoralis major and latissimus dorsi) muscle activity, and performance of a throwing task in softball players with glenohumeral internal rotation deficits244. Laudner, Compton, McLoda, and Walters (2014) examined the impact of an instrument assisted Graston technique delivered on the posterior shoulder on glenohumeral range of motion compared to a control group who did not receive any treatment227. Their results indicated those who received the treatment presented with increased glenohumeral horizontal adduction and internal rotation range of motion compared to the control group. Another study done by Laudner and Thorson (2020) demonstrated a SMFR of pectoralis minor significantly improved shoulder flexion, pectoralis minor length, and forward scapular posture compared to a placebo group225. Collectively, this suggests that MFR treatment in one area of the body is capable of modifying neuromuscular recruitment strategies of distant muscles and improve performance, range of motion, and FSP. Thus, while increasing the length of the pectoral myofascial complex is an important aspect of reducing the incidence and improving the rehabilitation of upper limb pathologies194,218,224, it is not currently known if practitioner administered MFR to the pectoral fascia improves shoulder posture or its associated neuromuscular abnormalities (i.e. altered activation patterns). 41

2.7.2d Combined Approaches Though each individual approach has demonstrated improvements of FSP as noted above, it is a combination approach that seems most effective in the treatment of FSP. Participants undergoing a rehabilitation regiment that included both stretching of the scapular protractors and strengthening of the scapular retractors experienced a reduction in FSP53,54 and improved shoulder kinematics187. A study by Kluemper, Uhl, and Hazelrigg (2006)53 implemented a six-week scapular protractor/retractor stretching and strengthening (respectively) program for 39 high school and college aged elite swimmers, half of which were assigned to a control group. Measurement of FSP was completed using the double-square method and was measured in both relaxed posture and upright military posture. Participants in the experimental group completed a stretching and scapular strengthening routine three times per week. Their results demonstrated a significant decrease in FSP in the experimental group compared to the control group after six weeks. Dewan et al. (2014)54 conducted a study that investigated the impact of a similar stretching-strengthening program in 38 asymptomatic individuals with FSP between the ages of 18-35. Participants were randomized into either an experimental group or control group, both of which completed the same stretching-strengthening program, but the experimental group also received a taping treatment thought to correct scapular position during each session. All participants completed 15 supervised stretching and strengthening sessions over the course of three weeks and were further randomly divided into two groups. Both experimental groups observed a decrease in scapular abduction (i.e. FSP). Similar results have been demonstrated in children245 and those with shoulder impingement syndrome216. Wang et al. (1999)187 had twenty asymptomatic individuals with FSP complete a combined stretching and strengthening protocol for 6-weeks where they were required to perform a pectoral stretch and four scapular strengthening exercises three times per week. Interestingly, isometric strength of external/internal rotation and horizontal abduction increased but resting scapular posture did not change187. Kaur and Jayaraman (2019)55 completed a 10 session strengthening protocol over two weeks with females with FSP. The participants were randomized to also receive an MFR treatment or complete stretching, both targeting pectoralis major and minor. FSP as well as muscle length of pectoralis major and minor were measured after the 10th day of intervention. 42

Both groups saw a significant decrease after the 10th treatment, with the MFR group exhibiting a significantly greater improvement than the stretching group. Other studies have demonstrated the effectiveness of combination rehabilitative programs involving manual therapy and stretching56–58. A study by Wong et al. (2010) randomized 28 participants with FSP into either an experimental group who received a soft-tissue mobilization and completed a specific stretch both to the scapular protractors; or a control group who received a passive placebo treatment and completed a non-specific stretch to a different muscle. The experimental group revealed greater immediate and delayed reduction in FSP compared to those in the control group. Similarly, programs incorporating scapular protractor manual techniques and stretching as well as scapular retractor strengthening have exhibited improvements in pain and disability within the shoulder complex57. A study by Bang & Deyle (2000) compared the impact of two intervention groups in 42 men and women with shoulder impingement syndrome on strength, pain, and function. The exercise group partook in scapular strengthening and stretching exercises while the manual therapy group received a manual treatment in addition to the exercises58. Though participants in both groups experienced a significant decrease in pain and increase in function, it was the manual therapy technique group that experienced a significantly greater improvement in these areas. Additionally, the manual therapy group saw significant increases in the strength component where the exercise group did not. The authors concluded that the superior treatment for this population was a combination of stretching, strengthening, and manual techniques.

3. Purpose Numerous studies have demonstrated the ability of an agonist contraction to cause a reciprocal reduction in activity within the antagonist musculature119,122,123,125. In those with FSP, it is assumed that the scapular protractors (i.e. pectorals) are shortened, hypertonic and theoretically contracted, leading to an increased state of activity within the musculature36,44. This will cause a reciprocal inhibition to their antagonist, the scapular retractors, causing them to be in a less active state and negatively altering the ratio of activity within this force-couple. If this is true, electromyographic data would exhibit greater levels of activity in the scapular protractors and smaller levels of activity within the scapular retractors in those with FSP in comparison to those without FSP. Moreover, elongating the hyperactive scapular protractors will return them to normal resting length, further decreasing the amount of active actin-myosin cross-bridges. This 43 proposed reduction in activity within the musculature would theoretically reduce reciprocal inhibition, leading to an increase of activity within the scapular retractors. However, this hypothesis has not been tested, making this concept purely theoretical. This gap that exists in the literature needed to be addressed to provide evidence for therapists performing these rehabilitative strategies who were taught on assumption that changes in scapular muscle activity will occur with pectoralis soft-tissue mobilization.

4. Objectives The objectives of the current study were to determine the impact of a 4-minute MFR to the pectoral fascia in individuals with FSP on: 1) FSP, 2) pectoral muscle length, and 3) individual muscle activity (upper, middle, and lower trapezius, pectoralis major), 4) the ratio of average muscle activity between the scapular retractors and protractors during a reaching task, and 5) movement performance (reaction time, movement time, and accuracy [constant error and variable error]) during a reaching task compared to a soft-touch, placebo treatment (control; CON).

5. Hypotheses I hypothesized that MFR will: 1) decrease FSP, 2) increase pectoral muscle length, 3) increase middle and lower trapezius activity and decrease upper trapezius and pectoralis major activity, 4) increase the scapular retractor to protractor muscle activity ratio during a reaching task, and 5) improve movement performance by decreasing reaction time, decreasing movement time, and decreasing constant and variable error, compared to CON.

6. Experimental Methods

6.1 Experimental Method

To achieve the objectives of the study, a within-subjects repeated measures crossover design was conducted. FSP and pectoral length were measured before and after two different treatment conditions (MRF and CON; Figure 6). Surface electromyography (EMG) of trapezius and pectoralis major, and movement performance were measured during a reaching task before and after the treatment conditions. Both treatment conditions (MFR and CON) were completed by an experienced (~19 years) Registered Massage Therapist (RMT) with specific training in 44

MFR. One treatment consisted of a four-minute MFR to the pectoral fascia (MFR), and the other treatment consisted of a four-minute “soft-touch” treatment that acted as a control (CON). The order of these experimental sessions was randomized and counterbalanced with a minimum of a 48-hour wash-out period between each.

6.2 Participants

A convenience sample of 26 right-hand dominant females were recruited from the student and faculty population at the University of Manitoba, and the surrounding community via posters and word of mouth. Based on the inclusion criteria, only 23 of those participants were eligible. In light of evolving COVID-19 research suspensions, only 18 participants (N=18; 27 years ± 10) completed both experimental sessions and were included in data analyses (Figure 7). This study was a part of a larger study that will recruit both males and females. Participants were assessed for eligibility through the following exclusion criteria via email prior to their first visit and were excluded if they reported any of the following: male, left-hand dominant, under the age of 18 or over the age of 60, a recent (<6 months) history of injuries or orthopedic disorders to the shoulder, upper back or neck (such as rotator cuff tears, whiplash, fractures), neurological (e.g. Epilepsy, Multiple Sclerosis, Parkinson’s Disease) or musculoskeletal disorders (e.g. Muscular Dystrophy, Myasthenia Gravis), or currently experiencing pain in the shoulder, upper back or neck. Potential participants were made aware that an additional inclusion criterion included the presence of FSP which could not be confirmed via email. Participants had the option of being assessed by the lead researcher for FSP prior to scheduling their first visit, or at the beginning of their first visit. Participants were asked to refrain from physical activity involving the upper body for 48-hours prior to each visit. 45

Figure 6: Schematic Representation of the Experimental Protocol.

(A) Participants were recruited and screened for eligibility based on the exclusion criteria and, if eligible, gave informed consent and completed a participant intake form. (B) Participants had the PRE-treatment measurements taken on the right side for forward shoulder posture (FSP) using the double square method (Figure 7), and pectoral length measurement (Figure 8). Bipolar electrodes for pectoralis major, upper trapezius, middle trapezius, and lower trapezius were then placed accordingly (Figure 9) and set up for surface electromyography (sEMG) collection. Four, five-second maximum voluntary isometric contractions (MVICs) of each the trapezius and pectoralis major were then completed with two minutes of rest in between each. After approximately two minutes, sEMG activity and movement performance data were collected while the participant completed a reaching task on a touch screen monitor (Figure 10), requiring them to reach towards one of five randomly appearing targets (Figure 11) for a total of 60 trials. (C) Participants were then randomized to receive one of two four-minute treatments: either a myofascial release to the right pectoral fascia (MFR), or a soft-touch control treatment (CON), completed by an experienced Registered Massage Therapist (RMT). (D) The RMT completed the appropriate treatment on the participant. (E) Participants then had the same measurements taken as the PRE-treatment measurement, apart from the MVICs (B). (F) Each participant underwent a washout period of a minimum of 48 hours between treatments (G). The PRE-treatment measurements were taken as previously completed during (B) prior to the second treatment condition, including MVICs. (H) Participants then crossed over from the treatment condition (MFR or CON) during their first visit to 46 receive the alternative treatment condition. (I) The same RMT who applied the first treatment during the first visit applied the second, alternative treatment (MFR or CON). (J) The same POST-treatment measurements were be taken for the fourth and final time as previously completed during (E).

47

Figure 7: Consort Diagram of Participant Recruitment and Experimental Protocol a) A total of 26 females were recruited to participate in the study, but 3 of which were excluded due to not meeting the inclusion criteria. b) Therefore, 23 female participants were randomized to receive either myofascial release (MFR) or soft-touch control (CON) for their first visit. c) 11 of the 23 received the MFR condition for their first visit and 12 received the CON. d) 18 of the 23 original participants attended a second session where they crossed over to receive the second of two conditions. e) 8 of the 12 participants who initially received CON completed their second session by receiving MFR and 10 of the 11 participants who initially received MFR completed their second session by receiving CON. f) All 18 participants who completed both experimental sessions were analyzed.

Participants were evaluated for the presence of FSP by visual observation of the participant’s right lateral plumb line (as previously described in section 2.2) by the lead researcher who is a Certified Athletic Therapist. The Athletic Therapist evaluated the anterior 48 position of the participant’s right acromion according to the lateral line of reference (Figure 5). This line should divide the body into front and back halves through the following anatomical landmarks: the external auditory meatus, the acromion process, and the high point of the iliac crest74. FSP was considered an anterior deviation of the acromion from this line by a minimum of one centimeter. Finally, participants completed the Participant Intake Medical Form (Appendix A) which was administered by the RMT to determine if the participant was eligible for treatment and if any considerations were needed (e.g. the presence of low blood pressure to advise the participant to sit up slowly after each treatment). Eligible participants received written and verbal details of the experimental procedures and potential risks involved in the study prior to signing an informed consent form approved by the Education/Nursing Research Ethics Board at the University of Manitoba (Appendix B).

6.3 Experimental Sessions

Each participant attended two experimental sessions (Figure 6). After being assessed for the presence of FSP at the beginning of their first session, participants then completed the participant intake form and consent form. The order of the treatments was randomized for each participant across the two experimental sessions and consisted of either 4-minutes of MFR (MFR) or soft-touch treatment (CON). Each participant completed one MFR session and one CON session with a minimum of a 48-hour washout period. All measurements were taken before (PRE) and after (POST) each treatment during both visits. These measurements included: FSP, pectoral length, EMG of the scapular protractors (pectoralis major) and retractors (upper, middle, and lower trapezius), and movement performance during a reaching task. Maximum voluntary isometric contractions (MVICs) of the trapezius and pectoralis major were performed prior to the PRE measurements during each visit to provide a maximal reference contraction in which muscle activity during the reaching task would be expressed as a percentage. 6.3.1 Forward Shoulder Posture (FSP) Measurement FSP was measured using the double-square method which has significant intrarater reliability 199 (Figure 8). Prior to measurement, the Athletic Therapist palpated the participant’s right anterior acromion and marked it with an “X” in permanent marker. Participants stood relaxed against a wall with their entire back touching the wall while the researcher used a 49 modified combination square (Swanson Tool Company 12-in Combo Square, Frankfurt, IL, United States) to measure the distance of the centre of the “X” on the anterior acromion of the right shoulder to the wall. The tool was modified to include a second square, one of which was flat against the wall, while the second was placed at the anterior surface of the acromion, at the centre of the marked “X”. This measurement (centimeters) was taken three separate times, where the participant was asked to take a step forward between each measurement and give their arms a shake to reduce the possibility of postural corrections. These measurements were converted to millimeters and the average of the three was used for statistical analysis.

Figure 8: Double-Square Method for Forward Shoulder Posture Measurement. Prior to taking the measurement, the participant’s right anterior acromion was marked with an “X” using a permanent marker. A combination square was modified by adding a second inversed square. The participant was instructed to stand up against the wall in a relaxed position (i.e. not pressing spine or shoulders up against the wall). (A) The modified combination square was then placed over the participant’s right shoulder with one flat end of the square pressed flat against the wall behind them. (B) The flat side of the second, inversed square was then moved along the ruler until it pressed against the centre of the marked “X” of the right anterior acromion process of the participant. (C) The measurement, in centimeters, was recorded and converted to millimeters. The participant was then asked to take a step forward, shake their arms, and then a step back to receive a second measurement completed in the same manner. This process was 50 repeated for a total of three measurements, converted to millimetres, and the average of the three measurements was used for statistical analysis. 6.3.2 Pectoral Muscle Length A measurement of the pectoral length was taken by measuring range of motion in horizontal abduction (Figure 9). Participants laid supine on a plinth with the right side of their torso lined up with the right side of the plinth. The participant was then instructed to bring their right shoulder and elbow to 90° of flexion. A meter stick held perpendicular to the ground by a custom base was placed beside the participant’s torso, approximately where the arm would abduct and the elbow would fall. The metre stick was placed vertically with the beginning of the measurement scale (i.e. zero) in contact with the floor. This resulted in a lower value indicating an increase in horizontal abduction range and thus, an increase in pectoral length. The participant was then asked to allow their arm to abduct off the table while keeping their elbow flexed at 90° (to mimic a pectoral stretch). The meter stick was used to measure the height of the inferior olecranon after the arm settled in abduction for ~2 seconds. The participant was then asked to horizontally adduct their arm back up to the starting position in flexion. This measurement (in centimeters) was repeated twice more, converted to millimeters, and the average of the three was used for statistical analysis.

Figure 9: Pectoral Length Measurement. (A) The participant laid supine on the table with the right side of their torso lined up with the right edge of the plinth and shoulder and elbow were flexed to 90°. (B) The participant horizontally abducted their right arm from this position to mimic a pectoralis major stretch. The participant was instructed to relax in this position. (C) A metre stick was placed perpendicular to 51 the ground using a custom made base and beside the right elbow (0 centimeters, CM at ground, 100 CM superior). (D) The metre stick was then used to measure the distance (in CM) from the ground to the elbow at the inferior olecranon. The participant was then instructed to adduct their arm back to 90° of shoulder flexion, then relax their arm back into horizontal abduction for the second measurement. This process was repeated for a total of three measurements, converted to millimetres, and the average of the three measurements was used for statistical analysis.

6.3.3 Muscle Activity - Surface Electromyography (sEMG) Surface electromyography (sEMG) of the upper (UT), middle (MT), and lower trapezius (LT), and pectoralis major (PEC) were measured during the reaching task using 4, semi- disposable pairs of bipolar electrodes (CDE-C, OT Bioelettronica, Torino, Italy). Electrode location was landmarked according to Surface Electromyography for the Non-Invasive Assessment of Muscles (SENIAM) Recommendations246,247 (Table 2). Prior to electrode application, the area was shaved with a disposable razor (if necessary), cleaned with an abrasive paste (Nuprep, Weaver and Company, Aurora, Colorado, USA), and wiped with an isopropyl alcohol swab (70%). The electrodes were then placed with each pair of electrodes running approximately parallel with the muscle fibres (Figure 10). The pectoral electrodes were outlined in permanent marker so they could be removed for the treatment and replaced in the exact position by the RMT following each treatment. A grounding reference strap was placed around the participant’s left wrist and on the C7 spinous process and connected to the Quattrocento bioelectrical signal amplifier (OT Bioelettronica, Torino, Italy). Raw data was collected using OT BioLab+ software (version 1.3.2, OT Bioelettronica, Torino, Italy) during the maximum voluntary isometric contractions (MVICs) and during a reaching task.

52

Table 1: Bipolar Electrode Placement for Upper, Middle, and Lower Trapezius, and Pectoralis Major.

Muscle Proximal Landmark Distal Landmark Details

Upper Trapezius C7 spinous process Acromion 50% of the distance between landmarks Middle Trapezius T5 spinous process Acromion 50% of the distance between medial border of scapula and the spine at T3 level in line with the landmarks Lower Trapezius T8 spinous process Superior Angle of the 2/3 of the distance Scapula from the superior angle to T8 Pectoralis Major Bipolar electrodes to be placed so that they run parallel to the middle sternal head muscle fibres; approximately 1 inch to the left from the sternum and 1 inch distal to the clavicle

Figure 10: sEMG Bipolar Electrode Setup for Pectoralis Major, Upper, Middle, and Lower Trapezius in Reaching Task. 53

A total of four pairs of bipolar electrodes were applied parallel to the muscle fibres of each participant’s right pectoralis major, upper trapezius, middle trapezius, and lower trapezius, according to SENIAM recommendations. Pectoralis major (A): the bipolar electrodes were applied to the sternal head of the pectoralis major between the right edge of the sternum and costal cartilages of ribs 1-6 and the greater tubercle (GT) of the right humerus. Upper trapezius (B): the electrodes were applied midway between the right acromion (AC) and C7, where a grounding electrode was placed. Middle Trapezius (C): the electrodes were placed half of the distance from the medial border of the scapula to T3, in the direction of T5 to the acromion. Lower Trapezius (D): the electrodes were placed 2/3 of the distance from the superior angle (SA) of the scapula to T8. A ground electrode was placed on C7 (E) and around the participant’s left wrist (F)

6.3.3a Maximum Voluntary Isometric Contractions (MVICs) Prior to completing the PRE measurement reaching task, each participant completed two sets of three maximum voluntary isometric contractions (MVICs). Participants first completed the trapezius MVIC followed by the pectoralis major MVIC. The maximum value obtained during the 3 repetitions for each muscle was used to serve as a maximal reference contraction that individual muscle activity would be expressed as a percentage of in the reaching task. For the trapezius MVIC, participants laid prone on a plinth and their right arm was placed in 120° of abduction. They were asked to hold a handle affixed to a weighted base using clips that allowed for adjustment of the length of the handle, to keep the arm abducted in the frontal plane. The participant was then instructed to pull the handle as hard as possible for five-seconds by pulling toward the ceiling (i.e. extension) and bringing their shoulder blades together. The researcher counted down from five at the beginning of each repetition and provided verbal encouragement during repetitions. Two-minutes of rest was provided between repetitions. This was repeated for a total of four repetitions, the first as a practice repetition, and the following three to be used for analysis of maximal activity. The contraction with the greatest maximal activity was used as the reference contraction for each individual muscle’s activity. This MVIC method was used for the trapezius as a recent report from our group demonstrated that this test position elicits the greatest activity in all three regions of the trapezius compared to test positions for the upper and middle trapezius248. The participant was then instructed to lay supine on the plinth where the same handle was placed in their right hand, adjusting the clips to keep their shoulder abducted to 90° and elbow straight in the frontal plane. The participant was instructed to perform the MVIC in the same manner as the trapezius MVIC, but to instead attempt to pull the handle up and across their body 54

(i.e. horizontal adduction or pec fly) as hard as they possibly could while focusing on using their pectoral muscle. The procedure was the same as for the trapezius. 6.3.4 Reaching Task The reaching task required participants to sit at a height adjustable workstation with a touchscreen monitor and microswitch in front of them (Figure 11). The participant sat on a stool adjusted so their hips were between 45-80° of flexion17 and feet were flat on the floor. The table’s height was adjusted so that the participants elbows were flexed around 80° as if working on a keyboard17. The participant was asked if the setup was comfortable, as if they were working at their own desk prior to proceeding. The monitor was set at a distance relative to the participant’s arm length so that when they reached to touch the centre of the monitor, their elbow would be at ~20° of flexion. A measuring tape was placed along the wall adjacent to the adjustable table, and a second measuring tape on the surface of the table under the monitor, to record each participant’s setup for their second visit. The stool remained at the shortest height for all participants as it did not need to be adjusted to accommodate any participant’s height. Prior to the second visit, the research assistant configured the experimental setup to be identical to the measurements taken from the first visit. Custom software designed in E-prime (v3.0 Psychology Software Tools Inc., Pittsburgh, PA, United States) was used to program the reaching task where participants were required to reach towards one of five randomly appearing targets. Before completing their first reaching task during the first experimental session, the participant completed a familiarization round with one of each of the targets. The program was designed to have five 1cm x 1cm boxes (Figure 12) appear in a random order, twelve times each, for a total of 60 targets. The location of the boxes was as follows: centre, top left, bottom left, top right, bottom right.

55

Figure 11: Reaching Task Setup. (A) Participants sat on a height adjustable stool adjusted so their feet were flat on the floor and their hips were flexed between 45-80°. (B) The stool was placed in an identical position for each participant as marked on the floor. (C) The participant sat on the stool that was placed in front of a height adjustable table and asked to put their hands flat onto the table. The table was raised or lowered to the height that was comfortable for the participant with their elbow flexed around 80°. (D) The table height measurement was recorded in order to replicate an identical setup for the second visit, as per the measuring tape on the wall. (E) A microswitch was embedded within the table near the closest edge of the table to the participant. (F) A touchscreen monitor was placed at a distance from the participant so that their elbow is flexed approximately 20° while reaching to touch the centre of the screen. The screen measurement was recorded in order to replicate an identical setup for the second visit, as per the measuring tape on the table.

56

Figure 12: Complete Target Setup for Reaching Task. The five targets that appeared were each 1cm x 1cm black boxes. The above figure demonstrates the position of all five targets as if they were to appear all at once. Each target appeared in random order, 12 times each for a total of 60 trials. The location of the boxes were as follows: centre, top left, bottom left, top right, bottom right.

Participants were instructed to press and hold a microswitch (Submini Snap Action Switch, Philmore Manufacturing, Rockford, Illinois, USA) key embedded on the table with their right hand. Once the microswitch was held, a “fixation” screen appeared before the presentation of one of the five possible targets. This screen remained there for a randomized time between 2000 and 2500 milliseconds so that the participant was unable to predict when the target would appear. The participant was instructed to release the microswitch once the target appeared and reach to press the centre of the target as quickly and accurately as possible using only their arm (i.e. not rotating at the trunk or swiveling on the stool). The release of the microswitch recorded reaction time (RT; time from target onset until release of microswitch) and movement time (MT; time from release of microswitch until touch of screen). Once the target was pressed, the screen prompted the participant to return to the microswitch and did not advance to the next fixation screen until the microswitch was held down. This process repeated for a total of 60 trials, or approximately four minutes. Each time the participant reached to touch the target, the x- and y- coordinates on the monitor were recorded by the E-prime program (in pixels) to measure end- point accuracy.

