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SERRATUS ANTERIOR MUSCLE FATIGUE EFFECTS ON SCAPULAR KINEMATICS

A Thesis

Presented in Partial Fulfillment of the Requirements for the Degree Master of Science in the Graduate School of The Ohio State University

By

Oren Costantini, B.S.M.E.

Graduate Program in Graduate Program in Mechanical Engineering

The Ohio State University

2011

Master’s Examination Committee:

Dr. John H. Bolte, Advisor Dr. John D. Borstad c Copyright by

Oren Costantini

2011 Abstract

Background : pain accounts for an average of 8.6 million physician visits each year in the United States. Subacromial Impingement syndrome is the most common diagnosis of shoulder pain, accounting for 44% to 65% of all complaints of shoulder pain during a physician’s office visits. Methods: A protocol to bias fatigue the Serratus Ante- rior was used in conjunction with an electromagnetic motion capture system to track the

3D motion of the and the electromyography signal of 4 muscles bilaterally in 17 subjects. The skin based motion sensors tracked humeral elevation and scapular upward rotation, internal rotation, and tilting relative to the in 2 planes of elevation. The skin based electromyography sensors recorded signal from , serratus an- terior, and upper and lower . Subjects performed 2 fatigue tasks and 3 sets of 2 kinematic tasks. Analysis: Scapular orientations relative to the thorax and electromyog- raphy signals for 3 fatigue conditions (Pre, Mid, Post) were analyzed in 10◦ increments for humeral elevations of 30◦ to 120◦ in the scapular plane and 30◦ to 110◦ in flexion.

Electromyography signals were also analyzed while subjects held the two isometric fa- tigue tasks. All data were analyzed with repeated measure analysis of variance. Results:

Non-dominant arms showed consistent increases in internal rotation, decreases in upward rotation, and increases in anterior tilting of the scapula relative to the thorax in flexion and the scapular plane as fatigue progressed. Dominant arms had a wider variety of motions, showing both increases and decreases in all scapular rotations. Indications of progressive

ii muscle fatigue were found qualitatively from the first fatigue task; however, the quantitative data was inconclusive. A state of global shoulder fatigue was reached following the second fatigue task. Individual muscle contributions to motion were inconclusive. Conclusions :

Non-dominant arms, when fatigue, show consistent kinematic alterations similar to those found in patients with subacromial impingement syndrome. Dominant arms show a variety of kinematic alterations, some of which similar to patients with subacromial impingement syndrome, suggesting compensation strategies are learned. If this is true, rehabilitation can affect these compensation strategies and, possibly, return patients to more healthy motions.

Further studies are needed to validate the fatigue task and protocol.

iii To my friends and loved ones.

You have helped to keep my dreams alive.

iv Acknowledgments

This research would not have been possible without the mentoring of my advisors, the loving support of my parents, and the help of my friends.

First, I want to thank my advisors, Dr. John Borstad and Dr. John Bolte. Thank you for allowing me the freedom to make this project truly my own. Dr. Borstad, thank you for your hours of mentoring, your patience, and for teaching me how to be a bio-mechanist.

Next, I want to thank my parents for supporting me through this process and allowing me to develop my interests in orthopedics, musculature, and biomechanics. Truly, I do not know if I would have had the ability to do this without you.

Finally, I want to thank all of my friends. Our conversations on a myriad of topics helped me to learn more about the world as well as myself. Our discussions and experiences together were as much a part of graduate school for me as the classes and my research. To my friends outside of graduate school, thank you for bearing with my long absences and keeping in touch. I cannot thank you enough for your continued support.

Special thanks go to:

Amitabh Dashottar, your advice and help were vital to this project. Your friendship, in and out of the lab, kept me sane even when I thought things might have fallen apart.

Bruce Noskowiak, your help and friendship were invaluable. Anytime I needed tech- nical help or advice you were there for me, and our conversations always lifted my spirits.

Thank you.

v Vita

January 10, 1987 ...... Born - Cincinnati, Ohio

June 2005 ...... B.S. Mechanical Engineering, The Ohio State University

Fields of Study

Major Field: Mechanical Engineering

vi Table of Contents

Page

Abstract ...... ii

Dedication ...... iv

Acknowledgments ...... v

Vita ...... vi

List of Tables ...... x

List of Figures ...... xiii

List of Acronyms and Abbreviations ...... xv

1. Introduction ...... 1

1.1 Background and Significance ...... 1 1.1.1 Rotator Cuff Pathology in the General Population ...... 1 1.1.2 Cost of Rotator Cuff Treatment ...... 2 1.1.3 Rotator Cuff Etiology ...... 2 1.1.4 Subacromial Impingement Syndrome and the Anatomy of the Subacromial Space ...... 3 1.1.5 Pathogenesis of Subacromial Impingement ...... 5 1.1.6 Scapular Dyskinesis ...... 6 1.2 The Scapula ...... 6 1.2.1 Normal and Altered Scapular Motions ...... 8 1.2.2 Rotations of the Scapula ...... 9 1.2.3 Reduction and Compression of the Subacromial Space ...... 10 1.3 Muscles of the ...... 11 1.3.1 Muscular Control of the Shoulder Girdle ...... 16

vii 1.3.2 Muscle Fatigue ...... 17 1.3.3 Serratus Anterior and Trapezius: Force Couples of Scapular Sta- bility ...... 18 1.3.4 Reasons For Examining Serratus Anterior ...... 19 1.4 Hypotheses ...... 21 1.4.1 Hypothesis 1: ...... 21 1.4.2 Hypothesis 2: ...... 22

2. Methods ...... 23

2.1 Subjects ...... 23 2.1.1 Sample Size Calculations ...... 23 2.1.2 Subject Recruitment ...... 23 2.2 Instrumentation and Equipment ...... 24 2.3 Procedure ...... 25 2.3.1 Setup ...... 25 2.3.2 Subject Preparation ...... 26 2.3.3 Testing ...... 33 2.4 Data Reduction and Processing ...... 37 2.4.1 MVC Task ...... 37 2.4.2 Kinematic Tasks ...... 37 2.4.3 Fatigue Tasks ...... 38 2.5 Data Analysis ...... 39 2.5.1 Verification of Data ...... 39 2.5.2 Analysis ...... 40

3. Results ...... 44

3.1 Hypothesis 1: Alterations in scapular muscle fatigue will be inconsistent between the dominant and non-dominant arms of subjects. This will result in differing kinematic and fatigue profiles between the dominant and non-dominant arms of subjects ...... 44 3.1.1 Hypothesis 1.1: Kinematic alteration of the scapula, relative to the thorax, will vary across fatigue conditions between the dom- inant and non-dominant arm as the arms are elevated in flexion and the scapular plane...... 44 3.1.2 Hypothesis 1.2: Patterns of normalized EMG activation levels for the dominant and non-dominant arms will be different and vary across condition, phase of motion, and humeral elevation. . 45 3.1.3 Hypothesis 1.3: Median power frequency (MPF) of EMG acti- vation levels for the dominant and non-dominant arms will differ across conditions...... 47

viii 3.2 Hypothesis 2: Serratus anterior fatigue will lead to a decrease in scapular upward rotation, posterior tilting, and scapular internal rotation . . . . . 48 3.2.1 Hypothesis 2.1: Scapular upward rotation, internal rotation, and posterior tilting will decrease progressively across fatigue con- ditions ...... 48 3.2.2 Hypothesis 2.2: Normalized EMG activation levels of the serra- tus anterior muscle will rise between fatigue conditions at a great rate than those of the upper and lower trapezius muscles . . . . . 62 3.2.3 Hypothesis 2.3: Median power frequency of EMG activation levels of the serratus anterior muscle will have a higher per- cent decline across fatigue conditions than those of the upper and lower trapezius muscles ...... 63