57

6.4 Treatment Conditions

6.4.1 Myofascial Release (MFR) The pectoral MFR treatment was completed by an experienced (~19 years) Registered Massage Therapist (RMT) with training and proficiency in MFR. Once PRE-measurements were taken, the bipolar electrodes were disconnected from the pre-amplifier. The three pairs of trapezius electrodes were left on the skin, but the pectoralis major electrodes were removed for the treatment conditions. Prior to removal, the electrodes were outlined in permanent marker, then placed back onto their plastic backings and given to the RMT to reapply after the treatment condition was completed. The MFR was performed to the pectoral fascia on the right side while the participant was positioned supine with arms resting at their side. Draping was secured underneath the posterior thorax and extended across a line at approximately the 4th rib (Figure 13A). The RMT stood on the participant’s right side slightly rotated to the left facing towards the participant’s left hip and applied a crossed-hand myofascial release technique to the superficial pectoral fascia (Figure 13B)249. The height of the hydraulic treatment plinth was adjusted so that it was at a similar height for all participants relative to the therapist’s height/treatment position and participants had a bolster placed under their knees. The same therapist applied the crossed-hand MFR technique to all participants. The contact area used on the therapist’s hands was the palmar surface, hypothenar and thenar eminences. The therapist began by placing the distal region of the anterior palm of the anchoring hand (therapist’s right hand) on the right edge of the anterior sternum at the level of the 3rd to the 6th ribs on the skin and the draping over the pectoral fascia. They then applied a gentle posterior pressure to “hold” the fascia in place. The therapist’s anchoring hand and fingers were directed to the participant’s left and were not in contact with the treatment area remaining elevated (i.e. not in contact with the skin or draping). The forearm of the mobilizing hand (therapist’s left hand) was directed to the right shoulder/elbow, with the right forearm crossing over top of the left allowing the distal region of the anterior palm of the mobilizing hand to contact the skin superficial to the pectoral fascia on the anterior aspect of the humerus, at the insertion point of the pectoralis major muscle. A light to moderate posterolateral pressure was applied to take up the slack within the fascial tissue without gliding, in order to apply a 58 mechanical stretch to elongate/mobilize the pectoral fascia. Participants were instructed to maintain normal breathing throughout the duration of the technique.

Figure 13: Treatment Condition Setup The participant was positioned supine with their arms by their side and the right pectoral region exposed. (A) The Registered Massage Therapist (RMT) secured the draping across approximately the 4th rib. (B) The RMT stood on the participant’s right side facing the participant’s left hip. The RMT applied a crossed-hand myofascial release technique to the superficial pectoral fascia by placing their right hand thenar/hypothenar eminences on the right edge of the anterior sternum from ribs 3-6 and their left hand thenar/hypothenar eminences on the anterior aspect of the humerus at the pectoralis major attachment. The right hand applied a gentle posterior pressure to “hold” the fascia, while the left hand applied a light to moderate posterolateral pressure to take up the slack in the fascia for the MFR treatment condition. For the CON treatment condition, the RMT assumed the same hand placements, but did not apply any pressure. This was held for four-minutes for both treatment conditions with the RMT wearing medical gloves.

According to Ercole et al. (2010), ~3.3 minutes of sustained pressure needs to be applied into a restricted tissue barrier to modify fascial fibrosis, therefore, the MFR intervention was 4- minutes in duration70. After the 4-minute intervention, the therapist slowly released the posterolateral pressure applied by the mobilizing hand (right) first and then removed the anchoring hand. 6.4.2 Soft-touch Control (CON) The soft-touch control (CON) treatment was completed by the same RMT for each participant. In order to control for changes that could result from therapeutic touch, the RMT completed a “soft-touch” treatment. Therapeutic touch is thought to act upon human energy fields250, providing therapeutic benefit by means of energy transfer by the therapist. The RMT 59 applied the CON treatment in the same method (i.e. draping, duration, participant and therapist position procedures) as the MFR, but did not apply the pressure required to mechanically stretch or elongate the pectoral facia. This control treatment would allow for differentiation in observed changes due to MFR or soft touch, determining if the benefits of the treatment were due to mechanical changes in tissue due to MFR or therapeutic touch.

6.5 Blinding

Blinding procedures were followed by the researchers and RMT to ensure single blinding of the researchers. A randomization chart was created by a third party using an online randomizer (Research Randomizer v 4.0, Social Psychology Network, Lancaster, PA, USA) that only the RMT had access to. The participant was informed that they would be receiving one of two treatments that would have different intensities of pressure; however, they would not be told which one they would be receive during each experimental session. The RMT educated the participant on what they may feel (e.g. discomfort, burning sensations) and informed them that the level of discomfort should not exceed 7/10. The participant was to notify the RMT if their pain or discomfort level reached a 7 or greater out of 10 (10 being the most intense amount of pain/discomfort they could tolerate). The removed electrodes were given to the RMT before beginning the treatment portion of the experimental session. The researcher and research assistants exited the room prior to the RMT preparing for or beginning the treatment to ensure total researcher blinding. After each treatment condition, the RMT reapplied the pectoralis major electrodes in the marker outlines on the participant’s anterior chest and asked the participant to put on a modified t-shirt that covered the pectoral area. The t-shirt was designed to cover the treatment area so that the researchers were unable to see any hyperemia (i.e. skin redness) that occurred as a result of the treatment, as we expected the MFR treatment condition to produce greater hyperemia. The t-shirt was modified to include a slit in the back to access all electrodes of the trapezius and ensure visibility of the acromion marker. The RMT ensured that the pectoralis major electrode wires were accessible to the researchers and that the acromion “X” mark was visible before the researchers re-entered. Upon conclusion of the POST measurements, the participant was asked to remove their pectoral electrodes to ensure blinding of the research assistants. 60

6.6 Data Processing

Data processing was performed by a blinded investigator prior to statistical analyses. 6.6.1 Electromyography (EMG) EMG signals were recorded and processed using a Dell laptop (Latitude 5500, Dell Canada, Toronto, ON, Canada), and acquired in a bipolar configuration for the trapezius and pectoralis major with a gain of 500, band-pass filtered (-3 dB bandwidth, 10-500 Hz), sampled at 2,048 samples/second, and digitally converted by a 16-bit A/D converter (Quattrocento, OT Bioelettronica, Torino, Italy). Signal differential spatial filtering were performed using OT Biolab + (OT Bioelettronica, Torino, Italy) and was digitally band-pass filtered at 30-500 Hz to remove electrocardiogram contamination from the EMG signal251. The root-mean-square (RMS) was calculated for the differential of each pair of bipolar electrodes. Data was exported from OT BioLab+ (version 1.3.2, OT Bioelettronica, Torino, Italy) as a .csv file in 0.001 epochs. Peak RMS for the last three repetitions of each MVIC were determined for each muscle/bipolar electrode pair. The highest of the three was used for relative reference for the RMS during the reaching task.

The release of the microswitch for each target sent a pulse to the EMG amplifier, marking the recording with the time the participant began their movement towards the target. That target trial’s MT recorded by E-prime was added to the marked beginning time for the respective target. This calculated timeframe for each target represented the beginning of the movement (i.e. release of the microswitch) to the touch of the target on the touch screen, which was the portion of the movement that muscle activity was analyzed from the trapezius and pectoral muscles. The average RMS for each muscle was calculated for each of the 60 targets individually, then averaged for the mean individual muscle activity, yielding a total of four average RMS values: one for UT, MT, LT, and PEC. These values were then divided by the respective muscles MVIC value to yield a percentage of activity for each muscle, which was used for statistical analysis. In addition, the mean scapular retractor (UT, MT, and LT) activity percentages were calculated and divided by the scapular protractor (PEC) activity percentage, providing a scapular retractor- protractor ratio (R/P) that was used for statistical analysis. 61

6.6.2 Movement Performance Constant and variable error for end-point accuracy were calculated. Constant error was calculated by adding or subtracting (depending on the target; Table 2) the true centre coordinates from the coordinates of the participant’s touch in both the X- and Y-axis. These calculations were determined so that a ‘short’ touch portrayed a negative value. To determine directional control in the X-axis, the mean constant error was calculated for both the left targets (top left and bottom left) and right targets (top right and bottom right). To determine amplitude control in the Y-axis, the mean constant error was calculated for the top targets (top left and top right) and bottom targets (bottom left and bottom right). Four values were used for statistical analysis of constant error of end-point accuracy: directional control in the X-axis for the left targets, directional control of the X-axis for the right targets, amplitude control in the Y-axis for the top targets, and amplitude control in the Y-axis for the bottom targets. Variable error was calculated by finding the standard deviation of the participants touch for each of the five targets in the X- and Y-axis; however, the mean was calculated using only four of the targets (top left, bottom left, top right, and bottom right). This was done to keep consistency between the constant and variable error measurements, as the centre target was not used for the calculation of constant error. Therefore, a total of two values were calculated and used for statistical analysis: variable error in the X-axis and variable error in the Y-axis.

Table 2: Target Centre Coordinates and Calculation of Constant Error. Target Centre X-axis Calculation Y-axis Calculation Coordinates Top Left (192, 108) 192 - participant touch 108 - participant touch

Bottom Left (192, 972) 192 - participant touch 972 - participant touch Centre (960, 540) 960 - participant touch 540 - participant touch

Top Right (1728, 108) Participant touch -1728 108 - participant touch Bottom (1728, 972) Participant touch -1728 972 - participant touch Right Constant error was calculated by subtracting or adding the true centre coordinates from the coordinates of the participant’s touch in both the X- and Y-axis, so that a short reaction was a negative value. Directional control was calculated by taking the average constant X-axis error for both left targets, then both right targets. Amplitude control was calculated by taking the average constant Y-axis error for both top targets, then both bottom targets. A total of four values were used for statistical analysis of constant error of end-point accuracy: directional control in the X- 62 axis for the left targets, directional control of the X-axis for the right targets, amplitude control in the Y-axis for the top targets, and amplitude control in the Y-axis for the bottom targets.

6.7 Statistical Analysis

Statistical analyses were performed using SPSS (25.0 for Mac, Chicago, Il, USA). A two- way (treatment*time) repeated measures two-tailed analysis of variance (ANOVA) was conducted to determine the effect of the independent variables (treatment condition [MFR or CON] and time [PRE and POST]) on dependent variables (forward shoulder posture, pectoral length, muscle activity, and movement performance). Significant interactions were followed up with a post-hoc T-test to determine main effects. In addition, a paired sample T-test analysis was conducted on the PRE-POST differences between MFR and CON treatment conditions on all dependent variables to confirm the significance of the ANOVA results (Appendix D). Before statistical analysis, normality of the data was determined using the Shapiro– Wilk test for normality. Data were considered normally distributed if p >.05. Data with deviations from normal distribution had two, two-way ANOVA analyses performed: one with the original data and one with a Log10 transformation applied to the data. If a Log 10 transformation was conducted, all data (PRE and POST of MFR and CON) for that variable analysis was transformed, even if it was considered normally distributed. A Log10 transformation was used on positively skewed data to compresses the upper tail and stretch the lower tail to conform to normality252. ANOVAs were run with the untransformed data, even if it did not fit the assumption of normality, to compare the results between the untransformed and transformed data. The untransformed data had few outliers, and due to the nature of the measurements, a positive skew is to be expected as the measurements are greater than zero. For example, muscle activity will not equal zero unless there is an equipment malfunction. Most participants’ average muscle activity will be grouped around the smallest recorded measurement of muscle activity with few participants measuring much greater than the grouped average; however, some participants may have muscle activity that is measured at a much greater level, yielding a positive skew. Thus, due to the nature of the measurements, ANOVAs were run on both untransformed and transformed data to interpret the effect the distribution may have on the results. Data were assumed to have met Mauchly’s test of sphericity as there were only two 63 levels of each independent variable. Outliers were considered to be studentized residuals greater than ±3 standard deviations253. The mean value of the 60 trials (for EMG activity and movement performance) for each condition (PRE and POST) and group (MFR and CON) was used for the statistical analyses. Individual trial outliers for muscle activity and movement performance variables were considered values that were greater than ±3 standard deviations from the mean. When a trial outlier was present, all variable data (muscle activity and movement performance) for that trial were removed from mean calculations and analysis (Appendix C). Differences in FSP, pectoral length, muscle activity (UT, MT, LT, PEC, and R/P), and movement performance (RT, MT, constant error [left directional control, right directional control, top amplitude control, bottom amplitude control], and relative error [X- and Y- axis standard deviation]) between groups (MFR and CON) and time (PRE and POST) were determined using separate 2-way repeated measures analysis of variance (ANOVA). Significant differences were followed by post-hoc Bonferroni corrected t-tests. The Bonferroni test reduced the chance of a Type I error by reducing the p- value. Results were reported as mean and standard deviation (SD). Statistical significance was accepted at p < 0.05. The minimum effect size representing an effect was considered n2= 0.04, a moderate effect size was considered n2= 0.25, and a large was considered n2= 0.64254. To determine the reliability of the FSP double square measurement, pectoral length measurement, and MVICs, an intraclass correlation coefficient (ICC) was calculated using the individual participants’ repeated PRE measures. A two-way mixed model absolute agreement was used for analysis of each ICC. ICC values less than .5 were considered poor, .5 to .75 were considered moderate, .75 to .9 were considered good, and values > .9 were indicative of excellent reliability253. A secondary Pearson Correlation analysis was conducted on PRE- and POST- changes in FSP and pectoral length to determine the relationship between the two dependent variables. Statistical significance was accepted at p< .05 and r values of < .3 were considered small, .3 to .5 were considered moderate, and > .5 were considered strong correlations. Individual participant change percentages were calculated using the original data (non- transformed) for each dependent variable by dividing the POST value by the PRE value, multiplying by 100 and subtracting that number from 100 to yield the change. 64

The required sample size for the study was calculated using an a priori power analysis. Using pilot results and G*Power (3.1.9.3, Faul, Erdfelder, Lang, & Buchner, 2007), alpha was set at 0.05 and power was set at 0.8. The number of groups was set to 1, the number of measurements was set to 4, and effect size was set to a medium size at n2=0.06. The calculation yielded a sample size required of 60 participants. Additionally, a post-hoc a priori analysis was done on each dependent variable to determine the sample size required to reach != .8 using G*Power (3.1.9.3, Faul, Erdfelder, Lang, & Buchner, 2007). While an a priori test should not be conducted post-hoc, post-hoc analyses does not indicate sample size required to reach != .8 given the pilot study’s findings. Thus, post-hoc a priori power analyses were done to determine the required sample size required to attain 80% power using != .8 and the effect size (n2) for each dependent variable.

7.0 Results The results of the two-way repeated measures ANOVAs are presented in Table 3 and change percentages are found on Table 4. Achieved power and effect sizes (η2 and d) are in Table 5. The results of the paired T-tests of the PRE and POST differences of each the MFR and CON resulted in the same p-value as the ANOVAs for each variable and can be found in Appendix D. The post-hoc a priori sample size calculation can be found in Appendix E. Individual participant dependent variable means can be found in Appendix F. 65

Table 3: Mean and Standard Deviations of PRE- and POST- MFR and CON Conditions (N= 18).

MFR CON ANOVA VARIABLE PRE Mean (SD) POST Mean (SD) PRE Mean (SD) POST Mean (SD) f p-value η2 FSP (MM) 124 (15) 118 (14) 124 (15) 122 (15) 6.66 0.019* 0.282 PECTORAL 601 (44) 588 (44) 595 (52) 597 (42) 2.162 0.16 0.113 LENGTH (MM) MUSCLE ACTIVITY UT (MV) 1.57 (1.07) 1.59 (1.08) 1.81 (1.38) 1.82 (1.41) 0.001 0.971 0 UT TRANSFORMED .10 (.29) .10 (.30) .17 (.26) .16 (.29) 0.157 0.697 0.009 MT (MV) 1.15 (.85) 1.14 (.90) 1.26 (.90) 1.16 (.76) 0.761 0.395 0.043 MT TRANSFORMED -.04 (.29) -.04 (.29) -.02 (.26) -.01 (.25) 0.674 0.423 0.038 LT (MV) 2.15 (.93) 2.25 (1.09) 1.90 (.80) 1.88 (.83) 1.317 0.267 0.072 LT TRANSFORMED .29 (.19) .30 (.24) .25 (.17) .24 (.17) 0.162 0.692 0.009 PEC (MV) 4.02 (2.26) 4.47 (2.49) 4.53 (2.98) 5.06 (3.66) 0.047 0.831 0.003 PEC .54 (.25) .58 (.27) .56 (.30) .59 (.33) 0.12 0.734 0.007 TRANSFORMED R/P (A.U.) .47 (.24) .45 (.30) .50 (.35) .46 (.32) 0.097 0.759 0.006 R/P TRANSFORMED -.37 (.20) -.41 (.24) -.38 (.26) -.41 (.28) 0.003 0.954 0 *Continued on next page 66

MFR CON ANOVA VARIABLE PRE Mean (SD) POST Mean (SD) PRE Mean (SD) POST Mean (SD) f p-value η2 MOVEMENT PERFORMANCE RT (MS) 315 (30) 309 (31) 309 (27) 306 (26) 0.304 0.589 0.018 RT TRANSFORMED 2.50 (.04) 2.49 (.04) 2.49 (.04) 2.48 (.04) 0.325 0.576 0.019 MvT (MS) 343 (103) 339 (93) 338 (94) 344 (96) 1.721 0.207 0.092 MvT 2.52 (.12) 2.52 (.11) 2.52 (.11) 2.52 (.12) 1.614 0.221 0.087 TRANSFORMED CEL (PIXELS) -10 (8) -8 (6) -10 (7) -8 (7) 0.005 0.945 0 CER (PIXELS) -7 (6) -6 (6) -8 (7) -6 (6) 0.497 0.49 0.028 CET (PIXELS) 7 (6) 5 (5) 6 (5) 6 (8) 0.213 0.65 0.012 CEB (PIXELS) 17 (6) 17 (6) 19 (7) 20 (7) 0.136 0.717 0.008 VEX (PIXELS) 17 (5) 17 (4) 18 (4) 17 (4) 0.156 0.698 0.009 VEY (PIXELS) 19 (6) 19 (5) 21 (5) 19 (4) 1.41 0.251 0.077 MFR- myofascial release; CON- soft-touch control; MFR- myofascial release; CON- soft-touch control; FSP- forward shoulder posture; UT- upper trapezius; MT- middle trapezius; LT- lower trapezius, PEC- pectoralis major; R/P- scapular retractor to protractor ratio of activity. Transformed variable- not normally distributed and therefore used log10 transformation. RT- reaction time; MvT- movement time; CEL- constant error left targets; CER- constant error right targets; CET constant error top targets; CEB- constant error bottom targets; VEX- variable error x-axis; VEY- variable error y-axis. Transformed variable- not normally distributed and therefore used log10 transformation.

67

Table 4: Percent Change from PRE to POST MFR and CON of Individual Participant Means.

Outcome Variable % change % change MFR CON FSP 4.7% decrease 1.1% decrease Pectoral Length 1.9% increase 0.5% decrease

Muscle Activity UT 1.1% increase 0.8% increase MT 0.9% decrease 3.8% decrease LT 2.2% increase 0.5% decrease PEC 20.9% increase 9.0% increase R/P 2.5% decrease 7.1% decrease Movement Performance RT 1.8% decrease 1.0% decrease MvT 0.8% decrease 1.9% increase CEL 20.3% increase 87.6% increase CER 16.5% increase 25.6% decrease CET 82.3% increase 128.8% increase CEB 42.5% increase 12.6% increase VEX 3.9% increase 0.3% increase VEY 4.5% increase 4.0% decrease MFR- myofascial release; CON- soft-touch control; FSP- forward shoulder posture; UT- upper trapezius ; MT- middle trapezius; LT- lower trapezius, PEC- pectoralis major; R/P- scapular retractor to protractor ratio of activity; RT- reaction time; MvT- movement time; CEL- constant error left targets; CER- constant error right targets; CET constant error top targets; CEB- constant error bottom targets; VEX- variable error x-axis; VEY- variable error y-axis.

7.1 Forward Shoulder Posture

There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). With a sample size of n=18 the observed power for this dependent variable was ß= .682 with an effect size of "2= .282, indicating the measurement of FSP was not adequately powered and achieved a moderate effect size254 (Table 2). 68

There was a statistically significant two-way interaction between treatment and time, F(1, 17) = 6.66, p = .019, partial η2= .282 (Figure 14). Therefore, simple main effects were explored by conducting T-tests. A post-hoc Bonferroni pairwise comparison revealed a significant decrease in FSP from PRE MFR (124 ± 4 mm) to POST MFR (118 ± 3 mm), F(1, 17)= 18.19, p= .001, a difference of 6 (95% CI, 3 to 9) mm. FSP was also statistically significantly different in the POST MFR (118 ± 3 mm) compared to POST CON (122 ± 4 mm), F(1, 17)= 4.484, p= .049, a difference of 4 (95% CI, 0 to 8) mm. There was no statistically significant difference in the PRE MFR to PRE CON, a difference of 1 (95% CI, -3 to 4) mm, p= .762, or PRE CON to POST CON, a difference of 1 (95% CI, -1 to 4) mm, p= .201.

Figure 14: FSP before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N=18. mm=millimeter 7.2 Pectoral Length

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for this measurement was ß= .284, making the sample size underpowered. The effect size of the interaction effect was η2= .113, indicating a small-moderate effect size254. 69

There was no statistically significant two-way interaction between treatment and time, F(1, 17)= 2.162, p= .160, partial η2= .113 (Figure 15). The main effect for treatment on pectoral length was not significant, F(1, 17) = .063, p= .805, partial η2= .004, a difference of 1 (95% CI, - 10 to 13) mm. The main effect for time on pectoral length was not significant, F(1, 17) = 1.533, p= .233, partial η2= .083, a difference of 5 (95% CI, -4 to 15) mm.

Figure 15: Pectoral length before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N=18. mm=millimeters

7.3 Muscle Activity

7.3.1 Upper Trapezius (UT)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE MFR p= .017, POST MFR p= .012, PRE CON p= .000, and POST CON p= .001. The observed power for the UT activity was ß= .050 with an effect size of "2= 0, indicating an overwhelmingly underpowered sample. 70

There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .001, p= .971, partial η2= .000 (Figure 16). The main effect for treatment on UT activity was not significant, F(1, 17)= 1.289, p= .272, partial η2= .070, a difference of .237 (95% CI, -.203 to .676) mV. The main effect for time on UT activity was not significant, F(1, 17)= .016, p= .901, partial η2= .001, a difference of .009 (95% CI, -.148 to .167) mV. Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. Some data was not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE CON p= .012. Data that was normally distributed as assessed by Shapiro-Wilks test of normality on the studentized residuals were: PRE MFR p=.852, POST MFR p=.598, and POST CON p=.447. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .157, p= .697, partial η2= .009. The main effect for treatment on UT activity was not significant, F(1, 17) = 1.910, p= .185, partial η2= .101, a difference of .062 (95% CI, -.033 to .156) mV. The main effect for time on UT activity was not significant, F(1, 17) = .187, p= .671, partial η2= .011, a difference of .007 (95% CI, -.026 to .040) mV.

PRE and POST Trapezius Activity

UT MT LT

Treatment Condition

Figure 16: Upper (UT), middle (MT), and lower trapezius (LT) activity before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N=18. mV= millivolts

71

7.3.2 Middle Trapezius (MT)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE MFR p= .002, POST MFR p=.001, PRE CON p= .001, and POST CON p= .000. The observed power for the middle trapezius activity was ß = .131 with an effect size of "2= .043, indicating an underpowered sample with a small magnitude of change254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .761, p= .395, partial η2= .043 (Figure 16). The main effect for treatment on MT activity was not significant, F(1, 17)= .292, p= .596, partial η2= .017, a difference of .062 (95% CI, -.182 to .308) mV. The main effect for time on MT activity was not significant, F(1, 17)= 1.643, p= .217, partial η2= .088, a difference of .051 (95% CI, -.033 to .135) mV. Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. The data were normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05). There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .674, p= .423, partial η2= .038. The main effect for treatment on MT activity was not significant, F(1, 17) = .916, p= .352, partial η2= .051, a difference of .045 (95% CI, -.054 to .145) mV. The main effect for time on MT activity was not significant, F(1, 17) = 1.231, p= .283, partial η2= .068, a difference of .018 (95% CI, -.016 to .051) mV.

7.3.3 Lower Trapezius (LT)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. Some of the data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE CON p= .016, and POST CON p= .005. The data that was normally distributed as assessed by Shapiro-Wilk’s test of normality on the studentized residuals were: PRE MFR p=.134 and POST MFR p= .323. The observed power for the lower trapezius activity was ß = .192 with an effect size of "2= .072, indicating an underpowered sample with a small magnitude of change254. 72

There was no statistically significant two-way interaction between treatment and time, F(1, 17)= 1.317, p= .267, partial η2= .072 (Figure 16). The main effect for treatment on LT activity was not significant, F(1, 17)= 1.821, p= .195, partial η2= .097, a difference of .311 (95% CI, -.175 to .798) mV. The main effect for time on LT activity was not significant, F(1, 17)= .570, p= .461, partial η2= .032, a difference of .043 (95% CI, -.077 to .162) mV. Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. The data were normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p > .05). There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .162, p= .692, partial η2= .009. The main effect for treatment on LT activity was not significant, F(1, 17) = 1.166, p= .295, partial η2= .064, a difference of .051 (95% CI, -.049 to .150) mV. The main effect for time on LT activity was not significant, F(1, 17) = .010, p= .923, partial η2= .001, a difference of .001 (95% CI, -.024 to .026) mV.

7.3.4 Pectoralis Major

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. Some of the data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE CON p= .022, and POST CON p= .017. The data that was normally distributed as assessed by Shapiro-Wilk’s test of normality on the studentized residuals were: PRE MFR p= .123 and POST MFR p= .262. The observed power for the pectoralis major was ß = .055 with an effect size of "2= .003, indicating and underpowered sample with no magnitude of change. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .047, p= .831, partial η2= .003 (Figure 17). The main effect for treatment on pectoral activity was not significant, F(1, 17)= .892, p= .358, partial η2= .050, a difference of .550 (95% CI, -.679 to 1.778) mV. The main effect for time on pectoral activity was not significant, F(1, 17)= 3.946, p= .063, partial η2= .188, a difference of .490 (95% CI, -.030 to 1.010) mV. Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. The data were normally distributed, as 73 assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p > .05). There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .120, p= .734, partial η2= .007. The main effect for treatment on PEC activity was not significant, F(1, 17) = .099, p= .757, partial η2= .006, a difference of .017 (95% CI, -.097 to .131) mV. The main effect for time on PEC activity was not significant, F(1, 17) = 2.269, p= .150, partial η2= .118, a difference of .036 (95% CI, -.085 to .014) mV.

Figure 17: Pectoralis major activity before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N=18. mV= millivolts

7.3.5 Scapular Retractor-Protractor Ratio of Activity (R/P)

There was one outlier, as assess by examination of studentized residuals for values greater that ±3 standard deviations: a POST MFR measurement with a studentized residual of 3.41. The data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE MFR p= .009, POST MFR p= .001, PRE CON p= .001, and POST CON p= .003. The observed power for the scapular retractor to protractor ratio of activity was ß =.060 with an effect size of "2= .006, indicating a severely underpowered sample with an extremely small effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .097, p= .759, partial η2= .006 (Figure 18). The main effect for treatment on R/P was 74 not significant, F(1, 17)= .128, p= .724, partial η2= .008, a difference of .022 (95% CI, -.151 to .107) A.U.. The main effect for time on R/P was not significant, F(1, 17)= .1.209, p= .287, partial η2= .066, a difference of .028 (95% CI, -.026 to .081) A.U..

Figure 18: Scapular retractor to protractor ratio of activity before (PRE) and after (POST) 4- minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N=18. A.U.= arbitrary units

Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. The data were normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p > .05). There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .003, p= .954, partial η2= .000. The main effect for treatment on R/P was not significant, F(1, 17) = .007, p= .936, partial η2= .000, a difference of .005 (95% CI, -.114 to .123) A.U.. The main effect for time on R/P was not significant, F(1, 17) = 2.576, p= .127, partial η2= .132, a difference of .038 (95% CI, -.012 to .089) A.U.. 7.4 Movement Performance

7.4.1 Reaction Time (RT)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. Some of the data were not normally distributed, as assessed 75 by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE CON p= .008, and POST CON p= .004. The data that was normally distributed as assessed by Shapiro-Wilk’s test of normality on the studentized residuals were: PRE MFR p= .093 and POST MFR p= .062. The observed power for RT was ß =.082 with an effect size of "2= .018, indicating an underpowered sample with an extremely small effect size254.

Figure 19: Reaction time before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N= 18. ms= milliseconds

The main effect for treatment on RT was significant, F(1, 17)=8.002 , p= .012, partial η2= .320, a difference of 5.001 (95% CI, 1.271 to 8.730) ms. The main effect for time on RT was not significant, F(1, 17)=3.792, p= .068, partial η2= .182, a difference of 4.746 (95% CI, -.396 to 9.889) ms. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .304, p= .589, partial η2= .018 (Figure 19). Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. Some of the data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE CON p= .017, and POST CON p= .006. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .325, p= .576, partial η2= .019. The main 76 effect for treatment on RT was significant, F(1, 17) = 7.737, p= .013, partial η2= .313, a difference of .007 (95% CI, -.002 to .012) ms. The main effect for time on RT was not significant, F(1, 17) = 4.224, p= .059, partial η2= .199, a difference of .007 (95% CI, .000 to .014) ms. 7.4.2 Movement Time (MvT)

There was one outlier, as assessed by examination of studentized residuals for values greater that ±3 standard deviations: PRE CON with a studentized residual of 3.14. Some of the data were not normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p < .05): PRE MFR p= .011, and PRE CON p= .011. The data that was normally distributed as assessed by Shapiro-Wilk’s test of normality on the studentized residuals were: POST MFR p= .086 and POST CON p= .095. The observed power for MT was ß =.236 with an effect size of "2= .092, indicating an underpowered sample with small-moderate effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= 1.721, p= .207, partial η2= .092 (Figure 20). The main effect for treatment on MvT was not significant, F(1, 17)= .000, p= .991, partial η2= .000, a difference of .087 (95% CI, - 15.346 to 15.521) ms. The main effect for time on MvT was not significant, F(1, 17)=.037, p= .850, partial η2= .002, a difference of .816 (95% CI, -8.125 to 9.757) ms. Due to the violation of the assumption of normality, a log10 transformation was performed on the data. There were no outliers, as assessed by examination of studentized residuals for values greater than ±3 standard deviations. The data were normally distributed, as assessed by Shapiro-Wilk’s test of normality on the studentized residuals (p > .05). There was no statistically significant two-way interaction between treatment and time, F(1, 17)= 1.614, p= .221, partial η2= .087. The main effect for treatment on MvT was not significant, F(1, 17) = .011, p= .919, partial η2= .001, a difference of .001 (95% CI, -.018 to .017) ms. The main effect for time on MvT was not significant, F(1, 17) = .105, p= .750, partial η2= .006, a difference of .002 (95% CI, -.012 to .008) ms.

77

Figure 20: Movement time before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment (individual and group means). N= 18. ms= milliseconds

7.4.3 End Point Accuracy

7.4.3a Constant Error X-Axis Left Targets (CEL)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for CEL was ß =.051 with an effect size of "2= .00, indicating an underpowered sample with an undetectable magnitude of change. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .005, p= .945, partial η2= .000 (Figure 21). The main effect for treatment on CEL was not significant, F(1, 17)= .087, p= .772, partial η2= .005, a difference of .283 (95% CI, -1.741 to 2.307) pixels. The main effect for time on CEL was not significant, F(1, 17)= 1.185, p= .291, partial η2= .065, a difference of .1.425 (95% CI, -4.185 to 1.336) pixels. 78

Figure 21: X-axis constant error before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment for the left and right targets (individual and group means). N= 18.

7.4.3b Constant Error X-Axis Right Targets (CER)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for CER was ß =.102 with an effect size of "2= .028, indicating an underpowered sample with a very small effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .497, p= .490, partial η2= .028 (Figure 21). The main effect for treatment on CER was not significant, F(1, 17)= .000, p= .997, partial η2= .000, a difference of .003 (95% CI, -1.558 to 1.564) pixels. The main effect for time on CER was not significant, F(1, 17)= 2.435, p= .137, partial η2= .125, a difference of 1.558 (95% CI, -.548 to 3.665) pixels.

79

7.4.3c Constant Error Y-Axis Top Targets (CET)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for CET was ß =.072 with an effect size of "2= .012, indicating an underpowered sample with a very small effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .213, p= .650, partial η2= .012 (Figure 22). The main effect for treatment on CET was not significant, F(1, 17)= .019, p= .893, partial η2= .001, a difference of .171 (95% CI, -2.461 to 2.803) pixels. The main effect for time on CET was not significant, F(1, 17)=.354, p= .560, partial η2= .020, a difference of .625 (95% CI, -1.591 to 2.840) pixels.

Figure 22:Y-axis constant error before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment for the top and bottom targets (individual and group means). N= 18.

7.4.3d Constant Error Y-Axis Bottom Targets (CEB)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for CEB was 80

ß =.064 with an effect size of "2= .008, indicating an underpowered sample with a very small effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .136, p= .717, partial η2= .008 (Figure 22). The main effect for treatment on CEB was significant, F(1, 17)= 7.938, p= .012, partial η2= .318, a difference of 2.787 (95% CI, .700 to 4.873) pixels. The main effect for time on CEB was not significant, F(1, 17)= .288, p= .598, partial η2= .017, a difference of .646 (95% CI, -3.185 to 1.893) pixels.

7.4.3e Variable Error X-Axis (VEX)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for VEX was ß =.066 with an effect size of "2= .009, indicating an underpowered sample with an extremely small effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= .156, p= .698, partial η2= .009 (Figure 23). The main effect for treatment on VEX was not significant, F(1, 17)= .473, p= .501, partial η2= .027, a difference of .423 (95% CI, -.875 to 1.720) pixels. The main effect for time on VEX was not significant, F(1, 17)= .098, p= .758, partial η2= .006, a difference of .162 (95% CI, =.929 to 1.253) pixels. 81

Figure 23: Variable error before (PRE) and after (POST) 4-minutes of myofascial release (MFR) or soft-touch control (CON) treatment for X- and Y- axes (individual and group means). N= 18.

7.4.3f Variable Error Y Axis (VEY)

There were no outliers, as assessed by examination of studentized residuals for values greater that ±3 standard deviations. The data were normally distributed, as assessed by Shapiro- Wilk’s test of normality on the studentized residuals (p > .05). The observed power for VEY was ß =.202 with an effect size of "2= .077, indicating an underpowered sample with small effect size254. There was no statistically significant two-way interaction between treatment and time, F(1, 17)= 1.410, p= .251, partial η2= .077 (Figure 23). The main effect for treatment on VEY was not significant, F(1, 17)= 1.180, p= .293, partial η2= .065, a difference of .787 (95% CI, - .741 to 2.314) pixels. The main effect for time on VEY was not significant, F(1, 17)= .738, p= .402, partial η2= .042, a difference of .568 (95% CI, -.827 to 1.964) pixels.

82

Table 5: Achieved Power and Effect Sizes

Outcome Variable Achieved Effect Size Power

ß η2 d FSP .682 .282 .608 Pectoral Length .284 .113 .347 Muscle Activity UT .050 .000 .009 MT .131 .043 -.206 LT .192 .072 -.270 PEC .055 .003 .051 R/P .060 .006 -.074 Movement Performance RT .082 0.018 .130 MvT .236 0.092 .309 CEL .051 0 .017 CER .102 0.028 .166 CET .072 0.012 .109

CEB .064 0.008 .087 VEX .066 0.009 -.093 VEY .202 0.077 -.280

FSP- forward shoulder posture; UT- upper trapezius; MT- middle trapezius; LT- lower trapezius, PEC- pectoralis major; R/P- scapular retractor to protractor ratio of activity; RT- reaction time; MvT- movement time; CEL- constant error left targets; CER- constant error right targets; CET constant error top targets; CEB- constant error bottom targets; VEX- variable error x-axis; VEY- variable error y-axis.

83

7.5 Reliability

ICC values are presented in Table 6.

Table 6: Intraclass Correlations of FSP, Pectoral Length, and Maximal Voluntary Isometric Contractions (MVICs).

Measurement ICC FSP .984 Pectoral Length .990 MVICs UT .980 MT .953 LT .979 PEC .980 FSP- forward shoulder posture; UT- upper trapezius; MT- middle trapezius; LT- lower trapezius, PEC- pectoralis major

8. Discussion

Forward shoulder posture is a postural deviation where the scapular protractors are shortened and hypothesized to inhibit the scapular retractors44. Additionally, FSP is a risk factor for neck-shoulder pain and pathology40,41. The purpose of the current study was to determine the effects of a 4-minute myofascial release (MFR) to the pectoral fascia on individuals with forward shoulder posture on: 1) forward shoulder posture (FSP), 2) pectoral length, 3) muscle activity of the upper, middle, and lower trapezius and pectoralis major, 4) the ratio of average muscle activity between the scapular retractors and protractors during a reaching task, and 5) movement performance (reaction time, movement time, and accuracy) during a reaching task, compared to a 4-minute soft-touch control (CON). It was hypothesized that compared to CON, MFR would 1) decrease FSP, 2) increase pectoral length, 3) increase upper, middle, and lower trapezius activity and decrease pectoralis major activity, 4) increase the scapular retractor to protractor muscle activity ratio during a reaching task, and 5) improve movement performance (i.e. decrease reaction time, decrease movement time, decrease constant and variable error) during a reaching task. In line with my hypothesis, MFR significantly reduced FSP compared to CON. However, the results for the remaining variables did not support my hypotheses as no significant changes were detected in pectoral length, muscle activity, or movement performance between MFR and CON. 84

8.1 Forward Shoulder Posture (FSP)

Consistent with my hypothesis, there was a significant decrease in FSP of 6mm (4.7%) in response to the MFR treatment, compared to a 1mm (1.1%) decrease in response to the CON treatment (Figure 14). The double-square method for FSP assessment is reliable with an ICC of .98 (Table 6) which agrees with previous literature199. Forward shoulder posture is considered an abduction or protraction of the scapulae where the scapular protractors (i.e. pectorals) are adaptively shortened due to the approximation of their proximal and distal attachments36,37,43, leading to an anterior deviation of the acromion process and glenohumeral joint. This shortening is hypothesized to increase activity within the protractors, and reciprocally inhibit their antagonists, the scapular retractors44. This muscular imbalance is associated with altered scapular kinematics such as greater scapular internal rotation and decreased posterior tilting37, each of which are consistent with kinematics observed with shoulder pathologies37,28,45,117,118 and are considered a risk factor for pathology40,41. Thus, treatments targeted at lengthening the pectorals and their connective tissue allow the glenohumeral and AC joint to return to a more neutral position and the scapula to retract, reducing the degree of FSP46,219,220,225 and the risk of pain and pathology40,41. The significant reduction in FSP observed in the current study in response to MFR supports recommendations that increasing the length and extensibility of the scapular protractors reduces FSP46,54–56,219,220,225,255. A variety of techniques exist to increase the length and extensibility of the scapular protractors and connective tissue to help reduce FSP including stretching and manual techniques46,53,54,56–58,216,219,220,225,245. Stretching of the pectorals decreases FSP after a single bout of static stretching220, after two weeks of static stretching46, after three- weeks of PNF stretching219, and in combination with exercise54–56,58,159,187,211–213,255,256. Alternatively, manual therapies such as massage or MFR can also increases the length and extensibility of the pectorals56,225, and has been shown to decrease FSP56,225 and increase LT strength56. MFR involves the application of mechanical pressure to fascia until deformation occurs which elongates and softens restricted fascia69. While MFR has been shown to increase the length of soft tissue in some areas of the body70,257–260, it is not known if therapist-administered MFR is capable of increasing the length of the pectorals or reducing FSP. However, existing literature has demonstrated that self-myofascial release (SMFR) is effective in the treatment of 85

FSP. Laudner and Thorson (2020)225 had participants complete either a myofascial self- mobilization with movement using a “T-Dot” device held perpendicular to the wall, or a placebo movement. The device was placed in the middle of the pectoralis minor and participants were instructed to perform 15 repetitions of flexion-extension, horizontal abduction-adduction, and internal-external rotation at 90 degrees of shoulder abduction and elbow flexion. Their results demonstrated significant improvements in flexion range of motion, pectoralis minor length, and forward scapular posture. These results are consistent with the results of the current study, as both forms of MFR designed to target the scapular protractors decreased FSP. The scapular protractors consist of pectoralis major and minor, and given their attachments from the thorax to the proximal humerus and coracoid process, respectively, shortening both will contribute to the development of FSP. The MFR treatment in the current study required the RMT to apply a sustained, moderate mechanical pressure at the origin and insertion of the pectoralis major sternal head for 4-minutes. Increasing the length and extensibility of the pectorals with MFR would reduce the anterior pull of the pectorals on the glenohumeral joint and scapula, allowing the shoulder complex to move more posteriorly and thus reduce FSP. However, the MFR administered in the current study would not have targeted the pectoralis minor given its attachments on the third to fifth costochondral junctions and coracoid process. Thus, it is not known whether MFR to the pectoralis minor would result in similar improvements in FSP. Future research should aim to explore the effects of manual techniques on both scapular protractors (pectoralis major and minor) as it is probable that the reduction in FSP observed may be even greater when both protractors are treated. Much of existing literature regarding the treatment of FSP uses a combined treatment approach comprised of protractor lengthening techniques (i.e. stretching or manual) and/or retractor strengthening54–56,58,159,187,211,213,255,256. These studies have reported reductions in FSP54– 56,159,211,213,255, increased strength56,58,187,256, and improved kinematics187, while other studies observed no changes in FSP187,256 or strength211. Collectively, the results from these studies support the results from the current study, in that a manual technique focusing on increasing the length and extensibility of the scapular protractors may improve FSP. However, it is important to note that all of these studies examined the cumulative effect of multiple treatment sessions on FSP54,55,58,159,187,211,213,255 whereas the current study examine the effect of one session of MFR on FSP. To the authors knowledge, only one other study has examined the effect of one session of 86 therapist applied soft tissue mobilization to the pectorals on FSP, but the pectoralis minor was treated and it was combined with stretching and a scapular tilting exercise56. Wong et al (2010)56 examined the acute and delayed effects of two different treatments in those with FSP. The experimental group received a soft tissue mobilization (STM) to pectoralis minor and completed a pectoralis minor stretch. The control group received a passive placebo light touch treatment and completed a pectoralis major stretch. Participants attended a total of three experimental sessions where FSP and LT strength were measured, while one of the two treatment conditions was provided only during the second session. The third and final follow-up session was held two weeks after the second session to examine the long-term effects of either treatment. They found that the group receiving STM and stretching of pectoralis minor had a greater immediate (post- treatment) and long-term decrease in FSP compared to the control group, though the long-term reduction in FSP was not as great as immediately post-treatment. As the current study only measured FSP immediately post-MFR, it is unknown how long the decrease in FSP observed would have remained after treatment. My results demonstrate that a 4-minute MFR to the pectoral fascia immediately reduces FSP. Ercole et al. (2010)7 demonstrated that only 3.3 minutes are required to observe changes in fascial fibrosis and tissue mobility in an MFR treatment. While we did not measure fascial fibrosis or tissue mobility directly, our results demonstrate that a 4-minute MFR to the pectoral fascia does elicit some change in the tissue that leads to a reduction in FSP. Fibrotic and immobile pectoral fascia would position the shoulder complex anteriorly due to its attachments, which would contribute to restricting the scapula’s ability to maintain a relaxed retracted position. While Ercole et al.’s work would suggest a 4-minute MFR to the pectoral fascia would result in a reduction in fascial fibrosis and increased tissue mobility, we cannot confirm these results as they were not measured. Further, it is unknown if FSP will remain decreased or return back to pre-intervention values within hours or days of the experimental session as we did not measure the time-course of the effects of treatment. Thus, future investigations should incorporate both immediate and delayed measurements of FSP to determine how long the effects last after one treatment, in conjunction with direct measures of fascial fibrosis/mobility and FSP. While statistical significance indicates there is some sort of probable relationship between variables, it does not provide information regarding the strength of the relationship or determine how meaningful the relationship is261. Clinical significance refers to the practical or 87 applied change in functioning that is due to therapy261,262, which determines how meaningful the relationship is. For FSP, although a statistically significant change (p <.05) was observed, it is not known if this change is clinically significant as a statistically significant decrease in FSP does not indicate a reduced risk of shoulder pathology. According to Jacobson et al. (1999)263, clinical significance can be quantitatively evaluated by determining if the resulting change falls within certain ranges of normal functioning. However, due to the inconsistency of FSP classification, we are not able to evaluate clinical significance based on this evaluation, as literature has not defined what is considered normal or different degrees (i.e. mild, moderate, or severe) of FSP. This inconsistency creates a challenge for researchers and clinicians attempting to classify and examine differences in degrees of FSP and treatments that may positively impact FSP. In addition, many researchers are questioning the impact shoulder posture truly has on injury development, stating the traditional criteria used to evaluate FSP is uncommon and unrealistic34,203,204. Future research should focus on developing a ‘gold-standard’ measurement of FSP, such as measuring the distance from the scapular medial border to spine, that would delineate degrees of FSP and further assist in classifying clinically significant changes with therapeutic interventions. This research should determine the level of reduction of FSP required to reduce the risk of developing shoulder pathology, and either confirm traditional criteria, or generate a new standard practice for evaluating FSP. 8.2 Pectoral Length