4. Discussion ...... 73

4.1 Primary Kinematic Findings ...... 73 4.1.1 Hypothesis: 1.1 ...... 74 4.1.2 Hypothesis: 2.1 ...... 75 4.2 Primary Fatigue Findings ...... 77 4.2.1 Hypothesis: 1.2 ...... 77 4.2.2 Hypothesis: 1.3 ...... 78 4.2.3 Hypothesis: 2.2 ...... 79 4.2.4 Hypothesis: 2.3 ...... 80 4.3 JASA Findings ...... 81 4.4 Limitations and Future Work ...... 83 4.4.1 Subjects ...... 83 4.4.2 Instrumentation ...... 83 4.5 Conclusions ...... 87

Appendices 89

A. Bi-Lateral Kinematic & EMG Testing Protocol Version 1.3 ...... 89

Bibliography ...... 100

ix List of Tables

Table Page

1.1 Upward/Downward Rotators & Stabilizers of The Scapula ...... 12

1.2 Extrinsic Dynamic Stabilizers ...... 13

1.3 Intrinsic Dynamic Stabilizers ...... 14

2.1 Subject Demographics ...... 24

3.1 Subject Demographics: Borg Scores ...... 44

3.2 Summary of Arm Dominance P-Values ...... 45

3.3 Summary of P-Values for Normalized EMG During Lifting Task ...... 46

3.4 Summary of % Change for Normalized EMG During Lifting Task by Side 47

3.5 Summary of P-Values for Normalized EMG During Waving Task . . . . . 47

3.6 Summary of Humeral Elevation Differences for Normalized EMG During Waving Task ...... 48

3.7 EMG Amplitude: Summary of Arm Dominance P-Values ...... 48

3.8 EMG MPF: Summary of Arm Dominance P-Values ...... 49

3.9 EMG MPF: Summary of Arm Dominance Mean Percent Change . . . . . 49

3.10 General P-Values of Condition ...... 50

3.11 Comparison of Mean IR Change: Non-Dominant ...... 50

x 3.12 Comparison of Mean IR Change: Dominant ...... 52

3.13 Comparison of Mean UR Change: Non-Dominant ...... 53

3.14 Comparison of Mean UR Change: Dominant ...... 53

3.15 Comparison of Mean Tilt Change: Non-Dominant ...... 55

3.16 Comparison of Mean Tilt Change: Dominant ...... 55

3.17 Summary of Wave Task Results ...... 56

3.18 General P-Values of Condition ...... 56

3.19 Comparison of IR Scenarios: Dominant ...... 58

3.20 Comparison of IR Scenarios: Non-Dominant ...... 59

3.21 Comparison of UR Groups: Dominant ...... 60

3.22 Comparison of UR Groups: Non-Dominant ...... 60

3.23 Comparison of Tilt Groups: Dominant ...... 62

3.24 Summary of Tilt Results: Non-Dominant ...... 62

3.25 Summary of Lift Task Results ...... 63

3.26 EMG Amplitude: Summary of Arm Dominance Average Mean Percent Change ...... 64

3.27 Summary of Task 1 JASA Chart ...... 66

3.28 Summary of Task 2 JASA Chart ...... 71

3.29 Task 1 JASA Results by Subject ...... 71

3.30 Task 2 JASA Results by Subject ...... 72

4.1 Key to Direction of Change for Each Scapular Rotation ...... 73

xi 4.2 Comparison of Kinematics to Literature: Scapular Plane ...... 74

4.3 Comparison of Kinematics to Literature: Flexion ...... 74

4.4 Key to JASA ...... 82

xii List of Figures

Figure Page

1.1 Subacromial Space: Green = Subscapularis Pink = The Tendon of Long Head of the Biceps Blue = Supraspinatus Purple = Infraspinatus ...... 4

1.2 The Three Rotations of the Scapula. (Left to Right) Posterior Tilting, In- ternal Rotation, Upward Rotation ...... 7

2.1 Guides Built to Aid Subjects ...... 26

2.2 EMG Sensor Placement of Upper and Lower Trapezius and of Pectoralis Major ...... 28

2.3 EMG Sensor Placement of Serratus Anterior ...... 29

2.4 EMG Sensor Placement of Ground Electrode ...... 30

2.5 Kinematic Sensor Placement: Anterior and Posterior Thorax ...... 31

2.6 Kinematic Sensor Placement: Arm ...... 32

2.7 Setup of the Fatigue Tasks ...... 35

2.8 Scapular Plane Elevations ...... 36

2.9 Weighted Frontal Elevation Task ...... 36

3.1 Plot of IR Mean Differences From Condition One ...... 51

3.2 Plot of UR Mean Differences From Condition One ...... 52

3.3 Plot of Tilt Mean Differences From Condition One ...... 54

xiii 3.4 Plot of IR Mean Differences From Condition One ...... 57

3.5 Plot of UR Mean Differences From Condition One ...... 59

3.6 Plot of Tilt Mean Differences From Condition One ...... 61

3.7 First fatigue task mean EMG amplitude changes over time ...... 64

3.8 Second fatigue task mean EMG amplitude changes over time ...... 65

3.9 First fatigue task mean MPF changes over time ...... 67

3.10 Second fatigue task mean MPF changes over time ...... 68

3.11 First Fatigue Task: Mean MPF change is plotted on the vertical axis and mean EMG change is plotted on the horizontal axis...... 69

3.12 Second Fatigue Task: Mean MPF change is plotted on the vertical axis and mean EMG change is plotted on the horizontal axis...... 70

A.1 EMG Sensor Placement of Upper and Lower Trapezius and of Pectoralis Major ...... 92

A.2 EMG Sensor Placement of Serratus Anterior ...... 93

A.3 EMG Sensor Placement of Ground Electrode ...... 94

xiv LIST OF ACRONYMS AND ABBREVIATIONS

EMG Electromyography SIS Subacromial Impingement Syndrome ER External Rotation IR Internal Rotation UR Upward Rotation SA Serratus Anterior UT Upper Trapezius LT Lower Trapezius Pec Pectoralis Major RM-ANOVA Repeated Measure ANOVA GGE Geisser Greenhouse Epsilon CMC Covariance Matrix Circularity HFE Huynh Feldt Epsilon JASA Joint Analysis of EMG Spectrum and Amplitude BW Body Wieght

xv Chapter 1: INTRODUCTION

1.1 Background and Significance

1.1.1 Rotator Cuff Pathology in the General Population

Shoulder pain accounts for an average of 8.6 million physician visits each year in the

United States[57]. Data obtained from the U.S. Department of Health and Human Services show that more than 6% of these cases annual cases were attributed to rotator cuff problems.

The American Academy of Orthopaedic Surgeons (AAOC) reported that between 1998 and

2004 the increase in these rotator cuff related vists increased nearly 40%[58] and the trend will continue to increase for the near future as research has shown that incidence of rotator cuff damage increase with age[78, 65, 46]. These statistics only account for symptomatic rotator cuff damage. Studies have shown that between 15% and 35% of the asymptomatic population may have a rotator cuff tear[79, 46, 62, 65, 71]. While these statisitics are highly influced by age, showing the majority of tears found in patients ≥50, they highlight a growing problem that needs to be addressed, as 25% of these patients will develop pain within 5 years[71].

Many of these patients are treated by conservative and surgical means that address the symptoms; pain, loss of range of motion, and weakness. Studies have shown re- duced pain and improved function in shoulder pathology populations following conser- vative treatments[36, 21] however long term out come studies have reported that between

1 22% and 68% of people continue to experience symptoms one year after the onset of shoul- der pain.[4] Surgical interventions show similar immediate outcomes however suffer from degredation of the repair. Patients followed for as long as 10 years show clinical results of

”good” to ”excellent” dispite a reported known rotator cuff rupture rate of 20% to 65%[76].

1.1.2 Cost of Rotator Cuff Treatment

In a study on work related musculoskeletal disorders between 1987 and 1995 conducted by the Safety and Health Assessment and Research for Prevention (SHARP) program of the

Department of Labor and Industries of Washington State, rotator cuff pathologies incurred the highest median cost per claim[66]. These claims averaged $15,790 per case and resulted in and average time away from work of 263 days[66]. These values are similar to those collected in 1994 by Liberty Mutual, who held 10% of the private workers compensation market in the United States at the time[26]. Though these studies are dated, more recently published data suggests little progress has been made. The costs associated with shoulder pain and disability, across all pathologies, result in an average of 20 workdays missed per incidence of injury [56], and an average cost of $16,542 incurred per injury claim[48]. A typical injury claim includes costs for physician’s appointments, conservative management, and lost productivity. Surgical intervention for conditions such as rotator cuff tears can cost an additional $7,000 - $9,000 [11].