Contrary to my hypothesis, I observed no significant changes in pectoral length in response to either treatment (MFR 1.9% increase, CON .5% decrease; Figure 15; Table 4). Due to the sample being underpowered, conclusions may not be able to be drawn based on this sample as the full sample size was not collected due to research suspension. The pectoral length measurement was considered reliable with an ICC of .99 (Table 6). The 4-minute static, moderate pressure MFR intervention to the pectoral fascia was applied at the origin and insertion of the pectorals and their fascia. Previous work has demonstrated that a treatment time of 3.3 minutes was required to observe a change in fascial mobility in those with low back pain (LBP)70, which is why we elected to complete a 4-minute intervention. However, these findings were established from a MFR to the musculature and connective tissue in the low back; thus, it was unknown if a 4-minute MFR to the pectoral fascia 88 would increase the length and extensibility of the pectorals and their fascia. The fascial structure in the thoracolumbar area is complex with multiple trains contributing to the development of LBP264. Myofascial trains refer to whole-body connective tissue patterns that vary in length and depth, originating and terminating at various anatomical landmarks throughout the body265. Alternatively, the pectoral fascia is more simple, originating medially on the sternum and extending laterally, encapsulating pectoralis major and minor, and continuing over the shoulder joint71. Furthermore, the findings by Ercole and colleagues70 demonstrated these changes in those with LBP, whereas my participants were asymptomatic, which may possibly contribute to differences in results as asymptomatic patients may respond differently than those in pain. It is possible a longer treatment time is required to see similar changes in asymptomatic individuals compared to symptomatic. To indirectly measure pectoral length, participants horizontally abducted their shoulder at 90° of shoulder and elbow flexion while laying supine and allow their arm to fall towards the floor (Figure 9). This is considered an indirect measurement as we did not directly measure the pectoral muscle length itself, but rather the extensibility of the myofascial tissue in an end range of motion that would mimic a pectoral stretch. Due to the nature of this measurement, a decrease is indicative of pectoral soft tissue lengthening, as the participant was able to horizontally abduct their arm inferiorly towards the ground (or closer to 0cm on the meter stick). This measurement was chosen to assess the changes in muscle and connective tissue length and extensibility, whereas directly measuring pectoralis major length would exclude fascia. Extensibility is referred to the ability of a muscle to extend to a predetermined endpoint, and increases in muscle extensibility are established by an increase in end-range joint angles due to decreasing muscle stiffness or increasing muscle length266. By having the participant lay supine and allow their arm to fall into their maximal range of horizontal abduction (without overpressure), we are able to quantify the soft tissue changes in extensibility in response to either treatment. Research to date predominantly uses measurements of pectoralis minor when examining changes in FSP due to the abundance of research demonstrating that, a shorted pectoralis minor contributes to the development of FSP37,193,267. However, given its attachments to the thorax and proximal humerus, a shortened pectoralis major will also contribute to FSP, yet research tends to overlook its role in the development of FSP. Pectoralis minor length is typically quantified by measuring muscle length from its origin to insertion using a soft measuring tape or caliper188,200. 89

While these measurements are valid and reliable200, they only consider pectoralis minor length, one of the two pectoral muscles responsible for anteriorly deviating the shoulder when shortened. Further, it is not known if resting pectoralis minor length provides an accurate measurement of the muscle’s extensibility180,266. FSP is a protraction or abduction of the scapula, and I wanted to measure changes in pectoral muscle and fascial length and extensibility in the opposite direction, as traditional pectoralis minor length measurements do not consider extensibility of the muscle or surrounding fascia. This horizontal abduction measurement allows us to assess changes in the available range of motion by placing the pectoralis major and fascia in a lengthened position, permitting us to assess the changes in soft tissue restriction that inhibit the scapula’s ability to maintain a more retracted resting position due to less restriction of the anterior soft tissue. While there is a lack of literature examining the impact of an isolated manual technique on pectoral length, several studies have examined the impact of stretching or combination approaches on those with FSP212,221,222. Laudner and Thorson (2020)225 saw a significant increase in pectoralis minor length with a self-mobilization of pectoralis minor. Stretching protocols have demonstrated immediate changes in pectoralis minor length221,222, while stretching and strengthening combination approaches have demonstrated immediate increases pectoral length212. Interestingly, a study by Rosa et al. (2017)224 demonstrated that a 6-week pectoralis minor stretching protocol did not result in an increase in resting pectoralis minor length, but did result in an improvement in pain and functionality in those with shoulder pain. These results demonstrate clinical significance by improving pain and function, despite not having statistical significance. While the current study cannot confirm that the reductions in FSP reached clinical significance, it is possible the MFR intervention may clinically improve FSP without a statistically significant increase in pectoralis length. Future research should explore what magnitude of change in FSP results in favorable changes in scapular kinematics, function and patient symptoms in those with shoulder pathology. The discrepancy between significant changes in pectoral length and FSP is interesting, as a significant change in FSP was not related to a change in pectoral length. The exploratory Pearson Correlation between changes in pectoral length and FSP yielded a correlation coefficient r= .240 at p= .338, indicating an insignificant small correlation252 between the two variables. As previously discussed, the scapular protractors attach from the sternum to the anterior shoulder and when shortened, pull the shoulder anteriorly and contribute to the development of FSP. 90

When the protractors are lengthened, theoretically, this change should correspond to changes seen in FSP. Indeed, the results of the current study indicated a significant change in FSP with a 4-minute MFR to the pectoral region; however, the change in pectoral length was insignificant, indicating that changes in pectoral length and extensibility is not related to changes in FSP. It is possible, however, that pectoralis minor plays a more significant role in FSP than pectoralis major, and the pectoral measurement we performed did not adequately quantify changes in pectoralis minor length. Furthermore, changes in resting pectoral length may have contributed to this change in FSP, which were not quantified by the measurement completed. Future research should aim to quantify the direct relationship between pectoralis major length, pectoralis minor length, their associated fascia, and FSP. Further, the lack of significant change observed in pectoral length may be due to the method chosen to quantify pectoral length and extensibility, as it is possible that changes in resting pectoral muscle length (i.e. measure origin to insertion at rest) were significant. However, as we did not perform this measurement, I am unable to confirm if resting pectoral length increased to allow for a reduction in FSP. Performing a measurement such as the Pectoralis Minor Index (PMI; measuring resting muscle length from origin to insertion while at rest) would allow researchers to directly relate changes in resting pectoralis minor muscle length to changes in FSP. PMI predicts 78% of FSP incidences, 268 therefore, future studies should quantify resting length using the PMI and measure changes in pectoralis major length.

8.3 Muscle Activity

Contrary to my hypothesis, there were no significant immediate changes in muscle activity of the upper, middle, and lower trapezius (UT, MT, LT; Figure 16) or pectoralis major (PEC; Figure 17), nor were there any changes in the ratio of activity of the scapular retractor and protractor (R/P; Figure 18) after a 4-minute MFR to the pectoral fascia. I hypothesized that the retractors (MT, and LT) would increase and UT and PEC would decrease in activity, therefore increasing the R/P. Collectively, the observed power for each of these dependent measures determined they were extremely underpowered and demonstrated relatively small effect sizes (Table 5). While reliability of the muscle activity during the reaching task was not analyzed for reliability, the MVICs performed prior to the reaching task were, each with an ICC of over .9, or excellent (Table 6). 91

While not a true joint, the scapulothoracic joint plays an integral role in the functioning of the shoulder complex74. The scapula serves as an attachment point for several muscles that connect the thorax to the upper extremity, such as the trapezius. The trapezius has three fibre orientations, upper, middle and lower, that individually elevate, retract, and depress the scapula, respectively269, but collaborate to stabilize and retract the scapula during arm movements. Upper extremity movement is complex and requires coordination of several muscles for pain-free movement166,172,270, and imbalances with the onset, timing, and force production of these muscles is associated with shoulder pathology33. Specifically, individuals with shoulder pathology have demonstrated increased UT activity26,28,29,31,166, and decreased SA26–29, MT and LT activity28,31. Forward shoulder posture is associated with scapular protractors that are shortened and retractors that are lengthened36,37,41,43,148,195,196. This alteration in muscle length is speculated to decrease muscle performance43, as the shortened scapular protractors are theorized to be hypertonic and cause a reciprocal, inhibitory weakness of the scapular retractors44. Together, it is speculated that these changes alter the levels of activity in the scapular protractors and retractors44, and further contribute to the development of neck-shoulder pain or pathology31,33,171,172. Literature to-date has yet to explore this relationship between the scapular retractor and protractor activity in those with FSP and has minimally explored electromyographic changes of individual muscles due to FSP and treatments thereof. The current study is the first to capture the electromyographic changes in retractor and protractor muscle activity in response to a 4-minute MFR to the pectoral fascia. While novel, this makes it difficult to compare my results to other studies.

8.3.1 Upper Trapezius (UT)

Percent changes in UT activity from pre- to post- MFR (1.1% increase) and CON (.8% increase) are indicated in Table 4. Due to the sample being underpowered, conclusions may be drawn based on this sample. However, given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia would affect UT activity (Figure 16). The UT elevates the scapula and is hyperactive in those with FSP40 and shoulder pathology28. It is theorized that the increase in UT activity occurs in part due to the decreased activity in the MT28, as well as to assist in stabilizing the humerus due to the altered scapular 92 position38,39. Increased UT activity is associated with shoulder pain and altered scapular mechanics28,45,166; thus, interventions capable of decreasing UT activity are of keen interest in the prevention of shoulder pathologies. Interestingly, Thigpen et al. (2010) found no differences in UT activity in those with asymptomatic FSP compared to those without FSP, suggesting changes in trapezius activity may only be observed in the presence of shoulder pain190. Furthermore, the findings by both Thigpen and the current study suggest UT activity does not influence FSP, as both studies observed changes in FSP but no change in UT activity. Thigpen et al (2010)190 postulated that changes in UT activity may only occur in the presence of pain, suggesting this may be the reason we did not see a change in UT activity. The lack of change observed for UT activity from pre- to post- intervention may be due to the fact that my participants were not experiencing pain or pathology, thus not having increased UT activity to begin with and not requiring a reduction to a “normal” level. Kwon et al. (2015)271 recruited individuals with FSP and forward head posture and investigated UT, LT, and SA muscle activity during natural, ideal, and corrected postural conditions. Natural posture was considered the participants’ typical posture, ideal posture was the posture participants considered as ‘balanced,’ and corrected posture had the participant placed in neutral posture by experienced therapists. Muscle activity was collected while the participants performed an overhead reaching task under each postural condition. Interestingly, their results demonstrated that there was a significant reduction in UT activity in participants’ ideal and corrected posture compared to their natural posture. These results are contrary to the results of the current study, as I did not observe a change in UT activity despite FSP improving. This may be due to the fact that, even with the reduction observed in FSP in the current study, posture may still not have been considered “ideal,” therefore changes in UT may not be observed.

8.3.2 Middle Trapezius

Percent changes in MT activity from pre- to post- MFR (.9% decrease) and CON (3.8% decrease) are indicated in Table 4. Due to the sample being underpowered, conclusions may not be drawn based on this sample. However, given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia would affect MT activity (Figure 16). 93

The MT is the primary medial stabilizer of the scapula167 that assists with scapular retraction269. It is theorized that weakness in MT and LT contribute to FSP and scapular anterior tilt185, and it has been shown that MT activity is decreased in those with FSP40. FSP has been shown to contribute to altered kinematics of the shoulder190, and has been identified as a risk factor for shoulder pathology40,41. Thus, identifying interventions that are capable of increasing MT activity are imperative to the prevention and rehabilitation of shoulder pathology. The MT is considered the main antagonist to the scapular protractors272 as its primary action is to retract the scapula. In those with FSP, the pectorals are shortened36,37,43,188,193,218 and overactive40, causing a lengthening36 and reciprocal inhibition of the scapular retractors41,43,148,195,196. Since pectoralis major activity was unchanged during the reaching task in response to the 4-minute MFR, it is not surprising that MT activity remained unchanged. Musculoskeletal therapists are commonly taught that individuals with FSP have shortened hyperactive pectorals which cause a reciprocal inhibition of the scapular retractors, and by lengthening the protractors, they will reverse the inhibition on the retractors. While no literature to-date has examined reciprocal inhibition in the scapular retractors and protractors in those with or without FSP, reciprocal inhibition has been demonstrated in the lower leg122,123, forearm119,124, and upper arm and shoulder in force-couples such as biceps/triceps and pectoralis major/posterior deltoid125. Furthermore, interventions aimed at increasing the length and extensibility of one muscle has been demonstrated to alter muscle activity within its antagonist. These results have been demonstrated in force-couples such as the plantar-dorsiflexors120 and hamstrings-quadriceps223. Collectively, this suggests increasing the length and extensibility of one muscle may alter its own activity as well as the activity of its agonist. Theoretically, this alteration should be observed in the scapular protractors and retractors, as well; however, the 4- minute MFR may not have been a sufficient intervention in inducing these changes.

8.3.3 Lower Trapezius

While the results for LT activity were insignificant, the MFR condition saw a 2.2% increase from PRE to POST while the CON condition saw a 0.5% decrease in activity Table 4. Due to the sample being underpowered, conclusions may not be drawn based on this sample. However, given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia would affect LT activity (Figure 16). 94

The LT produces posterior tipping and external rotation of the scapula during movements of the upper extremity and weakness or reduced activity contributes to scapular instability and kinematic changes that result in shoulder pathology28,31,185,273. A study by Wong et al. (2010)56 examined the effects of two different FSP treatments on FSP and LT strength. Participants were randomly assigned to receive either a soft tissue mobilization treatment and self-stretching to pectoralis minor, or a tensionless treatment and self-stretch of pectoralis major. Their results determined that both groups observed a significant increase in LT strength immediately post- treatment and at the two-week follow up. While activity of the LT was not measured, their results demonstrate the ability of two different interventions targeted at lengthening the scapular protractors to alter the contractility of the LT. Furthermore, a study by Lee et al. (2015)212 found that a treatment composed of stretching pectoral resulted in a significant increase in LT activity compared to other treatments that did not address pectoral length. However, all treatments included a scapular posterior tilt exercise. Collectively, these results are contrary to those of the current study, as I did not observe changes in LT recruitment after a 4-minute MFR to the pectoral fascia. However, it must be acknowledged that strength and muscle activity are not the same measurement; therefore, it is possible the LT strength of my participants increased while not observing an increase in LT activity, as I did not measure muscle strength. The differing results between those of Wong56 and Lee212 and the current study may be due to methodological differences. Wong56 and colleagues used a 3-minute STM followed by self-stretching of pectoralis minor for 3-minutes, while Lee212 and colleagues had participants perform a scapular posterior tilt exercise for 5-seconds and pectoralis minor stretch held for 4x 30-seconds. Both of these treatments were targeted at pectoralis minor which varies from that of the current study as the treatment in my study was concentrated on pectoralis major. Thus, treatments focusing on pectoralis major may not be as effective in increasing the length of the muscle as observed with Wong’s study, or LT activity and/or strength as treatments focused on pectoralis minor. As the current study did not observe an increase in pectoral length, it is unsurprising I did not see a change in muscle activity. Furthermore, the scapular posterior tilt exercise may play a role in inducing increased LT activity, and future research should examine differences in LT activity in response to MFR with and without inclusion of a scapular posterior tilt exercise.

95

8.3.4 Pectoralis Major (PEC)

Percent changes in PEC activity from pre- to post- MFR and CON are indicated in Table 4. Interestingly, while I did not observe a statistically significant change in PEC activity, the MFR and CON conditions observed a 20.9% and 9% increase from PRE to POST, respectively. However, due to the sample being underpowered, conclusions may not be drawn based on this sample. However, given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia would affect PEC activity (Figure 17). One of the most common indications of FSP is shortened pectorals193 which have been demonstrated to have increased activity compared to those without FSP274. A shortened pectoralis minor contributes to anteriorly tilting and protracting the scapula by pulling the coracoid process anteriorly194,218,268,275, while a shortened pectoralis major pulls the proximal humerus anteriorly. These adaptations are associated with altered scapular and shoulder kinematics and shoulder pathology28,194,200,218,276. Furthermore, the shortened and hyperactive pectorals are theorized to alter the length-tension relationship with the scapular retractors197, producing a reciprocal inhibitory weakness of the scapular retractors44, and further contributing to the instability of the scapula28,185. While lengthening pectoralis minor has demonstrated increases in muscle length218,220,225, reductions in FSP46,211,255,268, and improvements in scapular kinematics, little research has examined the impact it has on pectoralis muscle activity. Interestingly, my results demonstrated no change in PEC activity following both the MFR and CON treatments, results that are contradictory to other research examining the effect of massage techniques on EMG activity277– 279. In the shoulder, literature has demonstrated the ability of massage to the UT to significantly decrease activity of the UT277,278. Arroyo-Morales et al. (2008)279 demonstrated similar findings with an MFR to the quadriceps, finding reduced EMG activity post-treatment. However, other literature has demonstrated that massage to the hamstring280 and quadriceps281 did not affect EMG activity. In 1990 and 1991, Morelli et al.231,232 found that, during a triceps massage, EMG activity decreased for the duration of the intervention, but returned to baseline values upon termination of the treatment. As I did not measure muscle activity during the MFR intervention, I cannot confirm that the pectoralis major experienced a decrease in activity during the intervention; however, resulting post-treatment muscle activity demonstrates no change in activity, possibly supporting Morelli and colleagues’ previous findings. 96

Domingo et al. (2017) postulate that the observed decrease in muscular activity is due to a decreased number of active motor units or decreased frequency of motor unit firing with the massage intervention277. Much like the current study, participants completed one experimental massage treatment and one control treatment; however, the intervention, focusing on bilateral upper shoulder and neck regions, lasted approximately 30-minutes. A study by Sefton et al. (2011)278 had participants receive three treatments: one control, one light tough, and one therapeutic massage, each on separate days. The therapeutic massage consisted of a 20-minute standardized supine treatment intervention for neck and shoulder pain. The light touch treatment required the same therapist to lightly place their hands on the same contact areas as the massage intervention but apply no pressure, while the control treatment has the participant rest for the 20- minute treatment. Their results demonstrated the experimental intervention significantly decreased UT activity compared to the light touch and control treatments. Interestingly, their results also demonstrated the massage interventions ability to decrease the H-reflex in a distant muscle to the intervention, being the flexor carpi radialis. Collectively, this suggests that massage can alter physiological responses in the treatment area in addition to areas considerably removed from the treatment area. The discrepancies in treatment type length between these studies may explain the conflicting results with the current study, as Domingo and Sefton provided a 30- and 20-minute Swedish massage intervention, respectively, compared to the 4- minute intervention in my study. The Swedish massage targets muscle while the MFR targets fascia. This may exhibit that a treatment time of only 4-minutes targeting fascia is not sufficient in reducing the number of active motor units or firing frequency in the treatment area and areas at a distance to the treatment area. Thus, future research should examine the effect of longer treatment times on muscle activity in the pectoralis major and its antagonist.

8.3.5 Scapular Retractor to Protractor Ratio of Activity (R/P)

In addition to analyzing individual muscle activity of the pectoralis major and trapezius, I also wanted to analyze the ratio of activity between the retractors and protractors. The R/P decreased by 2.5% and 7.1% from PRE to POST in MFR and CON, respectively (Table 4). Due to the sample being underpowered, conclusions may not be drawn based on this sample. However, given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia does not affect the R/P activity (Figure 18). 97

The decrease observed in R/P is contrary to what I had hypothesized, as I had expected to see an increase in retractor activity and a decrease in protractor activity. An increase in R/P would be a result of protractors that decrease in activity and retractors that increase in activity after intervention, results that are desirable when treating those with FSP due to increases in stability and control of the scapula31. These results, however, are only desired if retractor activity is, in fact, inhibited due to increased protractor activity. The current study did not assess the presence of an altered R/P in these muscle groups in those with FSP, but rather the change observed in R/P due to either an MFR or CON treatment. A study by Rashed et al. (2019)282 compared pectoralis major EMG activity to MT activity in girls aged 15-20 with thoracic kyphosis. Their results determined there was no correlation, indicating no relationship between pectoralis major and MT activity. While they did not look at FSP specifically, they argued that thoracic kyphosis is associated with FSP. DiVeta et al. (1990)272 compared scapular abduction (i.e. FSP) and muscle force produced in the MT and pectoralis minor (Pm). Their results determined a low correlation between FSP-MT, FSP-Pm, and FSP-MT/Pm (ratio of MT to Pm), demonstrating a direct relationship between shoulder posture, resting muscle length, and force production does not exist, questioning the assumption that altered posture can induce muscular weakness272. Collectively, the results from these two studies suggest that an altered ratio of activity or muscle performance of the scapular retractors and protractors may not exist in those with FSP. Thus, changes in this ratio may not be expected after a 4-minute MFR intervention. Future research should confirm the presence of an altered ratio of activity in those with different degrees of FSP prior to determining the changes observed due to a 4-minute MFR treatment.

While the changes in FSP were not related to changes in pectoral length, there is a possibility that they may have been related to changes in postural muscle activity. Though I did not examine the scapular retractor to protractor ratio of activity while the participant maintains a static standing posture, it is possible that this ratio may have been altered while standing. For example, we may have observed an increase in static posture activity in the retractors, or decreased activity in the protractors, which may have contributed to decreasing standing FSP as measured by the double square method. Future research should consider including this type of measurement in order to better understand the mechanisms of decreasing FSP.

98

8.4 Movement Performance

Contrary to my hypothesis, there were no significant changes in movement performance in measurements of reaction time (RT), movement time (MvT), or end-point accuracy (constant and variable error) after a 4-minute MFR to the pectoral fascia. I hypothesized that movement performance would improve by decreasing RT, MvT, constant error, and variable error. Collectively, the observed power for each of these dependent measures determined they were underpowered and demonstrated relatively small effect sizes; thus, it does not appear that a 4- minute MFR to the pectoral fascia would have an effect on movement performance.

8.4.1 Reaction Time (RT)

Percent changes in RT from pre- to post- MFR (1.8% decrease) and CON (1% decrease) are indicated in Table 4. Due to the sample being underpowered, conclusions may not be drawn based on this sample. However, given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia would influence RT (Figure 19).

8.4.2 Movement Time (MvT)

Percent changes in MvT from pre- to post MFR and CON are indicated in Table 4. Interestingly, the MFR condition saw an improvement of .8% while CON saw an increase in MvT by 1.9%. However, these values are insignificant, and given the power, effect size, and required sample size to reach #= .8, it does not appear that a 4-minute MFR to the pectoral fascia would influence MvT (Figure 20).