1.1.3 Rotator Cuff Etiology

Rotator cuff pathology has been described as a progressive degradation of the rotator cuff tendons starting with acute tendinitis followed by tendinopathy, tears, and eventu- ally full rupture[52]. Etiology of rotator cuff pathology has been attributed to two types of mechanisms: Intrinsic and Extrinsic. Intrinsic mechanisms include tendinopathy due

2 to aging, inferior or degraded mechanical properties from mechanical overload, ischemia,

and genetics[64]. Extrinsic mechanisms are ones in which the tendons of the rotator cuff

are mechanically compressed. Potential extrinsic mechanisms are rotator cuff muscle fa-

tigue or weakness, anatomical factors, and deviant biomechanics[67, 64]. The true cause

of rotator cuff degeneration is most likely some combination of both types of mechanisms,

however the scope of this study is limited to extrinsic mechanisms. Neer originally pro-

posed an extrinsic mechanism for the etiology of rotator cuff degradation in 1972, where

the rotator cuff tendons were compressed in the subacromial space[51]. Neer’s description

of the combined extrinsic mechanisms from anatomic and biomechanical factor became

known as Subacromial Impingement Syndrome (SIS)[64]. While SIS may not be present

in all patients who have or will have a rotator cuff tear, its prevalence, similar features, and

progressive degeneration into rotator cuff damage make it a strong topic of examination.

1.1.4 Subacromial Impingement Syndrome and the Anatomy of the Subacromial Space

Since Neer’s original description, SIS has become a separate diagnosis and is the most common diagnosis of shoulder pain, accounting for 44% to 65% of all complaints of shoul- der pain during a physician’s office visit[41]. As the name implies, SIS is the increased contact forces on the soft tissue structures within the subacromial space due to chronic narrowing. The subacromial space is bordered superiorly, in a hemispherical manner, by the anterior third of the acromion, the coracoacromial ligament, and the acromoclavicular joint. This hemisphere is typically referred to as the Coracoacromial Arch. Inferiorly, the subacromial space is bounded by the humeral head. Within this space are the subacro- mial bursa, the tendon of the long head of the biceps, and the rotator cuff tendons.(Fig.1.1)

Structures most vulnerable to mechanical impingement and subsequent damage are the

3 subacromial bursa and the tendonds of the supraspinatus, infraspinatus, subscapulars, long head of the biceps[45, 51, 52]. Though all of these are at risk it is most often the supraspina- tus tendon that is described as tearing. This may be due to its superior position and relative volume[63] in the subacromial space. Reductions in this space lead to compression of these structures and SIS. Specifically the range of humeral elevation between 60◦ and 120◦ is associated with a decrease in the width of the subacromial space[23, 22, 60] and high subacromial pressures[18, 30, 55].

Figure 1.1: Subacromial Space: Green = Subscapularis Pink = The Tendon of Long Head of the Biceps Blue = Supraspinatus Purple = Infraspinatus

3D MRI studies of the subacromial space have measured the subacromial space. The results studies on healthy subjects that age match the current study show the distance be- tween the the humeral head and the closest point on the acromion to be between 6 and 7 mm while at rest[60, 22]. This distance was shown to decrease as the arm was abducted[22] and increase in forward flexion[60]. When examining the rotator cuff tendons, Roberts et al[60] showed that, in flexion, the rotator cuff tendon thickness maintained a nearly con- stant 1:2 ratio with the minimum distance of the humeral head to the acromion despite angle

4 of humeral elevation. Graichen et al[22] showed that, in abduction, the vector of the mini- mum distance of the humeral head to the acromion to pass through the supraspinatus in less subjects as the humeral abduction angle increased. This is not to imply contact between the structures was made in this study, but instead to highlight that if contact were to be made it would probably be made in the interval of 30◦ to 90◦ of abduction. In another study by

Graichen et al[23] 10 N of force was applied to the distal humerus of healthy subjects while imaging of the subacromial space took place. When the musculature of the shoulder was activated, the minimum distance of the humeral head to the acromion remained relatively constant with a mean of 4.5 mm for measurements at 60◦, 90◦, and 120◦. This is a reduction of 32% at 60◦ and increase of 44% at 120◦ from previously reported data[23].

1.1.5 Pathogenesis of Subacromial Impingement

Many mechanisms have been proposed for the development and progression of SIS.

Prevalent mechanisms described in literature are, but not limited to, faulty biomechan- ics, poor posture, posterior capsule tightness, acromial and coracoacromial arch morphol- ogy, muscle weakness and fatigue, presence of osteophytes in the subacromial space, and overuse[45, 64]. Most would agree that some combination of these mechanisms is at fault. Soslowsky et al.[68] demonstrated this point in a 2002 study using a rat model.

Rats exposed to both overuse activities and compression of the rotator cuff tendons had significantly worse tendon properties than rats exposed to only one of these conditions. In many instances, SIS is associated with populations that perform repeated overhead motions

[6, 14, 24, 37], such as throwing athletes and construction workers.

5 1.1.6 Scapular Dyskinesis

It would be preferable to treat the underlying causes of SIS, however, they remain elusive. Clinically, it is rare to find SIS patents presenting without multiple pathological factors[25, 78]. It has been hypothesized that a method of discovering underlying causes of the symptoms many patients experience every year is by first addressing the issue of scapu- lar dyskinesis[32, 34]. The claim Kibler et al.[32, 33, 34] implies is that by first treating scapular dyskinesis, or preventing it entirely, the underlying causes of pathology can be de- termined or, in the case of early treatment, the pathology can be avoided entirely. Scapular dyskinesis is defined by Kibler et al.[32] as observable deviations in the static or dynamic positions of the scapula relative to the thoracic cage. Scapular dyskinesis is a common clin- ical finding in shoulder pathologies[34] occurring in 68% to 100% of patients with shoulder injuries[75].In patients with atraumatic, symptomatic rotator cuff tears scapular dyskinesis has been flagged as having consistent presence[25]. Connections between general shoulder pathology and scapular dyskinesis are commonly found in liturature[32, 6, 25, 54, 64, 75] as are those specific to impingement[28, 37, 41, 45, 39, 7, 19]. Potential sources of scapular dyskinesia include: muscular fatigue[72, 9, 18, 44], strength imbalances[72, 75], changes in muscular activation patterns[14, 13, 20, 37, 69, 74],posterior glenohumeral capsule tight- ness, and length[8].

1.2 The Scapula

The primary role of the scapula is provide a stable articulating surface to the humeral head across a wide range of motions. It is integral to the glenohumeral articulation, which effectively is a ball-and-socket joint. To maintain this configuration, the scapula must move

6 in coordination with the moving humerus such that the instant center of rotation , the math- ematical point within the humeral head that is the axis of rotation of the glenohumeral joint, does not deviate from the physiologically constrained space throughout the full range of shoulder motion[32, 54]. Proper alignment of the glenoid allows for optimum function of shoulder musculature to position and stabilize the humeral head[80]. This is achieved by maintaining correct length-tension relationships[32, 33]. Daily living requires the humerus to be able to move through a volume consisting of a 120◦ arc in flexion/anteflexion and an arc of nearly 180◦ in abduction/adduction[40]. In order to do this the scapula must be able to effectively preform all three of its rotations: anterior/posterior tilting, internal/external rotation, and upward/downward rotation. (Fig. 1.2)

Figure 1.2: The Three Rotations of the Scapula. (Left to Right) Posterior Tilting, Internal Rotation, Upward Rotation

7 1.2.1 Normal and Altered Scapular Motions

Normal patterns of scapular motions have been described as a pattern of upward rota- tion, external rotation, and posterior tilting as the humerus is elevated[42, 41, 54, 73, 38, 7].