8.4.3 End-Point Accuracy

Collectively, given the achieved power, effect size, and required sample size to reach #= .8, indicate that it does not appear that a 4-minute MFR to the pectoral fascia influences end- point accuracy. 8.4.3a Constant Error X-Axis Left and Right Targets (CEL & CER)

Constant error in the X-axis for the left-oriented targets saw an insignificant decrease in performance in both the MFR (20.3% increase) and CON (87.6% increase) treatment conditions, while the right-oriented targets saw a decrease in performance in the MFR condition (16.5% 99 increase) and improvement during CON (25.6% decrease) (Table 4). X-axis constant error provides us with information on directional (i.e. left and right) bias. Both the left and right targets had negative values for their pre- and post- means, indicating that participants generally fell short of accurately hitting the centre of each respective target. This means that, for the left targets, participant hits fell to the right of the target centre, while hits for the right targets fell on the left side of the target centre. The decrease in these means from pre- to post- demonstrate that participant’s accuracy on the X-axis generally improved by averaging hits that are closer to the true target centre, though these changes are not considered significant. 8.4.3b Constant Error Y-Axis Top and Bottom Targets (CET & CEB)

Constant error in the Y-axis for the top-oriented targets saw an insignificant decrease in performance for both MFR (82.3% increase) and CON (128.8% increase). Similarly, the constant error in the Y-axis for the bottom-oriented targets saw insignificant decreases in performance in the MFR (42.5% increase) and CON (12.6% increase) conditions (Table 4). Y-axis constant errors provides us with information on amplitude (i.e. height) bias. The mean values for both the top and bottom targets were positive, indicating that participants generally ‘overshot’ the centre of the targets, as positive constant error values denote touches that were above the true target centres. 8.4.3c Variable Error X- and Y- Axis (VEX & VEY)

Variable error in the X- saw decreases in performance for both MFR and CON, with the X-axis insignificantly increasing by 3.9% and 0.3%, respectively. The Y-axis variable error insignificantly increased by 4.5% in the MFR condition, but decreased by 4% in the CON condition (Table 4). These values represent the mean standard deviation of the participant hits in both the X- and Y-axis for the four corner targets, demonstrating an insignificant improvement in accuracy from pre- to post- in the CON condition. Variable error provides us with information regarding the consistency of the participant’s accuracy. Reaction time is considered the time between the onset of stimulus presentation and beginning of a response while movement time is the time from reaction time to completion of the movement59. In the case of my experiment, RT would be the time from each target’s onset of appearance until the lift of the participant’s finger from the microswitch. Alternatively, MvT was 100 considered the time between the lift of the participant’s finger until the touch of the target. Each target’s individual MvT was the same time period in which muscle activity was analyzed. Fitts’ Law describes the inverse relationship between speed and accuracy, stating that as speed increases, accuracy decreases, and vice-versa60. Speed is considered the measurement of MvT, and a decrease in MvT would indicate greater speed, thus resulting in greater movement variability, or an increase in end-point accuracy. This relationship is confirmed by Poston et al.’s (2010)283 findings, demonstrating increased end-point accuracy with the slower of two movement speeds. While my results demonstrate an insignificant change in both MvT and end- point accuracy, an interesting trend was noted between these variables. As articulated above, MvT decreased (i.e. improved) in the MFR condition by 1.2%. According to Fitts’ Law, a proportional, inverse increase should be observed in end-point accuracy. However, my results demonstrated an insignificant decrease (or improvement) in constant error for X-axis left and right targets, and Y-axis top targets, demonstrating both MvT and accuracy improved. As for the CON condition, MvT increased, which resulted in an expected improvement in some end-point accuracy measures, such as a decrease of X-axis constant error for the left and right targets, as well as a decrease variable error in both the X- and Y-axis. However, due to the statistical insignificance and achieved power from this sample, it does not appear a 4-minute MFR to the pectoral fascia has an impact on movement performance. Analyzing simple goal-directed movements, such as pointing in the current study, allows researchers to analyze different components of movement performance by breaking down component parts that generally contribute to larger-scale movements61. Using Fitts’ tasks allows for the evaluation and prediction of human performance in practical enviornments136, and are often applied to real-life situations, such as aircraft navigation62, chiropractic spinal adjustments63,64, older adults65, autistic individuals66, and healthy individuals67. While literature has yet to examine the impact of a manual soft-tissue treatment on movement performance, some research has demonstrated the impact of a chiropractic adjustment on different movement performance variables. Smith et al. (2006)63 demonstrated the impact of a spinal chiropractic adjustment compared to a control treatment on MvT in those with diagnosed spinal dysfunctions. The group who received the adjustment demonstrated a significant decreased MvT compared to the control group. Similar findings have been demonstrated by Emlet et al. (2013)284 in those with neck pain receiving a cervical adjustment. DeVocht et al. 101

(2019)285 revealed an improvement in RT immediately following a chiropractic adjustment in military personnel. Future research should explore the impact a manual intervention to soft tissue has on different components of movement performance such as RT, MvT, and accuracy.

9. Limitations and Future Directions

There are several limitations to the current study. Firstly, as mentioned previously, the study sample was underpowered due to the inability to collect a full data set due to evolving COVID-19 restrictions. The post-hoc a priori calculated sample sizes for each dependent variable can be found in Table 7. An underpowered sample reduces the likelihood of detecting statistically significant changes as a large effect size would be required to detect these changes. The full sample size is considered 60 participants; however, given the power analysis and post- hoc a priori calculations, many of the outcome variables will still be underpowered and, thus, not reach significance.

Table 7: Post-hoc a priori calculated sample size. Outcome Variable Achieved Power Required Sample Size $

FSP .682 24 Pectoral Length .284 68 UT .050 96 902 MT .131 187

LT .192 110 PEC .055 3 020 R/P .060 1 436 RT .082 467 MT .236 85 CEL .051 27 161 CER .102 287 CET .072 663 CEB .064 1 039

VEX .066 910 VEY .202 103

Secondly, the generalizability of the study is limited to healthy, younger females with FSP who were recruited primarily from student and staff populations at the University of Manitoba. It is possible I would obtain differing results in males or those with symptomatic or pathological 102 shoulders. Our results cannot provide insight into the application of MFR to the pectoral fascia in those with shoulder pain or pathology. Furthermore, this sample may not be representative of all younger females with FSP but otherwise healthy shoulders. It is important to note that literature to-date has recruited both male and female participants for research involving treatment of FSP but has not conducted sex-based analyses. Thus, females may respond differently than males. It is my intention to explore female versus male responses to the 4-minute MFR treatment compared to the CON once the full sample is collected to determine if response differences vary. Thirdly, the use of the double-square method of measuring FSP only provides us with an absolute measure of FSP, not one relative to each participant. This measurement is capable of identifying changes in FSP due to either treatment condition but does not provide information regarding the degree in which the participant has FSP. This limitation relates to our inability to detect clinical changes in FSP that would reduce an individual’s risk for the development of shoulder pain or pathology. It is possible that those with greater degrees of FSP may observe greater effects due to a MFR intervention than individuals with a lesser degree of FSP. Furthermore, this absolute measurement of FSP in unable to be compared to other measures such as muscle activity and impacts our understanding of the relationship between degree of FSP and ratio of activity between the scapular retractors to protractors. Fourth, while we observed a significant reduction in FSP after a 4-minute MFR to the pectoral fascia, it is unknown if this reduction would last long-term as we did not perform a follow-up measurement. While previous work by Wong et al. (2010)56 demonstrated lasting effects of reduced FSP two-weeks after a single soft tissue mobilization and stretch to pectoralis minor, it is unknown if the intervention performed in my study will observe similar effects, or if these effects will be clinically significant. Another limitation related to my study was the chosen method for analyzing pectoral soft tissue length and extensibility. While the measurement demonstrated a high degree of reliability as determined by the intraclass correlation, it is unknown if this measurement is related to changes in resting pectoral tissue length or FSP. Recent advances in technology have allowed for the examination of soft tissue shear elastic modulus via Shear Wave Elastography (SWE) that quantifies muscle elongation and extensibility. A series of studies by Umehara et al (2017, 2018 and 2021)286–288 has investigated changes in shear elastic modulus of the pectoralis minor with different stretching techniques. Through these studies, they found that maximal horizontal 103 abduction of the shoulder at 90° and 150° of abduction effectively elongated and acutely decreased tissue stiffness of pectoralis minor286,287. This demonstrates that our method of measuring pectoral length not only quantifies changes in extensibility in pectoralis major, but also pectoralis minor. Future studies should use SWE to quantify the direct changes in pectoral soft tissue stiffness due to a 4-minute MFR to the pectoral fascia, as it is unknown if MFR will cause similar changes in tissue extensibility as stretching both immediately and long-term. These results will not only inform researchers of the differences in tissue extensibility between stretching and manual techniques to elongate restricted soft tissues, but also the differences in delayed effects which should be a consideration for rehabilitation purposes. There are several limitations to the analysis of changes in muscle activity in the current study. As previously mentioned, it is unknown if my participants had altered muscle activity in the scapular protractors and retractors due to having FSP, or if the degree of FSP would impact the severity of these alterations. Secondly, our analysis of muscle activity was conducted only on the motor phase of movement, or from the time the microswitch was released to the time the participant touched the target. This time period does not include the premotor phase of activity which consists of the initiation of muscular activity and overcoming gravity to produce movement. It is possible that changes in muscle activity may be observed more so in the premotor phase of movement compared to the motor phase, thus, significant changes not being detected. Furthermore, the reaching activity we had participants perform may not have required them to generate enough force or muscle activity required to detect changes. Future research should include both the premotor and motor phases of movement in their analysis and have participants perform a task that requires greater force production. Lastly are a few limitations in the MFR intervention performed by the RMT. While the RMT is clinically experienced in performing MFR, the treatment intensity applied in the experimental condition was subjective and we cannot confirm this pressure was uniform across all participants. A table of the RMT’s notes on each participant’s intervention response can be found in Appendix G. Secondly, this pressure is also subjective to participants and may have been perceived differently by different participants. Participants were told to communicate level of discomfort to the RMT throughout the treatment, especially as the level of discomfort approaches and/or exceeds a 7/10. Pain is subjective and individuals may tolerate different intensities of MFR, and thus, may receive different intensities of treatment if their level of 104 discomfort reached a 7/10 and the RMT reduced their applied pressure. These subjective differences may also impact the outcomes of the treatment, as perhaps more intense treatments observed a greater change in FSP, pectoral length, muscle activity, or movement performance compared to those who received a less intense treatment. On the other hand, it is suspected that individuals with greater degrees of FSP would have greater pectoral soft tissue restrictions, and therefore will observe greater changes in the outcome variables than those with lesser degrees of FSP. Lastly, we did not control for individuals who have a history or routinely attend massage therapy treatment sessions; nor did we control for individuals who have a level of understanding of musculoskeletal assessment and treatment. Thus, our participants who routinely receive massage treatments may respond differently than those who do not receive massage treatments. Furthermore, individuals who have background knowledge on musculoskeletal assessment and treatment such as MFR may understand the objectives of the current study and consciously or subconsciously alter their behaviour to suit the hypothesized outcomes.

10. Conclusion

The results of this study demonstrate that a 4-minute MFR to the pectoral fascia effectively reduces FSP compared to a 4-minute soft-touch control treatment in those with FSP; but neither a 4-minute MFR or soft-touch control appear to influence pectoral length, muscle activity, or movement performance. While the sample used in the current study was well underpowered and thus, some conclusions may not be drawn until power is reached. However, other conclusions may be confidently drawn, such as those for muscle activity, that neither treatment has an effect on inducing changes. Future research should aim to quantify relative degrees of FSP and the relationship it has to pectoral muscle and connective tissue length and muscle activity. Furthermore, future research should determine the minimally clinically important difference required in order to reduce an individual’s risk for the development of shoulder pathology.

105

References 1. Government of Canada. The cost of injury in Canada. (2010). Available at: https://www.canada.ca/en/public-health/services/injury-prevention/cost-injury- canada.html. (Accessed: 10th December 2019) 2. Depreli, Ö. & Angın, E. Review of scapular movement disorders among office workers having ergonomic risk. J. Back Musculoskelet. Rehabil. 31, 371–380 (2018). 3. Straker, L. M., Smith, A. J., Bear, N., O’Sullivan, P. B. & de Klerk, N. H. Neck/shoulder pain, habitual spinal posture and computer use in adolescents: the importance of gender. Ergonomics 54, 539–546 (2011). 4. Hill, J., Lewis, M., Papageorgiou, A. C., Dziedzic, K. & Croft, P. Predicting persistent neck pain. Spine (Phila. Pa. 1976). 29, 1648–1654 (2004). 5. Croft, P. R. et al. Risk factors for neck pain: A longitudinal study in the general population. Pain 93, 317–325 (2001). 6. van der Heijden, G. J. M. G. Shoulder disorders: A state-of-the-art review. Best Pract. Res. Clin. Rheumatol. 13, 287–309 (1999). 7. Daneshmandi, H., Choobineh, A. R., Ghaem, H., Alhamd, M. & Fakherpour, A. The effect of musculoskeletal problems on fatigue and productivity of office personnel: A cross-sectional study. J Prev Med Hyg. 58, 252–258 (2017). 8. Larsson, B., Søgaard, K. & Rosendal, L. Work related neck-shoulder pain: a review on magnitude, risk factors, biochemical characteristics, clinical picture and preventive interventions. Best Practice and Research: Clinical Rheumatology 21, 447–463 (2007). 9. Läubli, T. & Karpilow, C. Musculoskeletal disorders. in Global Occupational Health 277–299 (Oxford University Press, 2011). doi:10.1093/acprof:oso/9780195380002.003.0015 10. Gallagher, S. & Schall Jr., M. C. Musculoskeletal disorders as a fatigue failure process: Evidence, implications and research needs. Ergonomics 60, 255–269 (2017). 11. Delisle, A. Musculoskeletal disorders and computer work the impact of workstation layout on posture and muscle load of the upper limbs. (Canadian Electronic Company, 2006). 12. Valipour Noroozi, M., Hajibabaei, M., Saki, A. & Memari, Z. Prevalence of musculoskeletal disorders among office workers. Jundishapur J. Heal. Sci. 7, 1–5 (2015). 13. Gerr, F., Marcus, M. & Monteilh, C. Epidemiology of musculoskeletal disorders among 106

computer users: lesson learned from the role of posture and keyboard use. J. Electromyogr. Kinesiol. 14, 25–31 (2004). 14. Blatter, B. . & Bongers, P. . Duration of computer use and mouse use in relation to musculoskeletal disorders of neck or upper limb. Int. J. Ind. Ergon. 30, 295–306 (2002). 15. Eltayeb, S., Staal, J. B., Hassan, A. & de Bie, R. A. Work related risk factors for neck, shoulder and arms complaints: A cohort study among dutch computer office workers. J. Occup. Rehabil. 19, 315–322 (2009). 16. Juul-Kristensen, B., Søgaard, K., Strøyer, J. & Jensen, C. Computer users’ risk factors for developing shoulder, elbow and back symptoms. Scand. J. Work. Environ. Heal. 30, 390– 398 (2004). 17. Ming, Z., Närhi, M. & Siivola, J. Neck and shoulder pain related to computer use. Pathophysiology 11, 51–56 (2004). 18. Treaster, D. & Burr, D. Gender differences in prevalence of upper extremity musculoskeletal disorders. Ergonomics 47, 495–526 (2004). 19. Dunk, N. M. & Callaghan, J. P. Gender-based differences in postural responses to seated exposures. Clin. Biomech. 20, 1101–1110 (2005). 20. Vekiri, I. & Chronaki, A. Gender issues in technology use: Perceived social support, computer self-efficacy and value beliefs, and computer use beyond school. Comput. Educ. 51, 1392–1404 (2008). 21. Paksaichol, A., Janwantanakul, P., Purepong, N., Pensri, P. & van der Beek, A. J. Office workers’ risk factors for the development of non-specific neck pain: A systematic review of prospective cohort studies. Occup. Environ. Med. 69, 610–618 (2012). 22. Hooftman, W. E., van der Beek, A. J., Bongers, P. M. & van Mechelen, W. Is there a gender difference in the effect of work-related physical and psychosocial risk factors on musculoskeletal symptoms and related sickness absence? Scand. J. Work. Environ. Health 35, 85–95 (2009). 23. Côté, J. N. A critical review on physical factors and functional characteristics that may explain a sex/gender difference in work-related neck/shoulder disorders. Ergonomics 55, 173–182 (2012). 24. Wüst, R. C. I., Morse, C. I., De Haan, A., Jones, D. A. & Degens, H. Sex differences in contractile properties and fatigue resistance of human skeletal muscle. Exp. Physiol. 93, 107

843–850 (2008). 25. Côté, J. N. A critical review on physical factors and functional characteristics that may explain a sex/gender difference in work-related neck/shoulder disorders. Ergonomics 55, 173–182 (2012). 26. Peat, M. & Grahame, R. E. Electromyographic analysis of soft tissue lesions affecting shoulder function. Am. J. Phys. Med. 56, 223–240 (1977). 27. Scovazzo, M. L., Browne, A., Pink, M., Jobe, F. W. & Kerrigan, J. The painful shoulder during freestyle swimming: An electromyographic cinematographic analysis of twelve muscles. Am. J. Sports Med. 19, 577–582 (1991). 28. Ludewig, P. & Cook, T. Alterations in shoulder kinematics and associated muscle activity in people qith symptoms of shoulder impingement. Phys. Ther. 80, 276–291 (2000). 29. Lin, J. et al. Functional activity characteristics of individuals with shoulder dysfunctions. J. Electromyogr. Kinesiol. 15, 576–586 (2005). 30. Diederichsen, L. P. et al. The activity pattern of shoulder muscles in subjects with and without subacromial impingement. J. Electromyogr. Kinesiol. 19, 789–799 (2009). 31. Cools, A. M., Declercq, G. A., Cambier, D. C., Mahieu, N. N. & Witvrouw, E. E. Trapezius activity and intramuscular balance during isokinetic exercise in overhead athletes with impingement symptoms. Scand. J. Med. Sci. Sport. 17, 25–33 (2007). 32. Lin, J. J., Hsieh, S. C., Cheng, W. C., Chen, W. C. & Lai, Y. Adaptive patterns of movement during arm elevation test in patients with shoulder impingement syndrome. J. Orthop. Res. 29, 653–657 (2011). 33. Cools, A. M., Witvrouw, E. E., Declercq, G. A., Danneels, L. A. & Cambier, D. C. Scapular muscle recruitment patterns: Trapezius muscle latency with and without impingement symptoms. Am. J. Sports Med. 31, 542–549 (2003). 34. Griegel-Morris, P., Larson, K., Mueller-Klaus, K. & Oatis, C. A. Incidence of common postural abnormalities in the cervical, shoulder, and thoracic regions and their association with pain in two age groups of healthy subjects. Phys. Ther. 72, 425–431 (1992). 35. Putz-Anderson, V., Bernard, B., & N. I. for O. S. and H. Musculoskeletal disorders and workplace factors: a critical review of epidemiologic evidence for work-related musculoskeletal disorders of the neck, upper extremity, and low back. (Atlanta, Ga.: U.S. Dept. of Health and Human Services, Public Health Service, Centers for Disease Control 108

and Prevention, National Institute for Occupational Safety and Health ; Cincinnati, OH: U.S. Dept. of Health and Human Services, Public Health Servic, 1997). 36. Kendall, F., McCreary, E., & Provance, P. Muscles, testing and function : with Posture and pain (4th ed.). Baltimore, Md: Williams & Wilkins. (Baltimore, Md: Williams & Wilkins., 1993). 37. Borstad, J. D. Resting position variables at the shoulder: Evidence to support a posture- impairment association. Phys. Ther. 86, 549–557 (2006). 38. Moore, M. K. Upper crossed syndrome and its relationship to cervicogenic headache. J. Manipulative Physiol. Ther. 27, 414–420 (2004). 39. Christensen, K. Manual muscle testing and postural imbalance. Dyn. Chiropr. 18, (2000). 40. Yoo, W. G. Comparison of shoulder muscles activation for shoulder abduction between forward shoulder posture and asymptomatic persons. J. Phys. Ther. Sci. 25, 815–816 (2013). 41. Burkhart, S. S., Morgan, C. D. & Kibler, W. Ben. The disabled throwing shoulder: Spectrum of pathology part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthrosc. - J. Arthrosc. Relat. Surg. 19, 641–661 (2003). 42. Novak, C. B. & Mackinnon, S. E. Nerve injury in repetitive motion disorders. Clin. Orthop. Relat. Res. 10–20 (1998). 43. Sahrmann, S. Diagnosis and treatment of movement impairment syndromes. (Elsevier Health Sciences, 2002). 44. Janda, V., Frank, C. & Liebenson, C. Evaluation of muscular imbalance. Rehabilitation of the spine: a practitioner’s manual. (1996). 45. Ludewig, P. M. & Reynolds, J. F. The association of scapular kinematics and glenohumeral joint pathologies. J. Orthop. Sport. Phys. Ther. 39, 90–104 (2009). 46. Roddey, T. S., Olson, S. L. & Grant, S. E. The effect of pectoralis muscle stretching on the resting position of the scapula in persons with varying degrees of forward head/rounded shoulder posture. J. Man. Manip. Ther. 10, 124–128 (2002). 47. Powers, S. K. & Howley, E. T. Exercise physiology: Theory and application to fitness and performance. (1990). 48. Herbert, R. The passive mechanical properties of muscle and their adaptations to altered patterns of use. Aust. J. Physiother. 34, 141–149 (1988). 109

49. Witzmann, F. A., Kim, D. H. & Fitts, R. H. Hindlimb immobilization: Length-tension and contractile properties of skeletal muscle. J. Appl. Physiol. 53, 335–345 (1982). 50. Harvey, L., Herbert, R. & Crosbie, J. Does stretching induce lasting increases in joint ROM? A systematic review. Physiother. Res. Int. 7, 1–13 (2002). 51. Godges, J. J., MacRae, H., Longdon, C., Tinberg, C. & MacRae, P. The effects of two stretching procedures on hip range of motion and gait economy. J. Orthop. Sport. Phys. Ther. 10, 350–357 (1989). 52. Shrier, I. Does stretching help prevent injuries? in Evidence-based Sports Medicine 36–58 (Blackwell Publishing). doi:10.1002/9780470988732.ch3 53. Kluemper, M., Uhl, T. & Hazelrigg, H. Effect of stretching and strengthening shoulder muscles on forward shoulder posture in competitive swimmers. J. Sport Rehabil. 15, 58– 70 (2006). 54. Dewan, N., Raja, K., Balthillaya Miyaru, G. & MacDermid, J. C. Effect of box taping as an adjunct to stretching-strengthening exercise program in correction of scapular alignment in people with forward shoulder posture: A randomised trial. ISRN Rehabil. 2014, 1–12 (2014). 55. Kaur, P. & Jayaraman, G. To compare the effectiveness of myofascial release (MFR) with strengthening and stretching with strengthening to improve the rounded shoulder posture. Indian J. Physiother. Occup. Ther. 13, 116- (2019). 56. Wong, C. K., Coleman, D., DiPersia, V., Song, J. & Wright, D. The effects of manual treatment on rounded-shoulder posture, and associated muscle strength. J. Bodyw. Mov. Ther. 14, 326–333 (2010). 57. Peixoto, G. et al. Case report Swimmer’s shoulder in young athlete: Rehabilitation with emphasis on manual therapy and stabilization of shoulder complex. Man. Ther. 16, 510– 515 (2011). 58. Bang, M. D. & Deyle, G. D. Comparison of supervised exercise with and without manual physical therapy for patients with shoulder impingement syndrome. J. Orthop. Sport. Phys. Ther. 30, 126–137 (2000). 59. Schmidt, R., Lee, T., Winstein, C., Wulf, G. & Zelaznik, H. Motor Control and Learning. (2019). 60. Fitts, P. The information capacity of the human motor. J. Exp. Psychol. 47, (1954). 110

61. Bootsma, R. J., Fernandez, L. & Mottet, D. Behind Fitts’ law: kinematic patterns in goal- directed movements. Int. J. Hum. Comput. Stud. 61, 811–821 (2004). 62. van Zon, N. C. M., Borst, C., Pool, D. M. & van Paassen, M. M. Touchscreens for aircraft navigation tasks: comparing accuracy and throughput of three flight deck interfaces using Fitts’ law. Hum. Factors J. Hum. Factors Ergon. Soc. 62, 897–908 (2020). 63. Smith, D. L., Dainoff, M. J. & Smith, J. P. The effect of chiropractic adjustments on movement time: a pilot study using Fitts law. J. Manipulative Physiol. Ther. 29, 257–266 (2006). 64. Passmore, S. R. et al. Fitts’s Law using lower extremity movement: Performance driven outcomes for degenerative lumbar spinal stenosis. Hum. Mov. Sci. 44, 277–286 (2015). 65. Aloraini, S. M., Glazebrook, C. M., Sibley, K. M., Singer, J. & Passmore, S. Anticipatory postural adjustments during a Fitts’ task: Comparing young versus older adults and the effects of different foci of attention. Hum. Mov. Sci. 64, 366–377 (2019). 66. Glazebrook, C. M., Elliott, D. & Szatmari, P. How do individuals with autism plan their movements? J. Autism Dev. Disord. 38, 114–126 (2008). 67. Glazebrook, C. M., Welsh, T. N. & Tremblay, L. The processing of visual and auditory information for reaching movements. Psychol. Res. 80, 68. Schmidt, R., Lee, T., Winstein, C., Wulf, G., & Zelaznik, H. Motor control and learning : a behavioral emphasis. (2019). 69. Barnes, M. F. & Barnes, M. F. The basic science of myofascial release: morphologic change in connective tissue. Journal of Bodywork and Movement Therapies 1, (1997). 70. Ercole, B., Antonio, S., Julie Ann, D. & Stecco, C. How much time is required to modify a fascial fibrosis? J. Bodyw. Mov. Ther. 14, 318–325 (2010). 71. Gray, H., Standring, S., Ellis, Harold & Berkovitz, B. K. B. Gray’s anatomy: the anatomical basis of clinical practice. (New York: Elsevier Churchill Livingstone., 2005). 72. Punnett, L. & Wegman, D. H. Work-related musculoskeletal disorders: the epidemiologic evidence and the debate. J. Electromyogr. Kinesiol. 14, 13–23 (2004). 73. Moore, K. L., Dalley, A. F. & Agur, A. M. R. Clinically oriented anatomy. (Philadelphia : Wolters Kluwer Health/Lippincott Williams & Wilkins, [2014], 2014). 74. Magee, D. Orthopedic physical assessment. (Magee, D. (2014). Orthopedic physical assessment (Sixth edition.). St. Louis, Mo: Elsevier Saunders., 2014). 111

75. Wu, G. et al. ISB recommendation on definitions of joint coordinate systems of various joints for the reporting of human joint motion—Part II: shoulder, elbow, wrist and hand. J. Biomech. 38, 981–992 (2005). 76. Seth, A., Matias, R., Veloso, A. P. & Delp, S. L. A biomechanical model of the scapulothoracic joint to accurately capture scapular kinematics during shoulder movements. PLoS One 11, e0141028 (2016). 77. Serratus Anterior: Learn Your Muscles - Custom Pilates and Yoga. Available at: https://www.custompilatesandyoga.com/serratus-anterior-learn-your-muscles/. (Accessed: 30th December 2019) 78. Johnson, G., Bogduk, N., Nowitzke, A. & House, D. Anatomy and actions of the trapezius muscle. Clin. Biomech. 9, 44–50 (1994). 79. Klingler, W., Velders, M., Hoppe, K., Pedro, M. & Schleip, R. Clinical relevance of fascial tissue and dysfunctions. Curr. Pain Headache Rep. 18, 439 (2014). 80. Findley, T., Chaudhry, H., Stecco, A. & Roman, M. Fascia research – A narrative review. J. Bodyw. Mov. Ther. 16, 67–75 (2012). 81. Stecco, A. et al. The pectoral fascia: Anatomical and histological study. J. Bodyw. Mov. Ther. 13, 255–261 (2009). 82. Stecco, A. et al. Pectoral and femoral fasciae: common aspects and regional specializations. Surg. Radiol. Anat. 31, 35–42 (2009). 83. Hedley, G. Notes on visceral adhesions as fascial pathology. J. Bodyw. Mov. Ther. 14, 255–261 (2010). 84. Mccombe, D., Brown, T., Slavin, J. & Morrison, W. A. The histochemical structure of the deep fascia and its structural response to surgery. J. Hand Surg. Am. 26, 89–97 (2001). 85. Stecco, A., Gesi, M., Stecco, C. & Stern, R. Fascial components of the myofascial pain syndrome. Curr. Pain Headache Rep. 17, 352 (2013). 86. Simons, D. G. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction. J. Electromyogr. Kinesiol. 14, 95–107 (2004). 87. Donnelly, J. M. Travell, Simons & Simons’ myofascial pain and dysfunction: the trigger point manual. (Wolters Kluwer, 2019). 88. Lavelle, E. D., Lavelle, W. & Smith, H. S. Myofascial trigger points. Med. Clin. North Am. 91, 229–239 (2007). 112

89. Dommerhold, J. & Huijbregts, P. Myofascial trigger points: pathophysiology and evidence-informed diagnosis and management. (Jones and Bartlett Publishers, 2011). 90. Ibarra, J. M. et al. Latent myofascial trigger points are associated with an increased antagonistic muscle activity during agonist muscle contraction. J. Pain 12, 1282–1288 (2011). 91. Samuel, A. S., Peter, A. A. & Ramanathan, K. The association of active trigger points with lumbar disc lesions. J. Musculoskelet. Pain 15, 11–18 (2007). 92. Mohammadi, Z. et al. The effects of active trigger point of upper trapezius muscle on its electromyography activity and maximal isometric contraction force during scapular plane elevation (scaption). J. Rehabil. 14, (2014). 93. Fernández-de-las-Peñas, C. & Dommerholt, J. International consensus on diagnostic criteria and clinical considerations of myofascial trigger points: A delphi study. Pain Med. 19, 142–150 (2018). 94. Tough, E. A., White, A. R., Richards, S. & Campbell, J. Variability of criteria used to diagnose myofascial trigger point pain syndrome—Evidence from a review of the literature. Clin. J. Pain 23, 278–286 (2007). 95. Lucas, N., Macaskill, P., Irwig, L., Moran, R. & Bogduk, N. Reliability of physical examination for diagnosis of myofascial trigger points. Clin. J. Pain 25, 80–89 (2009). 96. Weisman, A., Meakins, A. & Rotem-Lehrer, N. A Delphi study: Defining a unicorn. Pain Med. 19, 1295–1295 (2018). 97. Quintner, J. L., Bove, G. M. & Cohen, M. L. A critical evaluation of the trigger point phenomenon. Rheumatology 54, 392–399 (2015). 98. Rathbone, A., Henry, J. & Kumbhare, D. Comment on: A critical evaluation of the trigger point phenomenon. Rheumatol. (United Kingdom) 54, 1126–1127 (2015). 99. Chen, Q. et al. Quantification of myofascial taut bands. Arch. Phys. Med. Rehabil. 97, 67– 73 (2016). 100. Chen, Q., Bensamoun, S., Basford, J. R., Thompson, J. M. & An, K.-N. Identification and Quantification of Myofascial Taut Bands With Magnetic Resonance Elastography. Arch. Phys. Med. Rehabil. 88, 1658–1661 (2007). 101. Day, J. A., Stecco, C. & Stecco, A. Application of Fascial Manipulation© technique in chronic shoulder pain—Anatomical basis and clinical implications. J. Bodyw. Mov. Ther. 113

13, 128–135 (2009). 102. Simons, D. G. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction. J. Electromyogr. Kinesiol. 14, 95–107 (2004). 103. Pedrelli, A., Stecco, C. & Day, J. A. Treating patellar tendinopathy with Fascial Manipulation. J. Bodyw. Mov. Ther. 13, 73–80 (2009). 104. Travell, JG & Simons, D. Myofascial pain and dysfunction: the trigger point manual. (Lippincott Williams & Wilkins, 1983). 105. Ge, H.-Y., Zhang, Y., Boudreau, S., Yue, S.-W. & Arendt-Nielsen, L. Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points. Exp. Brain Res. 187, 623–629 (2008). 106. Xu, Y.-M., Ge, H.-Y. & Arendt-Nielsen, L. Sustained nociceptive mechanical stimulation of latent myofascial trigger point induces central sensitization in healthy subjects. J. Pain 11, 1348–1355 (2010). 107. Hoyle, J. A., Marras, W. S., Sheedy, J. E. & Hart, D. E. Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. J. Electromyogr. Kinesiol. 21, 41–48 (2011). 108. Bohlooli, N., Ahmadi, A., Maroufi, N., Sarrafzadeh, J. & Jaberzadeh, S. Differential activation of scapular muscles, during arm elevation, with and without trigger points. J. Bodyw. Mov. Ther. 20, 26–34 (2016). 109. Ge, H.-Y., Arendt-Nielsen, L. & Madeleine, P. Accelerated muscle fatigability of latent myofascial trigger points in humans. Pain Med. 13, 957–964 (2012). 110. Langevin, H. M. et al. Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain. BMC Musculoskelet. Disord. 10, 151 (2009). 111. Langevin, H. M. et al. Reduced thoracolumbar fascia shear strain in human chronic low back pain. BMC Musculoskelet. Disord. 12, 203 (2011). 112. Ge, H. Y. & Arendt-Nielsen, L. Latent myofascial trigger points. Curr. Pain Headache Rep. 15, 386–392 (2011). 113. Raine, S. & Twomey, L. T. Head and Shoulder Posture Variations in 160 Asymptomatic Women and Men. 114. Liebenson, C. et al. Rehabilitation of the Spine - A Practitioner’s Manual Second edition 114

Part IV. (Lippincott Williams & Wilkins). 115. Taspinar, F., Aksoy, C. C., Taspinar, B. & Cimbiz, A. Comparison of patients with different pathologies in terms of shoulder protraction and scapular asymmetry. J. Phys. Ther. Sci. 25, 1033–1038 (2013). 116. Nijs, J., Roussel, N., Struyf, F., Mottram, S. & Meeusen, R. Clinical assessment of scapular positioning in patients with shoulder pain: state of the art. J. Manipulative Physiol. Ther. 30, 69–75 (2007). 117. Lukasiewicz, A. C. et al. Comparison of 3-dimensional scapular position and orientation between subjects with and without shoulder impingement. J. Orthop. Sport. Phys. Ther. 29, 574–586 (1999). 118. Kibler, W. Ben et al. Clinical implications of scapular dyskinesis in shoulder injury: The 2013 consensus statement from the ‘scapular summit’. Br. J. Sports Med. 47, 877–885 (2013). 119. Day, B. L., Marsden, C. D., Obeso, J. A. & Rothwell, J. C. Reciprocal inhibition between the muscles of the human forearm. J. Physiol. 349, 519–534 (1984). 120. Blazevich, A. J. et al. Plantarflexor stretch training increases reciprocal inhibition measured during voluntary dorsiflexion. J. Neurophysiol. 107, 250–256 (2012). 121. Leonard, C. T., Sandholdt, D. Y. & McMillan, J. A. Long-latency contributions to reciprocal inhibition during various levels of muscle contraction. Brain Res. 817, 1–12 (1999). 122. Shindo, M., Harayama, H., Kondo, K., Yanagisawa, N. & Tanaka, R. Changes in reciprocal ia inhibition during voluntary contraction in man. Exp. Brain Res. 53, 400–408 (1984). 123. Iles, J. F. Reciprocal inhibition during agonist and antagonist contraction. Exp. Brain Res. 62, 212–214 (1986). 124. Delwaide, P. J., Sabatino, M., Pepin, J. L. & La Grutta, V. Reinforcement of reciprocal inhibition by contralateral movements in man. Exp. Neurol. 99, 10–16 (1988). 125. McClelland, V. ., Miller, S. & Eyre, J. . Short latency heteronymous excitatory and inhibitory reflexes between antagonist and heteronymous muscles of the human shoulder and upper limb. Brain Res. 899, 82–93 (2001). 126. Goodman, S. R. Accuracy and variability of the movement in Fitts’ and Schmidt’s laws. 115

Behav. Brain Sci. 20, 309–310 (1997). 127. Kong, J. & Ren, X. The optimal calculation method to determine the effective target width for the application of fitts’ law. IEICE Trans. Inf. Syst. E90-D, 753–758 (2007). 128. Fitts, P. M. & Peterson, J. R. Information capacity of discrete motor responses. J. Exp. Psychol. 67, 129. Zhai, S., Kong, J. & Ren, X. Speed–accuracy tradeoff in Fitts’ law tasks—on the equivalency of actual and nominal pointing precision. Int. J. Hum. Comput. Stud. 61, 823– 856 (2004). 130. Adam, J. J. The effects of objectives and constraints on motor control strategy in reciprocal aiming movements. J. Mot. Behav. 24, 173–185 (1992). 131. Murata, A. Extending Effective Target Width in Fitts ’ Law to a Two-Dimensional Pointing Task Extending Effective Target Width in Fitts ’ Law to a Two-Dimensional Pointing Task. Int. J. Hum. Comput. Interact. 7318, 137–152 (1999). 132. Schmidt, R. A. A schema theory of discrete motor skill learning. Mind 82, 225–260 (1975). 133. Schmidt, R. A. & et al. Motor-output variability: A theory for the accuracy of rapid motor acts. Psychol. Rev. 86, 415–451 (1979). 134. Uno, Y., Kawato, M. & Suzuki, R. Formation and control of optimal trajectory in human multijoint arm movement. Biol. Cybern. 61, 89–101 (1989). 135. Takeda, M. et al. Explanation of fitts’ law in reaching movement based on human arm dynamics. Sci. Rep. 9, 19804 (2019). 136. Clark, L. D., Bhagat, A. B. & Riggs, S. L. Extending Fitts’ law in three-dimensional virtual environments with current low-cost virtual reality technology. Int. J. Hum. Comput. Stud. 139, 102413 (2020). 137. Zeng, X., Hedge, A. & Guimbretiere, F. Fitts’ law in 3D space with coordinated hand movements. Proc. Hum. Factors Ergon. Soc. Annu. Meet. 56, 990–994 (2012). 138. Billette, J. & Janz, T. Injuries in Canada: Insights from the Canadian community health survey. Statistics Canada (2010). Available at: https://www150.statcan.gc.ca/n1/pub/82- 624-x/2011001/article/11506-eng.htm. (Accessed: 10th December 2019) 139. Annual Report 2018 | Workers Compensation Board of Manitoba. Available at: https://www.wcb.mb.ca/annual-report-2018. (Accessed: 10th December 2019) 116

140. Hauret, K. G., Jones, B. H., Bullock, S. H., Canham-Chervak, M. & Canada, S. Musculoskeletal injuries. Am. J. Prev. Med. 38, S61–S70 (2010). 141. Burton, K. & Kendall, N. Musculoskeletal disorders. (2014). 142. da Costa, B. R. & Vieira, E. R. Risk factors for work-related musculoskeletal disorders: a systematic review of recent longitudinal studies. Am. J. Ind. Med. 53, n/a-n/a (2009). 143. Khan’, B. &. Clinical Sports Medicine. 144. Musculoskeletal conditions. Available at: https://www.who.int/news-room/fact- sheets/detail/musculoskeletal-conditions. (Accessed: 25th October 2019) 145. Bush, I. L. N. and P. M. Work-Related Musculoskeletal Disorders Assessment and Prevention. (2012). doi:10.5772/37229 146. Szeto, G. P. Y., Straker, L. M. & Sullivan, P. B. O. A comparison of symptomatic and asymptomatic office workers performing monotonous keyboard work — 2 : Neck and shoulder kinematics. 10, 281–291 (2005). 147. Page, P. Shoulder muscle imbalance and subacromial impingement syndrome in overhead athletes. Int. J. Sports Phys. Ther. 6, 51–8 (2011). 148. Kibler, B. W., Sciascia, A. & Wilkes, T. Scapular dyskinesis and its relation to shoulder injury. J. Am. Acad. Orthop. Surg. 20, 364–372 (2012). 149. Bone and Joint Initiative USA. The Impact of Musculoskeletal Disorders on Americans- Opportunities for Action. (2012). 150. Levy, B. Occupational and Environmental Health: Recognizing and Preventing Disease. (New York: Oxford University Press, 2011). 151. Etemadinezhad, S., Ranjbar, F. & Charati, J. Y. Investigation into the musculoskeletal disorders prevalence and postural assessment among barbers in Sari-2016. 6, 40–46 (2018). 152. Luttmann, A., Jager, M. & Griefahn, B. Preventing Musculoskeletal Disorders in the Workplace. Protecting Workers, Health Series 153. AWCBC. National Work Injury/Disease Statistics Program. (2018). Available at: https://awcbc.org/en/statistics/#injuries. (Accessed: 5th March 2021) 154. WSIB. 2019 WSIB Statistical Report. (2019). Available at: http://www.wsibstatistics.ca/S2/Part of Body _ WSIB By The Numbers_P.php. (Accessed: 6th March 2021) 117

155. Wilkins, K. & Mackenzie, S. G. Work Injuries. Heal. Reports (Statistics Canada Cat. 18, 1–18 (2007). 156. Organization, W. H. Identification and control of work-related diseases. (1985). 157. Most Common MSK Issues in the Workplace - HRHQ No1 Choice for HR News & Resources. Available at: https://www.hrheadquarters.ie/health-and-well-being/common- msk-issues-workplace/. (Accessed: 30th December 2019) 158. Aumann, K. & Galinsky, E. The state of health in the American workforce: Does having an effective workplace matter? (2009). 159. Hajihosseini, E., Norasteh, A., Shamsi, A. & Daneshmandi, H. The effects of strengthening, stretching and comprehensive exercises on forward shoulder posture correction. Phys. Treat. - Specif. Phys. Ther. J. 4, 123–132 (2014). 160. Hall, H., McIntosh, G., Alleyne, J. & Cote, P. A pain in the neck. 161. Côté, P., Cassidy, D. J., Carroll, L. J. & Kristman, V. The annual incidence and course of neck pain in the general population: a population-based cohort study. Pain 112, 267–273 (2004). 162. Haldeman, S., Carroll, L., Cassidy, J. D., Schubert, J. & Nygren, Å. The bone and joint decade 2000–2010 task force on neck pain and its associated disorders. Spine (Phila. Pa. 1976). 33, S5–S7 (2008). 163. Church, T. S. et al. Trends over 5 decades in U.D. occupation-related physical activity and their associations with obesity. PLoS One 6, e19657 (2011). 164. Tremblay, M. S., Colley, R. C., Saunders, T. J., Healy, G. N. & Owen, N. Physiological and health implications of a sedentary lifestyle. Appl. Physiol. Nutr. Metab. 35, 725–740 (2010). 165. Straker, L. M., O’Sullivan, P. B., Smith, A. & Perry, M. Computer use and habitual spinal posture in Australian adolescents. Public Health Rep. 122, 634–643 (2007). 166. Lopes, A. D., Timmons, M. K., Grover, M., Ciconelli, R. M. & Michener, L. A. Visual scapular dyskinesis: Kinematics and muscle activity alterations in patients with subacromial impingement syndrome. Arch. Phys. Med. Rehabil. 96, 298–306 (2015). 167. Phadke, V., Camargo, P. & Ludewig, P. Scapular and rotator cuff muscle activity during arm elevation: a review of normal function and alterations with shoulder impingement. Brazilian J. Phys. Ther. 13, 1–9 (2009). 118

168. Bandholm, T., Rasmussen, L., Aagaard, P., Jensen, B. R. & Diederichsen, L. Force steadiness, muscle activity, and maximal muscle strength in subjects with subacromial impingement syndrome. Muscle and Nerve 34, 631–639 (2006). 169. Moraes, G. F. S., Faria, C. D. C. M. & Teixeira-Salmela, L. F. Scapular muscle recruitment patterns and isokinetic strength ratios of the shoulder rotator muscles in individuals with and without impingement syndrome. J. Shoulder Elb. Surg. 17, 48–53 (2008). 170. Roy, J.-S., Moffet, H. & McFadyen, B. J. Upper limb motor strategies in persons with and without shoulder impingement syndrome across different speeds of movement. Clin. Biomech. 23, 1227–1236 (2008). 171. Cools, A. M., Witvrouw, E. E., Declercq, G. A., Vanderstraeten, G. G. & Cambier, D. C. Evaluation of isokinetic force production and associated muscle activity in the scapular rotators during a protraction-retraction movement in overhead athletes with impingement symptoms. Br. J. Sports Med. 38, 64–68 (2004). 172. Michener, L. A., Sharma, S., Cools, A. M. & Timmons, M. K. Relative scapular muscle activity ratios are altered in subacromial pain syndrome. J. Shoulder Elb. Surg. 25, 1861– 1867 (2016). 173. Malchaire, J. et al. Musculoskeletal complaints, functional capacity, personality and psychosocial factors. Int. Arch. Occup. Environ. Health 74, 549–557 (2001). 174. W M van der Windt, D. A. et al. Occupational risk factors for shoulder pain: a systematic review. Occup Environ Med 57, (2000). 175. Jensen, C. et al. Job demands, muscle activity and musculoskeletal symptoms in relation to work with the computer mouse. Scand. J. Work. Environ. ＆ Heal. 24, 418–424 (1998). 176. Hakala, P. T., Rimpelä, A. H., Saarni, L. A. & Salminen, J. J. Frequent computer-related activities increase the risk of neck–shoulder and low back pain in adolescents. Eur. J. Public Health 16, 536–541 (2006). 177. Nordander, C. et al. Gender differences in workers with identical repetitive industrial tasks: exposure and musculoskeletal disorders. Int. Arch. Occup. Environ. Health 81, 939– 947 (2008). 178. Lindman, R., Eriksson, A. & Thornell, L.-E. Fiber type composition of the human female trapezius muscle: Enzyme-histochemical characteristics. Am. J. Anat. 190, 385–392 119

(1991). 179. Lexell, J., Henriksson-Larsen, K. & Sjostrom, M. Distribution of different fibre types in human skeletal muscles 2. A study of cross-sections of whole m. vastus lateralis. Acta Physiol. Scand. 117, 115–122 (1983). 180. Hrysomallis, C. Effectiveness of strengthening and stretching exercises for the postural correction of abducted scapulae: A review. J. Strength Cond. Res. 24, 567–574 (2010). 181. Burkhart, S. S., Morgan, C. D. & Kibler, W. B. Shoulder injuries in overhead athletes: The ‘dead arm’ revisited. Clin. Sports Med. 19, 125–158 (2000). 182. Decker, M. J., Hintermeister, R. A., Faber, K. J. & Hawkins, R. J. activity during selected rehabilitation exercises. Am. J. Sports Med. 27, 784–791 (1999). 183. Finley, M. A. & Lee, R. Y. Effect of sitting posture on 3-dimensional scapular kinematics measured by skin-mounted electromagnetic tracking sensors. Arch. Phys. Med. Rehabil. 84, 563–568 (2003). 184. Ha, S. min et al. Comparison of electromyographic activity of the lower trapezius and serratus anterior muscle in different arm-lifting scapular posterior tilt exercises. Phys. Ther. Sport 13, 227–232 (2012). 185. Ludewig, P. M., Cook, T. M. & Nawoczenski, D. A. Three-dimensional scapular orientation and muscle activity at selected positions of humeral elevation. J. Orthop. Sports Phys. Ther. 24, 57–65 (1996). 186. Moseley, J. B., Jobe, F. W., Pink, M., Perry, J. & Tibone, J. EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am. J. Sports Med. 20, 128–134 (1992). 187. Wang, C.-H., Mcclure, P., Pratt, N. E. & Nobilini, R. Stretching and strengthening exercises: Their effect on three-dimensional scapular kinematics. (1999). 188. Lee, J.-H. H., Cynn, H. seock, Yi, C.-H. H., Kwon, O. yun & Yoon, T.-L. L. Predictor variables for forward scapular posture including posterior shoulder tightness. J. Bodyw. Mov. Ther. 19, 253–260 (2015). 189. Arshadi, R., Ghasemi, G. A. & Samadi, H. Effects of an 8-week selective corrective exercises program on electromyography activity of scapular and neck muscles in persons with upper crossed syndrome: Randomized controlled trial. Phys. Ther. Sport 37, 113–119 (2019). 190. Thigpen, C. A. et al. Head and shoulder posture affect scapular mechanics and muscle 120

activity in overhead tasks. J. Electromyogr. Kinesiol. 20, 701–709 (2010). 191. Weiser, W. M., Lee, T. Q., Mcmaster, W. C. & Mcmahon, P. J. Effects of simulated scapular protraction on anterior glenohumeral stability. (1999). 192. Karagiannakis, D., Athanasopoulos, S. & Mandalidis, D. Scapular muscles’ activity in female volleyball players with scapular asymmetry in the resting position. J. Bodyw. Mov. Ther. 22, 580–585 (2018). 193. Borstad, J. D. & Ludewig, P. M. The Effect of Long Versus Short Pectoralis Minor Resting Length on Scapular Kinematics in Healthy Individuals. J. Orthop. Sport. Phys. Ther. 35, 227–238 (2005). 194. Borstad, J. D. & Ludewig, P. M. The effect of long versus short pectoralis minor resting length on scapular kinematics in healthy individuals. J. Orthop. Sport. Phys. Ther. 35, 227–238 (2005). 195. Cools, A. M. et al. Descriptive profile of scapulothoracic position, strength and flexibility variables in adolescent elite tennis players. Br. J. Sports Med. 44, 678–684 (2010). 196. McClain, M., Tucker, W. S. & Hornor, S. D. Comparison of scapular position in overhead- and nonoverhead-throwing athletes using the pectoralis minor length test. Athl. Train. Sport. Heal. Care 4, 45–48 (2012). 197. Smith, J., Kotajarvi, B. R., Padgett, D. J. & Eischen, J. J. Effect of scapular protraction and retraction on isometric shoulder elevation strength. Arch. Phys. Med. Rehabil. 83, 367–370 (2002). 198. Singla, D. & Veqar, Z. Methods of postural assessment used for sports persons. Journal of Clinical and Diagnostic Research 8, (2014). 199. Peterson, D. E. et al. Investigation of the validity and reliability of four objective techniques for forward shoulder. JOSPT J. Orthop. Sport. Phys. Ther. Downloaded from www.jospt.org 25, (1997). 200. Borstad, J. D. Measurement of pectoralis minor muscle length: Validation and clinical application. J. Orthop. Sport. Phys. Ther. 38, 169–174 (2008). 201. Weber, C., Enzler, M., Wieser, K. & Swanenburg, J. Validation of the pectoralis minor length test: A novel approach. Man. Ther. 22, 50–55 (2016). 202. Slater, D., Korakakis, V., O’Sullivan, P., Nolan, D. & O’Sullivan, K. “Sit up straight”: Time to re-evaluate. J. Orthop. Sport. Phys. Ther. 49, 562–564 (2019). 121