While lowering the humerus from an elevated position the pattern is reversed but the path of motion has been shown to differ[38, 7]. Studies that used bone pins to record the motion of the scapula[42, 38] report that upward rotation of the scapula after 50◦ of humeral ele- vation follows approximately a 2:1 ratio, while posterior tilting and external rotation were non-linear and occurred more after 90◦ of humeral elevation. These studies were done in the scapular plane as well as in flexion and reported no differences in patterns of rotation between humeral elevation planes except in internal rotation where Ludwig et al[38] re- ported an average increase of 7◦ in scapular internal rotation between humeral elevation in the scapular plane and that in flexion. Reported range of motion, as the arm is elevated, for the healthy scapula are: 50◦ of upward rotation, 30◦ of posterior tilt, and 25◦ of external rotation.

Similar studies have been done in patients with SIS to track the motions of the scapula

[28, 37, 41, 39, 41]. The pattern of scapular kinematics associated with SIS is decreased scapular posterior tilting, decreased upward rotation, and increased scapular internal rota- tion [19, 37, 28, 54, 39]. This pattern of motion may result in an insufficient movement of the anterior aspect of the acromion leading to a reduction in the subacromial space[37].

Conversely, increased scapular upward rotation and posterior tilting have also been reported in those with SIS[41]. This may be a compensatory strategy aimed at reducing subacro- mial pressure and maintenance of the subacromial space[41]. While the magnitude of the kinematic deviations in the literature vary widely, changes as small as 4◦ from normal are of clinical significance[37].

8 1.2.2 Rotations of the Scapula

Upward/downward rotation of the scapula occurs about an axis perpendicular to the scapular plane with upward rotation occurring when the inferior angle moves laterally and superiorly. Anterior/posterior tilt occurs about an axis parallel to the spine of the scapula with posterior tilt depicting the superior scapular border moving posteriorly away from the thoracic cage. Internal/external rotation occurs about a vertical axis with external rotation taking place when the lateral scapular border moves posteriorly away from the thoracic cage[6].

External and upward rotation of the scapula are key to the flexion and abduction of the arm. By externally rotating the scapula as the arm is elevated, the glenoid is moved to a more lateral facing, posterior position bringing the base of the arm, the humeral head, around the thorax. This position has been described to be more stable due to the bony constraints of the thorax[33, 42]. Upward rotation of the scapula keeps the instant center of humeral head rotation on the glenoid as the humerus is elevated. Both of these motions allow for the force vector acting on the humeral head, from the stabilizing musculature, to be perpendicular to the glenoid[33, 1, 80]. This reduces shear forces on the glenoid, thereby reducing wear of its surface, and increases the effectiveness of the muscles applying the compressive force that stabilizes the humeral head[80]. Failure to properly position the glenoid may decrease the effectiveness of stabilizing musculature[1, 32, 80], such as the rotator cuff muscles, and result in aberrant humeral head translations[37, 80]. Posterior tilting and external rotation of the scapula move the acromion away from the humeral head in flexion and abduction of the arm[34, 37, 39]. The combination of increased upward rotation external rotation, and posterior tilting of the scapula aid in maintaining the size of the subacromial space[30, 45].

9 1.2.3 Reduction and Compression of the Subacromial Space

Deficits in any of the scapular rotations could cause a reduction in the subacromial space and increase the risk of bony interference with soft tissue structures, namely the tendons of the long head of the bicep and rotator cuff muscles. At this time there have been no studies that have shown the effect of variation of individual scapular rotations on the subacromial space in vivo. Solem-Bertoft et al. examined the effect of scapular protraction and retraction on the subacromial space in vivo using MRI. This study showed a reduction in the the subacromial space in protraction. This gives credence to the popular theory that a reduced degree of posterior tilting can result in a failure to reposition the acromion[30] and thereby decrease the minimum distance to the humeral head[34, 37, 39]. The findings of

Solem-Bertoft et al. also suggest an increase in scapular internal rotation would reduce the subacromial space. A cadaveric study by Karduna et al[30] showed the upward rotation of the scapula decreases the subacromial space. Therefore a decrease in upward rotation, as typically seen in patients with SIS, may be a compensatory motion utilized to decrease the contact pressures in the subacromial space. Because the subacromial space is small[23, 60] even a subtle change in its dimensions could result in compression of the subacromial tissues[55].

As previously noted, the degradation of the rotator cuff tendon is probably multi- factorial. The combination of overuse and increased compression of the rotator cuff ten- dons in rats demonstrated more degradation of the the tendons than either factor alone[68].

Inflammation of the rotator cuff tendons or subacromial bursa would also reduce the sub- acromial space[45]. An increased internal rotation of the scapula would could create a functional deficit with the glenoid by failing to position the corocoid process anterior to the humeral head. The coracoid process has been shown to limit anterior translation of the

10 humeral head in abduction[61, 35]. This may increase the shear stresses on the rest of the anterior stabilizing structures[32] and cause inflammation, thereby reducing the subacro- mial space.

1.3 Muscles of the Shoulder Girdle

Primary stability of the scapula on the thoracic cage occurs via numerous muscular at- tachments. Kibler [33] has classified these dynamic stabilizers into three categories. The

first group is primarily responsible for upward/downward rotation and stability and con- sists of the trapezius, rhomboids, serratus anterior and levator scapulae. The second group consists of extrinsic muscles including the deltoids, pectorals, biceps and triceps. And the third group consists of the intrinsic muscles, such as the subscapularis, infraspinatus, teres minor, and supraspinatus.

Pectoralis major is the most superficial muscle covering the anterio-superior thorax.

Its clavicular portion protracts the while its more lateral portions medially rotate the humerus. Pectoralis minor is deep to pectoralis major and located on the anterior boundary of the . Tightness in the pectoralis minor, which attaches to the coracoid process, can limit posterior tilting of the scapula during arm elevation[8, 32]. Biceps brachii is a two headed muscle. Its short head attaches to the coacoid process and, in the case of poor scapular stability, can anteriorly tilt the scapula. The tendon of the long head, for the scope of this study, enters the anterior portion of the shoulder capsule and is one of the soft tissue structure commonly irritated by SIS. Subscapularis, infraspinatus, teres minor and supraspinatus are the intrinsic muscles of the shoulder and form the rotator cuff. The tendons of these muscles insert into the lateral/humeral part of the capsule around the glenohumeral joint. The main purpose of the rotator cuff muscles is to protect the joint

11 Upward/Downward Rotators & Stabilizers of The Scapula Primary Actions Muscle Proximal Attachment Distal Attachment on The Scapula Upper: Lateral 1/3 of UR & Elevation Superior Nuchal line the Clavicle & Ligamentum Nuchae

Middle: Spinous Along the Spine of ER & Posterior Trapezius Process of C7 the Scapula to Tilt the Acromion

Lower: Spinous Spine of UR,ER Processes of T1-T12 the Scapula & Posterior Tilt Anterior Surface of UR, IR, Serratus Lateral Portions of the Medial Border Posterior Tilt Anterior 1-9 of the Scapula & Anterior Translation Major: Spinous Processes of T2-T5 Medial Border Rhomboids of the DR & ER Minor: Spinous Scapula Processes of C7-T1 Levator Transverse Processes Superior part of the Scapulae of C1-C4 Medial Border of the DR & Elevation Scapula

Table 1.1: Upward/Downward Rotators & Stabilizers of The Scapula

12 Extrinsic Muscles of the Scapula Muscle Proximal Attachment Distal Attachment Primary Actions Anterior: Flexion & Medial Acromion, Spine of Rotation of the arm Deltoid the Scapula, & Deltoid Tuberosity Middle: Lateral (third) of of the Humerus Arm Abduction the Clavicle Posterior: Extension & Lateral Rotation of the arm Clavicular Head: Anterior medial (half) Intertubercular Adduction & Pectoralis of the Clavicle groove of Medial Rotation Major Sternal Head: the Humerus of the Humerus Anterior surface of the Sternum DR, IR, Pectoralis Near the Costal Medial border Anterior Tilt Minor Cartilage of Ribs of the & Depression 3-5 Coracoid process of the Scapula

Short Head: Short Head: Tip of Coracoid Process Resist Humeral Biceps Radial Tuberosity Head Dislocation Brachii Long Head: of the Radius All: Flexion Supraglenoid Tubercle & Supination of the Forearm Triceps Long Head: Long Head: Brachii Infraglenoid Tubercle Olecranon Process Resist Humeral Medial & Lateral Heads: of the Ulna Head Dislocation Posterior Surface All: Extension of the Humerus of the Forearm

Table 1.2: Extrinsic Dynamic Stabilizers

13 and provide the compressive force on the humeral head to stabilize it on the glenoid. The deltoids are often considered force couple synergists in their combined action results in humeral elevation. However, a high ratio of deltoid to rotator cuff activation or muscle strength can result in a superior translation of the humeral head into the subacromial space and create excessive shear stresses on the cartilage of the glenoid[80]. The deltoids attach to the mid shaft of the humerus distally and medially to the spine of the scapula, acromion, and lateral 1/3 of the clavicle. Levator scapulae lies deep to the sternocleidomastoid and upper trapezius. This muscle serves to elevate and retract the scapula. The rhomboids serve mainly to aid the serratus anterior in stabilizing the scapula on to the .