203. Harrison, A. L., Barry-Greb, T. & Wojtowicz, G. Clinical measurement of head and shoulder posture variables. J. Orthop. Sports Phys. Ther. 23, 353–361 (1996). 204. Ferreira, E. A., Duarte, M., Maldonado, E. P., Bersanetti, A. A. & Marques, A. P. Quantitative assessment of postural alignment in young adults based on photographs of anterior, posterior, and lateral views. J. Manipulative Physiol. Ther. 34, 371–380 (2011). 205. Lewis, J. S., Green, A. & Wright, C. Subacromial impingement syndrome: The role of posture and muscle imbalance. J. Shoulder Elb. Surg. 14, 385–392 (2005). 206. Greenfield, B. et al. Posture in Patients With Shoulder Overuse Injuries and Healthy Individuals. J. Orthop. Sport. Phys. Ther. 21, 287–295 (1995). 207. McClure, P. W., Michener, L. a & Karduna, A. R. Shoulder Function and 3-Dimensional Scapular Kinematics in People With and Without Shoulder Impingement Syndrome. Phys. Ther. 86, 1075–1090 (2006). 208. Sarabadani Tafreshi, E., Nodehi Moghadam, A., Bakhshi, E. & Rastgar, M. Comparing scapular position and scapular dyskinesis in individuals with and without rounded shoulder posture. Phys. Treat. Specif. Phys. Ther. 5, 127–136 (2015). 209. Braun, B. L. & Braun, B. L. Postural differences between asymptomatic men and women and craniofacial pain patients. Arch. Phys. Med. Rehabil. 72, 653–656 (1991). 210. Lewis, J. S., Green, A. & Wright, C. Subacromial impingement syndrome: The role of posture and muscle imbalance. J. Shoulder Elb. Surg. 14, 385–392 (2005). 211. Lynch, S. S., Thigpen, C. A., Mihalik, J. P., Prentice, W. E. & Padua, D. The effects of an exercise intervention on forward head and rounded shoulder postures in elite swimmers. Br. J. Sports Med. 44, 376–381 (2010). 212. Lee, J. et al. The effect of scapular posterior tilt exercise, pectoralis minor stretching, and shoulder brace on scapular alignment and muscles activity in subjects with round-shoulder posture. J. Electromyogr. Kinesiol. 25, 107–14 (2015). 213. Fathollahnejad, K., Letafatkar, A. & Hadadnezhad, M. The effect of manual therapy and stabilizing exercises on forward head and rounded shoulder postures: a six-week intervention with a one-month follow-up study. BMC Musculoskelet. Disord. 20, 86 (2019). 214. Voight, M. L. & Thomson, B. C. The role of the scapula in the rehabilitation of shoulder injuries. J. Athl. Train. 35, 364–72 (2000). 122

215. Kibler, W. Ben, Sciascia, A. D., Uhl, T. L., Tambay, N. & Cunningham, T. Electromyographic analysis of specific exercises for scapular control in early phases of shoulder rehabilitation. Am. J. Sports Med. 36, 1789–1798 (2008). 216. Moezy, A., Sepehrifar, S. & Dodaran, M. S. The effects of scapular stabilization based exercise therapy on pain, posture, flexibility and shoulder mobility in patients with shoulder impingement syndrome: A controlled randomized clinical trial. Med. J. Islam. Repub. Iran 28, (2014). 217. Goodman, C. & Hrysomallis, C. A review of resistance exercise and posture realignment. J. Strength Cond. Res. 15, 385–390 (2001). 218. Borstad, J. D. & Ludewig, P. M. Comparison of three stretches for the pectoralis minor muscle. J. Shoulder Elb. Surg. 15, 324–330 (2006). 219. Brown, D., Golia, L., Lotwala, A. & McCandless, R. A comparison of three proprioceptive neuromuscular facilitation stretching techniques on correcting forward shoulder posture in young adults. Phys. Ther. 80, (2000). 220. Viriyatharakij, N., Chinkulprasert, C., Rakthim, N., Patumrat, J. & Ketruang, B. Change of pectoralis minor length, and acromial distance, during scapular retraction at 60° shoulder elevation. J. Bodyw. Mov. Ther. 21, 53–57 (2017). 221. Williams, J. G., Laudner, K. G. & McLoda, T. The acute effects of two passive stretch maneuvers on pectoralis minor length and scapular kinematics among collegiate swimmers. Int. J. Sports Phys. Ther. 8, 25–33 (2013). 222. Muraki, T., Aoki, M., Izumi, T., Fujii, M. & Hidaka, E. Lengthening of the pectoralis minor motions and stretching techniques. Phys. Ther. 89, 333–341 (2009). 223. Sandberg, J. B., Wagner, D. R., Willardson, J. M. & Smith, G. A. Acute effects of antagonist stretching on jump height, torque, and electromyography of agonist musculature. J. Strength Cond. Res. 26, 1249–1256 (2012). 224. Rosa, D. P., Borstad, J. D., Pogetti, L. S. & Camargo, P. R. Effects of a stretching protocol for the pectoralis minor on muscle length, function, and scapular kinematics in individuals with and without shoulder pain. J. Hand Ther. 30, 20–29 (2017). 225. Laudner, K. & Thorson, K. Acute effects of pectoralis minor self-mobilization on shoulder motion and posture: A blinded and randomized placebo-controlled study in asymptomatic individuals. J. Sport Rehabil. 29, 420–424 (2020). 123

226. Hopper, D. et al. Evaluation of the effect of two massage techniques on hamstring muscle length in competitive female hockey players. Phys. Ther. Sport 6, 137–145 (2005). 227. Laudner, K., Compton, B. D., McLoda, T. A. & Walters, C. M. Acute effects of instrument assisted soft tissue mobilization for improving posterior shoulder range of motion in collegiate baseball players. Int. J. Sports Phys. Ther. 9, 1–7 (2014). 228. Crosman, L. J., Chateauvert, S. R. & Weisberg, J. The effects of massage to the hamstring muscle group on range of motion. J. Orthop. Sports Phys. Ther. 6, 168–172 (1984). 229. Baker, R. T., Nasypany, A. & Seegmiller, J. G. Instrument-assisted soft tissue mobilization treatment for tissue extensibility dysfunction. Int. J. Athl. Ther. Train. 18, 16–21 (2013). 230. Threlkheld, J. The effects of manual therapy on connective tissue. Phys. Ther. 72, 893– 902 (1992). 231. Morelli, M., Seaborne, D. E. & Sullivan, S. J. Changes in H-reflex amplitude during massage of triceps surae in healthy subjects. J. Orthop. Sports Phys. Ther. 12, 55–59 (1990). 232. Morelli, M., Seaborne, D. E. & John Sullivan, S. H-reflex modulation during manual muscle massage of human triceps surae. Arch Phys Med Rehabll 72, (1991). 233. Huguenin, L. K. Myofascial trigger points: the current evidence. doi:10.1016/j.ptsp.2003.11.002 234. Barnes, J. F. Myofascial release for craniomandibular pain and dysfunction. Int. J. Orofacial Myology 22, 20–2 (1996). 235. Laimi, K. et al. Effectiveness of myofascial release in treatment of chronic musculoskeletal pain: a systematic review. Clin. Rehabil. 32, 440–450 (2018). 236. Kalichman, L. & Ben David, C. Effect of self-myofascial release on myofascial pain, muscle flexibility, and strength: A narrative review. J. Bodyw. Mov. Ther. 21, 446–451 (2017). 237. McKenney, K., Elder, A. S., Elder, C. & Hutchins, A. Myofascial release as a treatment for orthopaedic conditions: A systematic review. J. Athl. Train. 48, 522–527 (2013). 238. Ajimsha, M. S., Al-Mudahka, N. R. & Al-Madzhar, J. A. Effectiveness of myofascial release: Systematic review of randomized controlled trials. J. Bodyw. Mov. Ther. 19, 102– 112 (2015). 124

239. Fairall, R. R., Cabell, L., Boergers, R. J. & Battaglia, F. Acute effects of self-myofascial release and stretching in overhead athletes with GIRD. J. Bodyw. Mov. Ther. 21, 648–652 (2017). 240. Nielsen, A. Gua sha research and the language of integrative medicine. J. Bodyw. Mov. Ther. 13, 63–72 (2009). 241. Barnes, J. F. John F. Barnes, PT - Myofascial Release. Available at: https://www.myofascialrelease.com/about/johnfbarnes.aspx. (Accessed: 28th April 2021) 242. McLeod, M. The acute effect of a myofascial release intervention on resting scapular position. (The University of North Carolina at Chapel Hill, 2007). 243. Smythe, A. Effect of myofascial release to the chest on glenohumeral internal rotation: A comparison of practitioner-applied vs self-applied techniques. (2014). 244. Fairall, R. Acute effects of self-myofascial release and static stretching on shoulder range of motion and performance in overhead athletes with glenohumeral internal rotation deficit. (Seton Hall University, 2017). 245. Ruivo, R. M., Carita, A. I. & Pezarat-Correia, P. The effects of training and detraining after an 8 month resistance and stretching training program on forward head and protracted shoulder postures in adolescents: Randomised controlled study. Man. Ther. 21, 76–82 (2016). 246. SENIAM. Recommendations for sensor locations in shoulder or neck muscles. Available at: http://seniam.org/. (Accessed: 29th October 2019) 247. Criswell, E. & Cram, J. Cram’s introduction to surface electromyography. (Sudbury, MA : Jones and Bartlett, 2011). 248. Henderson, Z. J., Bohunicky, S., Rochon, J. A., Dacanay, M. & Scribbans, T. D. Muscle activation in specific regions of the trapezius during modified Kendall manual muscle tests. J. Athl. Train. (2021). 249. Fritz, S. Mosby’s fundamentals of therapeutic massage. Mosby’s fundamentals of therapeutic massage (Elsevier Mosby, 2013). 250. Rosa, L. A close look at therapeutic touch. JAMA 279, 1005 (1998). 251. Drake, J. D. M. & Callaghan, J. P. Elimination of electrocardiogram contamination from electromyogram signals: An evaluation of currently used removal techniques. J. Electromyogr. Kinesiol. 16, 175–187 (2006). 125

252. Field, A. Discovering Statistics Using IBM SPSS Statistics. (Thousand Oaks, California : SAGE Publications Inc., 2018). 253. Portney, L. G. Foundations of clinical research : applications to practice. Foundations of clinical research : applications to practice (F.A. Davis Company). 254. Ferguson, C. J. An effect size primer: A guide for clinicians and researchers. Prof. Psychol. Res. Pract. 40, 532–538 (2009). 255. Kluemper, M., Uhl, T. & Hazelrigg, H. Effect of Stretching and Strengthening Shoulder Muscles on Forward Shoulder Posture in Competitive Swimmers. J Sport Rehabil 15, (2006). 256. Wang, C.-H. H., Mcclure, P., Pratt, N. E. & Nobilini, R. Stretching and strengthening exercises: Their effect on three- dimensional scapular kinematics. Arch. Phys. Med. Rehabil. 80, 923–929 (1999). 257. Stanek, J., Sullivan, T. & Davis, S. Comparison of compressive myofascial release and the graston technique for improving ankle-dorsiflexion range of motion. J. Athl. Train. 53, 160–167 (2018). 258. Abu-Taleb Walaa, P. T. Ms., Youssef Aliaa Rehan, P. T. Ms. P. & Saleh Amir, P. T. Ms. P. The effectiveness of manual versus algometer pressure release techniques for treating active myofascial trigger points of the upper trapezius. J. Bodyw. Mov. Ther. 20, 863–869 (2016). 259. Ichikawa Kazuna, P. T. Ms. P. C. O., Takei Hitoshi, P. T. P. O., Usa Hideyuki, P. T. P. O., Mitomo Shoh, P. T. Ms. P. C. & Ogawa Daisuke, P. T. Ms. P. C. O. Comparative analysis of ultrasound changes in the vastus lateralis muscle following myofascial release and thermotherapy: A pilot study. J. Bodyw. Mov. Ther. 19, 327–336 (2014). 260. Warren, A. J., LaCross, Z., Volberding, J. L. & O’Brien, M. S. Acute outcomes of myofascial decompression (cupping therapy) compared to self-myofascial release on hamstring pathology after a single treatment. Int. J. Sports Phys. Ther. 15, 579–592 (2020). 261. Kraemer, H. C. et al. Measures of clinical significance. J. Am. Acad. Child Adolesc. Psychiatry 42, 1524–1529 (2003). 262. Kazdin, A. E. The meanings and measurement of clinical significance. J. Consult. Clin. Psychol. 67, 332–339 (1999). 126

263. Jacobson, N. S., Roberts, L. J., Berns, S. B. & McGlinchey, J. B. Methods for defining and determining the clinical significance of treatment effects. J. Consult. Clin. Psychol. 67, 300–307 (1999). 264. Stecco, L. & Stecco, C. Fascial Manipulation. Practical Part. (Piccin, 2012). 265. Blanchard, S. Anatomy trains: myofascial meridians for manual and movement therapists. Phys. Ther. Sport 15, 269 (2014). 266. Weppler, C. H. & Magnusson, S. P. Increasing muscle extensibility: a matter of increasing length or modifying sensation? Phys. Ther. 90, 438–449 (2010). 267. Borstad, J. D. Measurement of pectoralis minor muscle length: Validation and clinical application. J. Orthop. Sports Phys. Ther. 38, 169–174 (2008). 268. Lee, J. H., Cynn, H. seock, Yi, C. H., Kwon, O. yun & Yoon, T. L. Predictor variables for forward scapular posture including posterior shoulder tightness. J. Bodyw. Mov. Ther. 19, 253–260 (2015). 269. Johnson, G., Bogduk, N., Nowitzke, A. & House, D. Anatomy and actions of the trapezius muscle. Clin. Biomech. 9, 44–50 (1994). 270. KRONBERG, M., NEMETH, G. & BROSTROÊM, L.-A. Muscle activity and coordination in the normal shoulder : an electromyographic study. Clin. Orthop. Relat. Res. 76–85 (1990). 271. Kwon, J. W., Son, S. M. & Lee, N. K. Changes in upper-extremity muscle activities due to head position in subjects with a forward head posture and rounded shoulders. J. Phys. Ther. Sci. 27, 1739–1742 (2015). 272. DiVeta, J., Walker, M. L. & Skibinski, B. Relationship between performance of selected scapular muscles and scapular abduction in standing subjects. Phys. Ther. 70, 470–476 (1990). 273. Cools, A. M., Witvrouw, E. E., Danneels, L. A. & Cambier, D. C. Does taping influence electromyographic muscle activity in the scapular rotators in healthy shoulders? Man. Ther. 7, 154–162 (2002). 274. Yoo, W.-G. G. Comparison of shoulder muscles activation for shoulder abduction between forward shoulder posture and asymptomatic persons. J. Phys. Ther. Sci. 25, 815– 816 (2013). 275. Burkhart, S. S., Morgan, C. D. & Kibler, W. B. Ben. The disabled throwing shoulder: 127

Spectrum of pathology part I: Pathoanatomy and biomechanics. Arthrosc. J. Arthrosc. Relat. Surg. 19, 404–420 (2003). 276. Hébert, L. J., Moffet, H., McFadyen, B. J. & Dionne, C. E. Scapular behavior in shoulder impingement syndrome. Arch. Phys. Med. Rehabil. 83, 60–69 (2002). 277. Domingo, A. R. et al. Short-duration therapeutic massage reduces postural upper trapezius muscle activity. Neuroreport 28, 108–110 (2017). 278. Sefton, J. E. M., Yarar, C., Carpenter, D. M. & Berry, J. W. Physiological and clinical changes after therapeutic massage of the neck and shoulders. Man. Ther. 16, 487–494 (2011). 279. Arroyo-Morales, M. et al. Psychophysiological effects of massage-myofascial release after exercise: a randomized sham-control study. J. Altern. Complement. Med. 14, 1223– 1229 (2008). 280. Barlow, A. et al. Effect of massage of the hamstring muscles on selected electromyographic characteristics of biceps femoris during sub-maximal isometric contraction. Int. J. Sports Med. 28, 253–256 (2007). 281. Hunter, A. M., Watt, J. M., Watt, V. & Galloway, S. D. R. Effect of lower limb massage on electromyography and force production of the knee extensors. Br. J. Sports Med. 40, 114–118 (2006). 282. Rashed, S. S., Youssef, A. M., Eldeeb, A. M. & Ellithy, A. Correlation between myoelectric activity of middle trapezius muscle and pectoralis major muscle in patients with postural kyphosis. 178–185 (2019). 283. Poston, B., Christou, E. A., Enoka, J. A. & Enoka, R. M. Timing variability and not force variability predicts the endpoint accuracy of fast and slow isometric contractions. Exp. Brain Res. 202, 189–202 (2010). 284. Emlet, J. A single blind randomized controlled trial of the effects of spinal manipulative therapy on Fitts’ Law performance in participants without neck pain. (2013). 285. DeVocht, J. W. et al. Effect of chiropractic manipulative therapy on reaction time in special operations forces military personnel: a randomized controlled trial. Trials 20, 5 (2019). 286. Umehara, J. et al. Shoulder horizontal abduction stretching effectively increases shear elastic modulus of pectoralis minor muscle. J. Shoulder Elb. Surg. 26, 1159–1165 (2017). 128

287. Umehara, J. et al. Scapular kinematic alterations during arm elevation with decrease in pectoralis minor stiffness after stretching in healthy individuals. J. Shoulder Elb. Surg. 27, 1214–1220 (2018). 288. Umehara, J. et al. Acute and prolonged effects of stretching on shear modulus of the pectoralis minor muscle. J. Sport. Sci. Med. 20, 17–25 (2021).

129

Appendices

Appendix A- Participant Intake Medical Form

*Please note the top right corner was not filled out by participants other than their age

Patient Intake Form Name: ______Date: ______Patient information contained within this form is considered Insurance: ______(dd/mm/yr) strictly confdential. Date of Birth: ______□ male □ female Your responses are important to help us better understand Address: ______the health issues you face and ensure the delivery of the ______Marital status best possible treatment. ______S M W D SEP Phone #: home: ______work: ______E-mail address: ______Occupation: ______Employer: ______

Check and indicate the age when you had any of the following: General Gastrointestinal Cardiovascular Check any of the conditions □ Allergies □ Abdominal pain □ High blood pressure you have or have had: □ Alcoholism □ Depression □ Bloody or tarry stool □ Low blood pressure □ Anemia □ Dizziness □ Colitis / Crohn’s □ Hardening of the arteries □ Appendicitis □ Fainting □ Colon trouble □ Irregular pulse □ Arteriosclerosis □ Fatigue □ Constipation □ Pain over heart □ Asthma □ Fever □ Diarrhea □ Palpitation □ Bronchitis □ Headaches □ Difficult digestion □ Poor circulation □ Cancer □ Loss of sleep □ Diverticulosis □ Rapid heart beat □ Chicken pox □ Mental illness □ Bloated abdomen □ Slow heart beat □ Cold sores □ Nervousness □ Excessive hunger □ Swelling of ankles □ Diabetes □ Tremors □ Gallbladder trouble □ Eczema □ Weight loss / gain □ Hernia Respiratory □ Edema □ Hemorrhoids □ Chest pain □ Emphysema Muscle / Joint □ Intestinal worms □ Chronic cough □ Epilepsy □ Arthritis / rheumatism □ Jaundice □ Difficulty breathing □ Goiter □ Bursitis □ Liver trouble □ Hay fever □ Gout □ Foot trouble □ Nausea □ Shortness of breath □ Heart burn □ Muscle weakness □ Painful deification □ Spitting up phlegm / blood □ Heart disease □ Low back pain □ Pain over stomach □ Wheezing □ Hepatitis □ Neck pain □ Poor appetite □ Herpes □ Mid back pain □ Vomiting Women only □ High cholesterol □ Joint pain □ Vomiting of blood □ Congested breasts □ HIV/AIDS □ Hot flashes Skin □ Influenza Genitourinary □ Lumps in breast □ Boils □ Malaria □ Bed-wetting □ Menopause □ Bruise easily □ Measles □ Bladder infection □ Vaginal discharge □ Dryness □ Miscarriage □ Blood in urine Menstrual flow □ Hives or allergies □ Multiple sclerosis □ Kidney infection □ Reg. □ Irreg. □ Pain / cramps □ Itching □ Mumps □ Kidney stones Days of flow: ____ Length of cycle: _____ □ Rash □ Numbness/tingling □ Prostate trouble Date - 1st day last period: ______□ Varicose veins □ Pace maker □ Pus in urine Are you pregnant? □ yes, □ no □ Osteoporosis □ Stress incontinence If yes, how many months? _____ Eye, Ear, Nose & Throat Pneumonia Urination How many children do you have? _____ □ □ Colds □ Polio □ Overnight more than twice Birth control method: ______□ Deafness □ Rheumatic fever □ More than 8x in 24hrs Date of last PAP test: ______□ Ear ache □ Stroke □ Decreased flow/force □ normal, □ abnormal □ Eye pain □ Thyroid disease □ Painful urination Date of last mammogram: ______□ Gum trouble □ Tuberculosis □ Urgency to urinate □ normal, □ abnormal □ Hoarseness □ Ulcers □ Nasal obstruction □ Nose bleeds Please list any medication you are currently taking and why: □ Ringing of the ears ______□ Sinus infection ______□ Sore throat □ Tonsillitis ______□ Vision problems ______

Reproduction is permitted for personal use, not for resale or redistribution. www.prohealthsys.com ©2012 by Professional Health Systems Inc. “Dedicated to Clinical Excellence.”