However, in forced lowering of the arm from a raised position they are used more intensely.

Intrinsic Muscles of the Scapula The Rotator Cuff Muscle Proximal Attachment Distal Attachment Primary Actions on The Scapula Subscapular Fossa Lesser Tubercle Adduction & Subscapularis (Anterior Surface of of the Humerus Medial Rotation the Scapula) of the arm Infraspinous Fossa Greater Tubercle Lateral Rotation Infraspinatus (Posterior Surface of of the Humerus of the arm the Scapula) (Middle facet) Superior portion of Greater Tubercle Lateral Rotation Teres Minor the Lateral border of of the Humerus of the arm the Scapula (Inferior facet) Supraspinatus Supraspinatus Fossa Greater Tubercle Abduction of the Humerus of the arm (Superior facet)

Table 1.3: Intrinsic Dynamic Stabilizers

14 The trapezius is the largest and most superficial scapulothoracic muscle. It spans, in a diamond shape from the muchal line to the spinous process of T12 and from the spine to the acromion. There are three sections of this muscle; upper, middle, and lower.Though the trapezius is innervated by the spinal accessory (CN11) as a whole[47], histolog- ical examination shows a fine branch of this nerve traveling to and innervating the upper trapezius, whereas the middle and lower trapezius are innervated by the larger portion of the nerve. An intra-operative EMG study has shown that stimulating the spinal accessory nerve below the branch will activate the middle and lower portions of trapezius, but not the upper portion of this muscle[70]. Similarly, stimulating the branch of the spinal accessory nerve will activate the upper portion only. EMG studies have shown different activation patterns for each of the three portions of the trapezius[13, 17, 20]. The upper trapezius has been described as originating at the superior nuchal line of the cranium and ligamentum nuchae and inserting on the distal third of the clavicle[47]. The middle trapezius origi- nates at the spinus process of C7 and distally attaches along the spine of the scapula to the acromion. The lower trapezius originates at spinus process of T1 to T12 and attaches distally to the spine of the scapula[47]. As a whole the trapezius serves as a scapular re- tractor though, due to the lines of action for each portion of the trapezius, each section has a different role in the motion of the scapula. The middle trapezius stabilizes the scapula on the thorax and prevents excessive internal rotation of the scapula[35, 47] Upper trapezius and lower trapezius act as a force couple with serratus anterior to stabilize and upwardly rotate the scapula [35, 61].

The Serratus anterior is a fan shaped muscles comprised of a series of digits origi- nating on the lateral portions of ribs 1 though 9 and attaching distally to the medial border of the scapula along is anterior face. Serratus anterior is divided into three divisions called

15 slips[35, 61]. The upper slip runs from ribs 1 and 2 and the intercostal space to superior angle of the scapula. Slips originating from ribs 2,3 and 4 comprise the middle slips and attach the to medial portion of the medial border of the scapula. The remaining 4 or 5 slips, anatomic variation is typical in the final slip[61], form the lower slips which attach to the inferior angle of the scapula. This is the most powerful portion of the serratus anterior due, in part, to the long moment arm they have for upward rotation of the scapula. Serratus anterior is the primary internal rotator of the scapula[61, 48]. Also, in conjunction with the rhomboids, the serratus maintains contact of the medial border of the scapula with the wall of the thorax [35, 61].

1.3.1 Muscular Control of the Shoulder Girdle

For the muscles of the shoulder girdle to best perform their roles they must have at least one stabilized attachment site. Muscles without a stabilized attachment site cannot develop appropriate or maximal torque with a concentric contraction, thereby decreasing their strength and contributing to problems not only with strength production but also of muscular imbalance[33]. The stability of the scapula is especially important as it has been described as attaching to as many as eighteen muscles.

Several studies have recorded scapular motion alterations due to fatigue[72, 18, 9, 44].

Though the results vary between these studies, due in part to the variety of fatigue tasks chosen, they consistently reflect changes in scapular kinematics. A previous set of studies in our lab[9, 69] showed increases in scapular IR, decreases in scapular posterior tilting, and altered activation ratios in the SA, UT, and LT. Ludewig and Cook[37] reported increased upper and lower trapezius activation and decreased serratus anterior activation in addition to decreased posterior tilting during arm elevation in construction workers with SIS. Cools

16 et al[14] showed imbalances between the muscle activation ratios of upper trapezius and

serratus anterior in athletes with SIS.

1.3.2 Muscle Fatigue

Acute fatigue is defined as the reversible reduction in force or power generating capacity

of the neuromuscular system[2, 5]. The results of muscle fatigue are weakness of the

muscle[12, 18, 27] and dulling of proprioception[50]. This loss of coordination is two fold.

The first being a loss of ability to accurately detect the position of the limb in space and

the second being a loss in fine motor controls, due to the weakening of the musculature,

to accurately place the limb in space. These combined effects make the idea that injury

is more than likely in this state plausible. Physiologic changes of fatigue include blood

flow impairment,accumulation of Ca+2, and accumulation of lactic acid. While muscles are activated they produce lactic acid, a product of anaerobic metabolism. Blood flow to to musculature typically removes this waste product, however, a sustained contraction of ≈20% MVC can restrict the blood flow[12]. This effect is exacerbated in sustained contractions and static poses because the effects of vascular return are also limited from the lack of movement. Higher force contractions can even stop blood flow, making the muscle ischemic. A contraction at this level would produce a more rapid acute fatigue although muscles would also recover rapidly[2]. Lower level contractions require longer peroids of time to elicit a fatigue response however the recovery time is also lengthend[2].

A cumulation of sub-maximal contractions of the course of a prolonged period of time has been theorized to contribute to overuse injuries in overhead athletes[6, 14, 13, 33, 74] and construction workers[8, 37, 36].

17 1.3.3 Serratus Anterior and Trapezius: Force Couples of Scapular Stability

Serratus anterior works in synergy with upper trapezius and lower trapezius to upwardly rotate the scapula[35, 49, 61]. The SA and trapezius are the only muscles responsible for upward rotation of the scapula and no other muscle has an adequate line of action for this task[35]. Together they form a force couple for controlled upward rotation of the scapula.

This force couple provides a consistent motion regardless of the plane of elevation[35, 38].

To do this activation ratios are altered, providing more activation to the muscles in the couple that provide optimal support for the given orientation[3, 35]. If SA were to fatigue this relationship would be altered and the trapezius would have to compensate via increased activations. In the case of abduction the trapezius is the primary upward rotator in the force couple and have been shown to compensate well, allowing the scapula a full range of upward rotation, albeit with a decrease in strength[35]. This is not the case in flexion, where the SA is the primary upward rotator and solely responsible for the anterior positioning of the scapula[35]. In flexion, without SA, not only is there loss of strength but also range of motion losses up to 50◦.

The loss of strength during flexion also has implications outside of the force couple.

Normally the deltoid and gravity put torsion on the scapula resulting, in the absence of the trapezius and SA, in a downward rotation of the scapula. The SA and trapezius counteract these effects continuously, however in the absence of SA, the trapezius must counteract these effects alone and, when the trapezius begins to fatigue which is more likely in flexion, maybe too weak to prevent some downward rotation of the scapula. This is evident in a clinical examination when drooping of the scapula is found[47, 61]. Also the length of the deltoid is affected by excessive scapular downward rotation dynamically as the arm

18 elevates, resulting in inflammation of subacromial tissues and reduced effectiveness of the

deltoid. This was discussed earlier (Sec. 1.2.2) as a repercussion of excessive movement

of the instant center of rotation of the humeral head.

1.3.4 Reasons For Examining Serratus Anterior

Serratus anterior is positioned to contribute to all three normal scapula rotations, up-

ward and internal rotation, and posterior tilting[49]. Also, the serratus anterior muscle

is has been identified as the primary contributor to normal 3-Dimensional scapular rota-

tions [18, 9, 20, 37] and is involved in multiple muscle synergies that control the shoulder

complex. In upward rotation the serratus anterior couples with the trapezius. This is best

seen in the raising and lowering of the arm. Serratus anterior and upper trapezius activate

within the initial 2◦ of arm elevation. Lower trapezius activates within the initial 10◦ of arm elevation to work with serratus anterior to rotate the scapula on the thorax and provide stabilization at higher angles of arm elevation[3, 35, 69]. While both the lower trapezius and the serratus anterior are responsible for scapular upward rotation after this angle, the lower trapezius subsequently causes scapular external rotation, while the serratus anterior causes scapular internal rotation and posterior tilting[3, 35]. Therefore, co-contraction of the two muscles causes a balance between their respective movements allowing for stabi- lization of the scapula on the thorax while still producing upward rotation and posterior tilting[6]. The serratus and especially the lower trapezius muscles appear to be the first muscles involved in inhibition-based muscle dysfunction[33]. These two muscles form a crucial part of the force couple responsible for elevating the acromion. Lack of acromial elevation can be a secondary source of impingement in other shoulder pathologies, such as rotator cuff tendinitis and glenohumeral instability[32, 18, 28, 37, 39, 51, 54]. Clinically

19 this source of secondary impingement can be seen early in many shoulder problems and can play a major role in defining and treating the clinical problems that are associated with these pathologies[33, 68, 75].

SA is the primary muscles which serves to anteriorly translate and internally rotate the the scapula about the thorax[47]. SA also is responsible for maintaining the contact of the scapula and the thoracic wall and serves to posteriorly tilt the scapula as the humerus is elevated. Posterior tilt is the effect of the SA lines of action during upward rotation and protraction. This motion is not unique to the SA, being shared by other scapular retractor, however is highly influenced by SA. Because the SA is attached to the ribs, a contraction of the lower fibers of the SA will result in bringing the medial border of the scapula closer to the ribs which, due to the curvature of the thorax, results in posterior tipping[47, 35].

By stabilizing the scapula against the thoracic wall the SA allows other muscles to use the scapula as a fixed base off which to manipulate the humerus[47, 61].Lack of a stable mus- cular anchor affects all of the functions of the muscles attached to the scapula. Muscles without a stable base of origin cannot develop appropriate or maximal torque with a con- centric contraction, thereby decreasing their strength and contributing to problems not only with strength production but also in muscular imbalance[33].

SA would fatigue for the same reasons any muscle fatigues. Prolonged or repeated arm

flexion and elevation would utilize the SA and fatigue it. Depending on the task, the SA could fatigue in its entirety or just the activated portions. Escamilla et al.[20] summarized the role of the serratus anterior in various upper extremity sports, showing a consistent trend of having one of the highest, if not the highest, activation to maximal voluntary activation ratios of all muscles studied. This is not surprising given that SA has been reported to have high levels of activation in healthy subjects while performing any tasks that activates

20 it. Cools and colleagues have shown imbalances between muscle activation ratios for the

UT, LT, and SA force couple, and altered intramuscular activation balance of the upper and lower trapezius muscle in subjects with SIS during an isokinetic abduction and external rotation exercise[14]. Ludewig and Cook reported increased upper and lower trapezius ac- tivation and decreased serratus anterior activation in addition to decreased scapula upward rotation and posterior tilting during arm elevation in construction workers with SIS[37].

1.4 Hypotheses

1.4.1 Hypothesis 1:

Alterations in scapular muscle fatigue will be inconsistent between the dominant and non-dominant arms of subjects. This will result in differing kinematic and fatigue profiles between the dominant and non-dominant arms of subjects

Hypothesis 1.1:

Kinematic alteration of the scapula, relative to the thorax, will vary across fatigue con- ditions between the dominant and non-dominant arm as the arms are elevated in flexion and the scapular plane.

Hypothesis 1.2:

Patterns of normalized EMG activation levels for the dominant and non-dominant arms will be different and vary across condition, phase of motion, and humeral elevation.

Hypothesis 1.3:

Median power frequency of EMG activation levels for the dominant and non-dominant arms will differ across conditions.

21 1.4.2 Hypothesis 2:

Serratus anterior fatigue will lead to a decrease in scapular upward rotation, pos- terior tilting, and scapular internal rotation.

Hypothesis 2.1:

Scapular upward rotation, internal rotation, and posterior tilting will decrease progres- sively across fatigue conditions.

Hypothesis 2.2:

Normalized EMG activation levels of the serratus anterior muscle will rise between fatigue conditions at a great rate than those of the upper and lower trapezius muscles.

Hypothesis 2.3:

Median power frequency of EMG activation levels of the serratus anterior muscle will have a higher percent decline across fatigue conditions than those of the upper and lower trapezius muscles.

22 Chapter 2: METHODS

2.1 Subjects

2.1.1 Sample Size Calculations

Sample size estimates were based on achieving statistical significance of 0.05 with

80% power. For the scapular kinematic variables, this required a sample of 26 ,

13 subjects, to detect differences in orientation of 10◦ between tests. However, due to the increased variability in EMG signal data, there is a lower effect size, which raised the sample requirement to 35 shoulders. Twenty-four subjects were requested to account for potential drop-outs during data collection or to account for poor data.

2.1.2 Subject Recruitment

All testing was conducted by the protocol approved by The Ohio State University

Biomedical Sciences Institutional Review Board (IRB #: 2010H0311).

Seventeen healthy subjects, ages 18 to 33 years, with no history of shoulder pathology or current shoulder pain were recruited to participate in this study. Subjects were recruited using IRB approved fliers in academic buildings and by word of mouth. All subjects filled out a short questionnaire ([Ref to Appendix]) to verify they fit within the inclusion criteria of this study and to collect demographic information. Subjects over 40 years, below 18 years, with shoulder pain, or a history of shoulder pathology were excluded from this study.

23 Forty years of age was chosen based on physiological changes and reported rates of joint

degradation reported in the literature[53, 46]. Similarly, the low bound of the age criteria

was chosen based on the available subject population. Prior to the start of testing each

volunteer was given a description of the study and required to give informed consent.

Standard Range Mean Deviation Age 18 - 33 24.24 4.32 Weight (lbs) 100 - 230 156.59 38.40 Male 10 Sex Height (in) 59-76 67.06 4.93 Female 7 Reach (in) 22.5 - 31 26.04 2.29 Force (% BW) 6.42 - 13.16 8.73 1.63 Time to Max 80-490 217.06 132.42 Fatigue

Table 2.1: Subject Demographics

2.2 Instrumentation and Equipment

This study measured the kinematics and EMG of subjects bilaterally while they per-

formed fatigue and kinematic tasks. To record EMG signals from four muscles bilaterally

a Delsys Bagnoli 8-channel EMG system (Delsys Inc., Boston, MA) was used with eight

surface EMG pickups. This system is differentially amplified and has an input impedance

of > 1015Ω/0.2pF. The common mode rejection rate ratio was 92 dB at 60 Hz. Signals were

pre-amplified x1000 and sampled at 2000 Hz to ensure accurate signal detection. Bipolar

Ag-AgCl parallel bar electrodes were taped to the skin overlying the muscle bellies in par-

allel with the direction of the muscle fiber. The electrodes had a detection area of 10mm2.