130

Patient Intake Form (side 2) Give a brief detailed description of the problem you are currently experiencing: ______How long have you had this condition? ______Is it getting worse? □ yes, □ no ______Does it bother you (check appropriate box): □ work, □ sleep, □ other: ______What seemed to be the initial cause: ______Please mark you area(s) of pain on the fgure below Please place a mark at the level of your pain on the scale below: Worst Possible Pain

No Pain

Past health history Habits none light mod. heavy Have you... Yes No If yes, explain briefly Alcohol □ □ □ □ ... been hospitalized in the last 5 year? □ □ ______Coffee □ □ □ □ ... had any mental disorders? □ □ ______Tobacco □ □ □ □ ... had any broken bones? □ □ ______Drugs □ □ □ □ ... had any strains or sprains? □ □ ______Exercise □ □ □ □ ... ever used orthotics? □ □ ______Sleep □ □ □ □ Do you take minerals, herbs or vitamins? □ □ ______Soft drinks □ □ □ □ How is most of your day spent? □ standing, □ sitting, □ other: ______Salty foods □ □ □ □ How old is your mattress? ______Water □ □ □ □ When was your last physical exam? ______Sugar □ □ □ □

Family history If any blood relative has had any of the following conditions, please check and indicate which relative(s) □ Alcoholism □ Cancer □ High blood pressure □ Anemia □ Diabetes □ High cholesterol □ Arteriosclerosis □ Emphysema □ Multiple sclerosis □ Arthritis □ Epilepsy □ Osteoporosis □ Asthma □ Glaucoma □ Stroke □ Bleed easily □ Heart disease □ Thyroid disease Do you have any other health issues or concerns that our staff should be made aware of? ______Reproduction is permitted for personal use, not for resale or redistribution. www.prohealthsys.com ©2012 by Professional Health Systems Inc. “Dedicated to Clinical Excellence.”

131

Appendix B- Research Ethics Board Approval

PROTOCOL APPROVAL

TO: Trisha Scribbans Principal Investigator

FROM: Joseph Gordon, Chair Education/Nursing Research Ethics Board (ENREB)

Re: Protocol #E2019:019 (HS22668) Myofascial Release (MFR) of Pectoral Fascia: Effects on Shoulder Posture, Upper Limb Reaching Strategies and Performance

Effective: April 1, 2019 Expiry: April 1, 2020

Education/Nursing Research Ethics Board (ENREB) has reviewed and approved the above research. ENREB is constituted and operates in accordance with the current Tri-Council Policy Statement: Ethical Conduct for Research Involving Humans.

This approval is subject to the following conditions: 1. Approval is granted for the research and purposes described in the application only. 2. Any modification to the research or research materials must be submitted to ENREB for approval before implementation. 3. Any deviations to the research or adverse events must be submitted to ENREB as soon as possible. 4. This approval is valid for one year only and a Renewal Request must be submitted and approved by the above expiry date. 5. A Study Closure form must be submitted to ENREB when the research is complete or terminated. 6. The University of Manitoba may request to review research documentation from this project to demonstrate compliance with this approved protocol and the University of Manitoba Ethics of Research Involving Humans. Funded Protocols: - Please mail/e-mail a copy of this Approval, identifying the related UM Project Number, to the Research Grants Officer in ORS.

Research Ethics and Compliance is a part of the Office of the Vice-President (Research and International) umanitoba.ca/research

132

Appendix C- Individual Trial Number Outliers for RT, MvT, End-Point Accuracy and EMG Variables During the Reaching Task

Measurement Outliers Time RT MvT End-Point EMG P1 V1 Pre 9, 20 41 P1 V1 Post 16 27 P1 V2 pre 12 2, 15 1 P1 V2 Post 33 19 P2 V1 pre 55 59 P2 V1 post 4 47 P2 V2 Pre 1 P2 V2 Post 19, 60 21 P3 V1 Pre 17 39 47 P3 V1 Post 42 1 P3 V2 Pre 52 45, 44, 37, 29, 13 P3 V2 Post 34 P4 V1 Pre 20, 29, 53 60, 28 P4 V1 Post 1, 25 24 37, 42, 47 P4 V2 Pre 51 23, 25, 40 P4 V2 Post 31, 54 P5 V1 Pre 7, 10 11 1, 45 P5 V1 Post 7, 18 P5 V2 Pre 27, 34 P5 V2 Post 27 P6 V1 Pre 2, 32 P6 V1 Post 5, 20, 58 2, 48 P6 V2 pre 22 P6 V2 Post 29, 57 P7 V1 Pre 29 P7 V1 Post 16, 22, 34, 39 19 133

P7 V2 Pre 47 P7 V2 Post 31 5, 7 12, 17, 35 P8 INCOMPLETE P9 V1 Pre 54 P9 V1 Post 36 28 P9 V2 Pre 2 10, 46, 49 P9 V2 Post 1, 19 56 P10 V1 Pre 25, 48 32 36 P10 V1 Post 16 16 8 10 V2 Pre 51 P10 V2 Post 34 5 47 P11 V1 Pre 24 P11 V1 Post 1, 20 P11 V2 Pre 30 7, 9, 15, 38 P11 V2 Post 1 6,10, 22, 33 P12 V1 Pre 20, 45 50 57 P12 V1 Post 27 35 P12 V2 Pre Missing Movement Performance Data 1, 24, 36, 54, 52 P12 V2 Post 52 14, 23, 24, 28 P13 INCOMPLETE P14 V1 Pre 20 P14 V1 Post 12, 49, 55 P14 V2 Pre 49 P14 V2 Post 8, 36 38 10 P15 V1 Pre 35, 56 P15 V1 Post 45 P15 V2 Pre 10 37, 40, 43 P15 V2 Post 18, 26, 44 P16 V1 Pre 9, 23 P16 V1 post 50 45 P16 V2 Pre 37, 45 47 134

P16 V2 Post 23 36 P17 V1 Pre 7 9, 56, 60 P17 V1 Post 4, 30 P17 V2 Pre 23 23 1 P17 V2 Post 45 7 3, 33 P18 V1 Pre 3, 4 47 27 P18 V1 Post 2 2 P18 V2 Pre 2 P18 V2 Post 51 P19 V1 Pre 42, 56 P19 V1 Post 57 49 P19 V2 pre 26, 50 35 P19 V2 Post 15 53 9 P20 V1 Pre 2 P20 V1 Post 1, 44 27 P20 V2 Pre 33 P20 V2 Post 30 8, 21 1 P21 INCOMPLETE P22 INCOMPLETE P23 INCOMPLETE

RT- reaction time; MvT- movement time; End-point- end-point accuracy; EMG- electromyography

135

Appendix D- Paired T-test Results

MFR CON Outcome Variable Mean (SD) Mean (SD) MFR-CON t p-value FSP (mm) 6 (6) 1 (5) 4.65 2.581 .019 Pectoral Length (mm) 12 (25) -1 (28) 13.40 1.470 .160

Muscle Activity UT (mV) -.01 (.30) -.01 (.67) -.01 -.037 .971 MT (mV) .01 (.20) .10 (.34) -.09 -.872 .395 LT (mV) -.10 (.34) .01 (.30) -.11 -1.148 .267 PEC (mV) -.45 (1.10) -.53 (1.53) .08 .216 .831

R/P (A.U.) .02 (.22) .04 (.07) -.02 -.312 .759 Movement Performance RT (ms) 6 (16) 3 (13) 2.61 .551 .589 MvT (ms) 4 (26) -6 (24) 10.51 1.312 .207 CEL (pixels) -1 (7) -1 (7) .11 .070 .945 CER (pixels) -1 (5) -2 (7) 1.47 .705 .490 CET (pixels) 1 (6) 0 (7) 1.15 .462 .650 CEB (pixels) 0 (6) -1 (7) .68 .369 .717 VEX (pixels) 0 (3) 0 (4) -.45 -.394 .698 VEY (pixels) 0 (3) 1 (4) -1.54 -1.188 .251

MFR- myofasical release; CON- soft touch control; FSP- forward shoulder posture; UT- upper trapezius; MT- middle trapezius; LT- lower trapezius, PEC- pectoralis major; R/P- scapular retractor to protractor ratio of activity; RT- reaction time; MvT- movement time; CEL- constant error left targets; CER- constant error right targets; CET constant error top targets; CEB- constant error bottom targets; VEX- variable error x-axis; VEY- variable error y-axis.

136

Appendix E- Post-hoc a priori sample size calculation to reach 80% power

Outcome Variable Achieved Required Power Sample $ Size

FSP .682 24 Pectoral Length .284 68 UT .050 96 902

MT .131 187 LT .192 110 PEC .055 3 020 R/P .060 1 436 RT .082 467 MT .236 85

CEL .051 27 161 CER .102 287 CET .072 663 CEB .064 1 039 VEX .066 910 VEY .202 103

137

Appendix F- Individual Participant Dependent Variable Means

Forward Shoulder Posture (mm) PARTICIPANT MFR CON PRE POST PRE POST 1 149 138 154 158 2 139 140 137 138.3 3 122 115 122 119.3 4 127 120 125 119 5 125 126 132 123 6 105 106 115 110.3 7 119 115 118 122 8 9 123 122 123 121 10 145 135 137 134.7 11 121 116 104 101.3 12 103 103 109 104 13 14 141 138 134 136 15 99 93 103 101.67 16 146 129 153 143.3 17 128 113 118 122 18 113 105 123 121 19 122 105 110 110.3 20 107 107 108 114.7 Pectoral Length (mm) PARTICIPANT MFR CON PRE POST PRE POST 1 566 540 503 565 2 535 534 583 586 3 582 558 575 585 4 569 582 590 571 5 553 544 554 533 6 598 542 557 546 7 640 607 642 604 8 9 642 646 661 658 10 579 574 534 578 11 629 639 625 621 12 547 572 564 547 13 14 534 516 518 538 15 637 589 688 667 16 629 635 579 634 17 673 625 624 641 138

18 657 657 659 638 19 632 600 613 604 20 606 634 644 623 Upper Trapezius Muscle Activity (% Max) PARTICIPANT MFR CON PRE POST PRE POST 1 2.02 1.66 4.09 3.10 2 3.87 3.64 1.94 4.03 3 0.77 0.75 1.30 1.35 4 0.85 1.10 1.15 1.06 5 1.11 0.97 1.83 2.45 6 1.61 2.22 1.08 1.30 7 1.37 1.41 1.00 1.15 8 9 0.39 0.37 0.80 0.45 10 3.70 3.45 5.24 5.73 11 3.10 2.92 1.42 1.29 12 0.62 0.65 1.03 0.86 13 14 1.30 1.22 1.09 1.03 15 0.71 0.58 0.73 0.70 16 1.37 1.35 2.07 1.82 17 1.61 1.51 1.28 1.28 18 2.54 3.42 4.67 3.49 19 0.91 0.83 0.88 0.76 20 0.47 0.51 1.04 0.91 Middle Trapezius Muscle Activity (% Max) PARTICIPANT MFR CON PRE POST PRE POST 1 3.23 3.50 3.13 2.66 2 1.28 0.91 1.55 0.83 3 0.38 0.41 0.73 0.84 4 2.19 2.69 3.70 2.77 5 1.11 1.01 0.71 0.63 6 0.72 0.92 0.41 0.57 7 0.75 0.58 0.89 1.07 8 9 0.52 0.51 0.51 0.39 10 0.65 0.64 0.64 0.68 11 2.75 2.36 1.32 1.44 12 0.82 0.78 0.66 0.62 13 14 0.58 0.57 0.83 0.79 15 0.40 0.40 1.32 1.19 16 1.98 1.98 2.15 2.73 17 1.41 1.43 1.22 1.08 139

18 2.54 3.42 4.67 3.49 19 0.91 0.83 0.88 0.76 20 0.47 0.51 1.04 0.91 Lower Trapezius Muscle Activity (% Max) PARTICIPANT MFR CON PRE POST PRE POST 1 2.94 3.65 1.36 1.31 2 1.46 1.43 2.86 3.67 3 1.13 1.03 0.91 0.87 4 3.85 4.22 4.11 4.10 5 0.92 0.57 1.04 0.98 6 2.17 2.87 1.49 1.75 7 1.74 1.58 1.47 1.41 8 9 1.90 1.94 2.29 2.15 10 2.88 3.29 1.88 2.04 11 3.68 3.37 1.64 1.85 12 1.56 1.39 1.51 1.57 13 14 1.54 1.58 1.38 1.44 15 2.21 1.85 3.07 2.38 16 3.50 3.55 2.44 2.21 17 2.93 3.18 1.41 1.44 18 1.58 1.78 1.45 1.31 19 0.94 0.89 1.82 1.65 20 1.79 2.34 1.99 1.73 Pectoralis Major Muscle Activity (% Max) PARTICIPANT MFR CON PRE POST PRE POST 1 9.38 10.91 8.55 10.45 2 2.20 3.19 6.30 12.02 3 1.45 0.97 1.60 1.92 4 2.33 1.84 1.97 2.01 5 4.04 4.28 3.46 4.14 6 6.15 6.76 9.98 12.00 7 3.86 3.37 2.42 2.48 8 9 2.58 2.40 1.57 1.24 10 6.67 6.97 7.98 7.02 11 6.92 7.03 3.76 4.61 12 1.30 5.24 0.91 0.91 13 14 2.91 3.79 3.47 3.93 15 2.47 1.91 2.67 2.30 16 3.70 3.52 7.05 7.15 17 4.98 6.15 4.02 3.60 140

18 6.17 5.47 9.99 8.93 19 3.68 4.72 3.22 3.96 20 1.53 1.85 2.52 2.34 Scapular Retractor to Protractor Ratio Of Activity (A. U.) PARTICIPANT MFR CON PRE POST PRE POST 1 0.29 0.27 0.33 0.23 2 1.00 0.62 0.34 0.24 3 0.52 0.75 0.61 0.53 4 0.98 1.45 1.51 1.32 5 0.26 0.20 0.34 0.33 6 0.24 0.30 0.10 0.10 7 0.33 0.35 0.46 0.49 8 9 0.36 0.39 0.76 0.80 10 0.36 0.35 0.32 0.40 11 0.46 0.41 0.39 0.33 12 0.77 0.18 1.17 1.12 13 14 0.39 0.30 0.32 0.28 15 0.45 0.49 0.64 0.62 16 0.62 0.65 0.32 0.32 17 0.40 0.33 0.32 0.35 18 0.26 0.37 0.24 0.22 19 0.23 0.16 0.35 0.25 20 0.59 0.60 0.53 0.51 Reaction Time (ms) PARTICIPANT MFR CON PRE POST PRE POST 1 391 369 383 351 2 350 360 341 349 3 288 299 290 286 4 342 362 333 337 5 293 271 283 279 6 315 303 325 308 7 314 309 298 294 8 9 306 308 295 299 10 305 317 306 292 11 304 293 307 292 12 294 292 286 290 13 14 298 276 286 296 15 278 286 285 278 16 319 277 301 295 17 364 340 327 353 141

18 332 325 341 330 19 304 296 291 293 20 279 283 284 277 Movement Time (ms) PARTICIPANT MFR CON PRE POST PRE POST 1 408 397 383 351 2 288 295 341 349 3 301 318 290 286 4 225 216 333 337 5 250 252 283 279 6 629 597 325 308 7 338 369 298 294 8 9 295 303 295 299 10 298 292 306 292 11 228 224 307 292 12 369 390 286 290 13 14 362 375 286 296 15 260 242 285 278 16 370 376 301 295 17 289 268 327 353 18 381 363 341 330 19 536 453 291 293 20 354 371 284 277 Constant Error X-Axis Left Targets (Pixels) PARTICIPANT MFR CON PRE POST PRE POST 1 -12.3 -11.9 -15.6 -7.8 2 -14.0 -18.0 -18.6 -14.7 3 -4.3 -6.8 -7.3 -13.4 4 -4.2 7.3 -4.9 2.9 5 -21.5 -13.1 -21.2 -7.6 6 -8.5 -7.5 -3.6 -12.8 7 -6.1 -5.3 -5.1 0.6 8 9 -0.5 -0.5 -0.8 6.5 10 -14.0 -7.9 -16.9 -19.7 11 -10.0 -10.5 -2.8 -6.8 12 -2.5 -13.8 -14.4 -10.4 13 14 -22.6 -7.9 -17.3 -8.9 15 -5.0 -5.0 -9.0 -8.0 16 -6.7 -11.1 -7.4 -16.2 17 5.7 -2.1 -2.3 -7.0 142

18 -19.9 -13.1 -18.4 -15.7 19 -7.0 -5.8 -0.5 -2.7 20 -22.3 -18.3 -15.9 -13.6 Constant Error X-Axis Right Targets (Pixels) PARTICIPANT MFR CON PRE POST PRE POST 1 -3.7 -3.4 -5.5 -1.1 2 1.3 -2.1 3.6 -3.3 3 -4.7 -13.1 -8.8 -1.6 4 -17.0 -3.9 -16.9 -13.4 5 -16.9 -17.0 -10.6 -11.0 6 -3.2 -0.7 -5.1 -3.1 7 -8.3 -5.2 -9.1 -8.2 8 9 -10.8 -14.7 -16.8 -14.1 10 -13.7 -11.0 -16.3 -4.8 11 -3.3 -1.1 -7.0 -6.2 12 -1.8 -7.0 -7.7 -9.8 13 14 -1.8 2.0 4.5 -3.1 15 -2.3 -3.0 -7.7 11.1 16 -8.0 -1.3 -7.1 1.0 17 -4.0 -9.9 -6.4 -5.0 18 -14.9 -14.0 -20.3 -11.4 19 -12.8 -12.2 -12.0 -15.7 20 -5.5 1.1 4.8 -3.5 Constant Error Y-Axis Top Targets (Pixels) PARTICIPANT MFR CON PRE POST PRE POST 1 0.5 7.5 2.5 -8.9 2 -5.4 -1.2 5.3 4.6 3 2.2 5.0 5.3 14.4 4 2.4 9.1 0.9 -7.6 5 7.8 8.3 8.3 15.1 6 11.6 2.9 6.3 1.8 7 9.9 5.0 7.4 8.9 8 9 9.7 3.7 4.2 10.4 10 12.7 1.7 5.6 -6.7 11 7.2 6.9 12.9 13.9 12 10.6 -0.7 1.4 13.6 13 14 10.6 13.7 11.6 19.4 15 14.0 17.1 15.5 7.0 16 -0.7 1.3 -6.8 -3.0 17 13.6 0.8 5.7 4.4 143

18 5.2 3.0 5.5 8.1 19 -1.0 0.7 2.7 6.3 20 7.0 11.6 10.2 1.8 Constant Error Y-Axis Bottom Targets (Pixels) PARTICIPANT MFR CON PRE POST PRE POST 1 18.3 16.4 10.6 16.6 2 11.9 16.3 15.2 12.2 3 14.0 23.2 21.0 30.3 4 10.7 5.6 16.1 4.4 5 18.9 10.8 21.0 14.7 6 1.7 15.3 12.5 17.7 7 11.4 11.4 13.6 24.9 8 9 14.1 11.4 23.8 23.5 10 25.3 19.1 11.8 24.1 11 22.5 27.8 35.1 29.6 12 17.7 18.8 17.5 25.9 13 14 14.0 19.5 17.0 22.4 15 25.1 19.6 29.8 24.6 16 15.3 15.3 13.8 11.2 17 17.3 17.1 21.7 14.8 18 26.3 26.0 30.5 26.7 19 16.9 10.8 11.2 14.5 20 22.2 24.9 25.7 27.3 Variable Error X-Axis (Pixels) PARTICIPANT MFR CON PRE POST PRE POST 1 18.3 22.2 21.7 24.6 2 14.8 15.8 16.5 15.8 3 16.5 15.8 12.0 16.2 4 21.4 18.4 20.8 18.9 5 21.9 20.6 26.9 19.5 6 8.7 10.8 14.2 13.0 7 13.5 15.5 15.5 14.4 8 9 16.0 19.1 20.2 18.7 10 21.2 18.9 17.5 22.7 11 21.4 20.7 18.3 19.7 12 12.5 14.7 17.2 15.5 13 14 20.0 19.6 18.9 12.3 15 25.9 19.2 24.7 23.6 16 15.7 14.6 15.2 17.9 17 21.6 23.4 20.4 14.7 144

18 13.5 14.7 11.8 11.1 19 7.9 11.8 12.3 13.9 20 14.5 10.5 12.8 17.3 Variable Error Y-Axis (Pixels) PARTICIPANT MFR CON PRE POST PRE POST 1 20.3 20.4 20.3 25.7 2 23.6 17.3 20.3 20.8 3 17.9 15.7 23.2 23.8 4 30.5 27.1 26.3 25.9 5 28.8 27.3 35.5 24.0 6 11.5 13.3 14.0 12.9 7 14.1 14.8 16.7 14.2 8 9 14.6 19.6 20.7 16.4 10 20.6 18.0 23.1 19.9 11 24.0 22.6 23.3 21.3 12 14.9 17.6 14.5 18.1 13 14 18.8 17.9 25.0 17.1 15 23.3 29.6 24.4 21.5 16 16.4 16.8 16.5 19.2 17 24.2 22.8 13.8 18.6 18 15.1 13.4 18.1 12.0 19 8.7 13.1 15.9 12.8 20 15.4 19.2 19.1 22.4

145

Appendix G- Registered Massage Therapist Notes on Treatment Condition

PARTICIPANT INTERVENTION MFR CON ORDER 1 CON-MFR Moderate release Minimal release; lots of heat 2 MFR- CON Moderate release; No release responded well- quite a bit of release and heat 3 CON-MFR Large release; very good Minimal release; some response and tons of heat release with heat 4 MFR-CON Large release; very good Minimal release response- heat and tissue release 5 MFR-CON Large release; very nice Minimal release reaction- increased heat and release 6 MFR-CON Moderate release; Minimal release; good moderate to almost large increase in heat release- especially at the 3:30 minute mark. Large increase in heat 7 MFR-CON Moderate release Minimal release 8 INCOMPLETE 9 CON-MFR Moderate release; not No release; increased much give until 3:30 heat minutes into treatment. Then increased heat and good but not large release 10 CON-MFR Moderate release; lots of Minimal release; lots of heat; some release heat; felt some release 11 MFR-CON Large release; increased Minimal release heat, good release 12 MFR-CON Large release; really nice Minimal release; very release and tons of heat good heat increase 13 INCOMPLETE 14 MFR-CON Large release; really nice Minimal release release with increased heat 15 CON-MFR Moderate release; fairly Minimal release; lots of good release with lots of heat heat 16 CON-MFR Moderate release No release 17 MFR-CON Large release; good Minimal release; a lot of release with increased heat- some redness heat 146

18 CON-MFR Moderate release; good Minimal release; some increase in heat, good heat, felt slight release release 19 MFR-CON Large release; lots of heat Minimal release; a lot of generated and felt a lot of heat generated near the release but near the end last 20s of treatment (30s left)- Right hand felt if I took up more slack I’d slide into left pec-had to lift off slightly to keep from happening 20 CON-MFR Moderate release Minimal release; increased heat