The system was linked to a 16 bit A to D board. Motion was measured and recorded with a

24 Flock of Birds miniBIRD electromagnetic tracking sensor system (Ascension Technology,

Burlington, Vermont) and Motion Monitor software (Innovative Sports Training, Chicago,

Illinois). This allowed simultaneous tracking of five sensors at a sampling rate of 100 Hz

per sensor. Static accuracy[15] has been reported at 1.8 mm for position and 0.5◦ RMS for

orientation. All data was collected on a computer, running Windows 7 using the Innova-

tive Sports Training Motion Monitor software, especially assembled by Innovative Sports

Training for the purpose of this type of data collection.

Subjects were required to lay supine on a standard examination table and stretch a

therapeutic exercise band (Theraband), chosen based on their arm length and body weight,

at 30◦. To more accurately achieve this goal and to reduce the use of other muscles a

custom built table (Fig.2.1) was employed with a 30◦ shelf for subjects to use as a guide and vertical stabilizer. This custom table was also used as a guide during the lifting portion of the functional kinematic task. To assist subjects in keeping to the scapular plane a single guide plane was constructed (Fig.2.1). Wheels were mounted to the base of the plane so it could be removed and stored when not in use and to clear the testing area for other tasks.

Subject height and weight were quantified using a standard examination scale and arm length was measured using a tape measure.

2.3 Procedure

Two testers were required for each testing session. Appendix (A) is the full working protocol of the experiment. This section is a descriptive overview of that protocol.

2.3.1 Setup

The testing area was arranged such that the subject would have to move from their original position as little as possible. They were also asked to stand on a 24” x 24”half inch

25 Figure 2.1: Guides Built to Aid Subjects

foam mat. This was used to highlight boundaries of motion and for subject comfort. This served three functions:

• The subject never left the 30” range of the transmitter

• The subject was far less likely to get tangled and detach a sensor

• The time between tasks, for the subject to recover from fatigue, was minimized

All necessary testing materials were also layed out and readied before subjects were sched- uled to arrive. This was also a means of minimizing recovery time as well as to reduce overall fatigue of the subject from standing and waiting.

2.3.2 Subject Preparation

Upon arrival, each subject was given a packet including an IRB approved informed consent document and a questionnaire. The first tester would explain the step of testing to

26 the subject and obtain the subject’s signed informed consent form. Next, this tester would ask the subject demographic information and measure the subjects arm length. Arm length was defined as the distance from the acromioclavicular joint to the base of the thumb. The second tester readied the data collection computer, tape, and testing area. Demographic information was used to determine the appropriate resistive band weight and stretch length, using a force length data table[59], to provide a force of approximately 10% body weight on each arm; therefore a total force of approximately 20% body weight.

While tester two determined the correct band weight and length, tester one began ap- plying the EMG and kinematic sensors on the subject bilaterally. In total 14 sensors were placed on each subject, eight EMG sensors and five electromagnetic kinematic sensors.

EMG Sensor Placement

• Serratus Anterior sensor was placed on the lateral mid-line of the subject at the 6th

anterior to Latissimus dorsi. (Fig.A.2)

• Lower Trapezius sensor was placed at the middle of the line between the root of the

spine of the scapula and T8. (Fig.A.1)

• Pectoralis Major sensor was placed 2cm below the medial convexity of the clavicle.

(Fig.A.1)

• Upper Trapezius sensor was placed at the midpoint of the line between the PLA and

C7.(Fig.A.1)

• The placement of the ground electrode was on the right Anterior Illiac Spine. In

subjects where this bony landmark was obscured or who had high risk of electrode

detachment the right Lateral Malleouls was used.(Fig.A.3)

27 Figure 2.2: EMG Sensor Placement of Upper and Lower Trapezius and of Pectoralis Major

28 Figure 2.3: EMG Sensor Placement of Serratus Anterior

29 Figure 2.4: EMG Sensor Placement of Ground Electrode

Kinematic Sensor Placement

The positioning of these sensors was determined using the International Society of

Biomechanics Shoulder protocol[77] altered to accommodate bilateral data collection as specified by Innovative Sports Training. Only five sensors were required to do this as the thoracic sensor did not need to be duplicated. These sensors were placed on the body, as follows, and the bony landmarks were then digitized using the protocol recommended by the ISB[77] to establish a local coordinate system for motion capture.

• One sensor on each upper arm below the body of the triceps. (Fig.2.6)

• One on each Acromion process. (Fig.2.6,2.3.2)

• One on the Sternum after digitization was completed.(Fig.2.3.2)

30 Figure 2.5: Kinematic Sensor Placement: Anterior and Posterior Thorax

31 Figure 2.6: Kinematic Sensor Placement: Arm

32 2.3.3 Testing

Each subject was asked to participate in a single measurement session consisting of two types of tasks: Fatigue and Kinematic. The testing session began with the collection of baseline measurements of the subject which included a single maximum 3 second voluntary contraction task, resting posture, and resting EMG. These resting values were collected for

5 seconds without the subjects knowledge. The subject was then asked to perform a set of two kinematic tasks to establish pre-fatigue kinematics. This was followed by a one minutes long fatigue task and a repetition of the two kinematic tasks. This process was then repeated with the subject holding the fatigue task for as long as possible. Kinematics and

EMG were recorded for all tasks. Before the first fatigue task and after each fatigue task, subjects were asked to rate thier level of fatigue based on the Borg CR10 scale. Subjects were asked for a final Borg score 4-minutes after testing was completed. This subjective measure of fatigue allowed for the testers to assess fatigue and recovery while testing. For clarity, the order of testing was:

• Resting EMG and Posture

• Three Second MVC Task

• Two Pre-Fatigue Kinematic Tasks

• Record the First Borg

• One minute Long Fatigue Task

• Record the Second Borg

• Two Mid-Fatigue Kinematic Tasks

33 • Fatigue Task to Failure

• Record the Third Borg

• Two Post-Fatigue Kinematic Tasks

• After 4-minutes Record the Fourth Borg

MVC Task

The MVC task used was a bilateral break task in the scapular plane. This involved the subject hold both arms at 90◦ of abduction in the scapular plane while one tester applied a downward force. While it may have been preferable to preform a separate MVC task for each muscle examined, it was not feasible due to the time constraints of the study.

Literature has shown an accurate approximation of the MVC of individual muscles can be derived from a single MVC task[10]. The MVC task used was verified on several subjects in a pilot study.

Fatigue Task

The fatigue task consisted of a resisted supine reaching task previously demonstrated, in pilot testing, to isolate and bias fatigue the Serratus Anterior. The resistance given to each subject was determined based on their body weight and arm length and was be applied using a therapeutic resistance band. Subjects maximally protracted their arms at a 30◦

angle, supported by an inclined table, against this resistance and held this position for

the duration of the task or failure. Subjects were continuously encouraged and visually

monitored throughout the task.(Fig.2.7)

34 Figure 2.7: Setup of the Fatigue Tasks

Kinematic Tasks

There were two kinematic task in this study. In the first, subjects raised and lowered their arms in the scapular plane five times at a self selected slow pace. Subjects were asked to take 2-seconds raising their arm to vertical and 2-seconds lowering their arm to their side. To aid subjects in maintaining the correct plane of motion, a guide was positioned in the correct orientation relative to the subject. Figure (2.8) shows a representation of this task.

The second kinematic task required subjects to lift a one gallon ergonomic bottle of water to between an imagined high shelf five times at a self selected slow pace. Subjects were asked to pause for 1 second at the top of this motion. The height of elevation was kept constant at 72” delineated by a line drawn onto the post of the custom table. Figure (2.9) shows a representation of this task.

35 Figure 2.8: Scapular Plane Elevations

Figure 2.9: Weighted Frontal Elevation Task

36 2.4 Data Reduction and Processing

2.4.1 MVC Task

All raw EMG data were root mean square(RMS) rectified with a period of 20ms, a low pass filter of 500Hz, and a high pass filter of 20Hz[16]. This data was then exported into a custom made MATLAB script where the 1-second period of maximum EMG amplitude was manually selected for each of the eight muscles analyzed of each subject. This portion of the data was then averaged and recorded as the MVC.

2.4.2 Kinematic Tasks

Local coordinate systems for each humerus and scapula were defined following the rec- ommendations of the International Society of Biomechanics[77] and the thorax coordinate system was defined by the internal coordinates of the electromagnetic sensor. To insure the same orientation of the thorax sensor was used across all subjects a non-ferrous housing was constructed around the sensor with a fused digitizing stylus. Figure (A.1) shows the thorax sensor within its housing.

Each segment digitized was compared to the local coordinate system of the thorax.

Using Euler angle sequences (Z, Y’, Z”) and (Z, Y’, X”), the 3-dimensional orientation of the humerus and scapula, respectively, were calculated relative to the thorax.

For the scapula:

• Z described internal/external rotation

• Y’ described upward/downward rotation

• X” described anterior/posterior tilting

37 For the humerus:

• Z described the plane of elevation

• Y’ described the angle of elevation

• Z” described internal/external rotation

Euler angles for humeral elevation, scapular internal rotation, scapular upward rotation, and scapular tipping were calculated and exported into a custom made series of MATLAB scripts using MotionMonitor. Kinematic and EMG data was reduced to 10◦ intervals be-

tween 30◦ & 120◦ of humeral elevation. For each of the scapular rotations, all data ±1◦ for each 10◦ interval were averaged to represent the mean scapular position at each 10◦ of humeral elevation. This process was done for both kinematic tasks as the arm was elevated and lowered. The direction (positive or negative) of the elevation of the humerus and the three scapular rotations were determined by the right hand rule for the left side. This was done to standardize all data for simplified analysis.

The same was done for the EMG data. All raw EMG data were RMS rectified with a period of 20ms, a low pass filter of 500Hz, and a high pass filter of 20Hz[16]. These individual subject mean EMG values were divided by the subjects’ MVC value and multi- plied by 100 to calculate the percentage of the maximum voluntary contraction and make it possible to compare muscle activation between muscles and subjects.

2.4.3 Fatigue Tasks

EMG data from the fatigue tasks was collected in 10-second intervals of the course of each fatigue task. Each 10-second interval was exported into a custom made series of

MATLAB scripts using MotionMonitor. Data in each interval consisted of RMS rectified

38 EMG signals, as in the kinematic and MVC tasks, and and power density spectrum (PSD) data calculated using MotionMonitor. PSD data was subject to the same high and low pass

filtering of all the EMG data of this study with an additional filter for 60Hz. To determine the median power frequency (MPF) of each 10-second interval a custom made MATLAB script was used, which extracted the weighted MPF.

To compare fatigue tasks across subjects For the first fatigue task data was recorded in

10 second intervals for 70 seconds. To determine the amplitude EMG for each interval, the mean amplitude of the EMG signal was taken. To normalize the data, the first 10- second mean was used as a base value and the remaining 6 time points were reported as a percentage change from that point. The second fatigue task was to failure and ranged in time from 80 - 490 seconds with an average of 217 seconds. To standardize this data, quartiles were compared to each other. The reported values for the second fatigue task are percentage changes of the first quartile.

2.5 Data Analysis

2.5.1 Verification of Data

Before the data was analyzed in detail an initial inspection of the data was done to verify no errors were made in processing. To determine the qualitative validity of the data from each kinematic sensor, two main guidelines were used. The first guideline was the amount of data collected on the sensor. Data from some subjects was missing from the higher and lower humeral elevation angles. In cases where the number of missing data points was small, the data from the nearest humeral elevation angle was repeated. In one case this was not possible, as the subject had not given sufficient data to allow for this estimation, and the

39 subject was removed from further analysis. This guideline was also used to verify EMG data for the kinematic tasks.

The second guideline used to determine the qualitative validity of the data was to com- pare the data to normal ranges of motion for the scapular rotations. Because the method of measuring the motion of the scapula was not in clinical terms it was not possible to simply examine the values of the data to make an assessment of how much the scapula had rotated on any of its axes. Instead the range of the the motion was examined for each of the ro- tations. All data fell within physiologically acceptable bounds. To further assess the data, the rotations of the unfatigued condition were compared to the rotations of the subsequent conditions. This was done by taking subtracting the values of condition one from those of the subsequent conditions and then taking a mean of those values. Figure(3.1) shows a representative plot of what the outcomes looked like. Each side and rotation was calcu- lated separately. At this stage the change scores were compared to what was believed to be physically possible. A mean change in UR of 25◦, IR of 20◦, or Tilt of 15◦ resulted in a subject’s exclusion from the analysis of that rotation.

A similar method was used to assess the validity of the EMG data however the thresh- olds were set much higher, excluding data larger than 500% of the mean of all subject data for any individual task.

2.5.2 Analysis

Statistical analysis was ubiquitously performed using the method of repeated mea- sure ANOVAs (RM-ANOVA). The factors examined for each subject were Gender, Phase of Motion (Upswing/Downswing) of the Humerus, Arm Dominance, Fatigue Condition,

40 Time, and Humeral Elevation Angle. Due to the lack of significance found for the fac- tors Gender and Phase of Motion they are not reported. Post-hoc testing was always done using Bonferroni tests. For ease of reporting Arm Dominance and Side are hence forth interchangeable terms.

Hypothesis 1.1: Kinematic alteration of the scapula, relative to the thorax, will vary across fatigue conditions between the dominant and non-dominant arm as the arms are elevated in flexion and the scapular plane.

To determine the effect of arm dominance on the three rotations of the scapula in each of the planes of humeral elevation, a series of RM-ANOVAs was performed. This set of

RM-ANOVAs was the most general and consisted of three factors: Condition, Side, and

Humeral Elevation Angle.

Hypothesis 1.2: Patterns of normalized EMG activation levels for the dominant and non-dominant arms will be different and vary across condition, phase of motion, and humeral elevation.

To determine the effects of the factors Side, Condition, Phase, and Humeral Eleva- tion on the normalized EMG activation levels during the kinematic tasks, a series of RM-

ANOVAs was performed. A second set of analysis was performed using EMG amplitude data from the two fatigue tasks. A series RM-ANOVAs was performed on the factors: Side and Time.

Hypothesis 1.3: Median power frequency (MPF) of EMG activation levels for the dom- inant and non-dominant arms will differ across conditions.

Statistical analysis of the effect of side on the MPF of each of the four muscles examined bilaterally was done using RM-ANOVAs. This set of RM-ANOVAs consisted of factors:

Time and Side.

41 Hypothesis 2.1: Scapular upward rotation, internal rotation, and posterior tilting will decrease progressively across fatigue conditions

To determine the effects of Condition on the three rotations of the scapula during the kinematic tasks, a series of RM-ANOVAs was performed on the factors: Humeral Eleva- tion and Condition for each arm. Qualitative inspection of the data reveled variability in the direction subjects moved between fatigue conditions. Subjects were grouped together based on the sign of their mean rotations changes across conditions. A subject with a posi- tive mean change meant that the subject had, on average, greater Euler angles in subsequent conditions than their corresponding baseline Euler angles. The reverse was true for subjects with a negative mean change. The reported results are from analysis of these groupings.

Hypothesis 2.2: Normalized EMG activation levels of the serratus anterior muscle will rise between fatigue conditions at a great rate than those of the upper and lower trapezius muscles

To determine the effects of fatigue condition on the normalized EMG activation levels during the kinematic tasks, a series of RM-ANOVAs was performed on factors: Condition and Humeral Elevation for each arm.

This original series of analysis gave insufficient information to make claims about the fatigue status of the muscles. To gain a better understanding of the effect the fatigue tasks on the muscles, further analysis was needed. EMG amplitude data from the two fatigue tasks was analyzed both statistically and qualitatively. A second series of RM-ANOVAs was performed for the factor Time. Qualitative analysis of the data was then performed.

42 Hypothesis 2.3: Median power frequency of EMG activation levels of the serratus anterior muscle will have a higher percent decline across fatigue conditions than those of the upper and lower trapezius muscles

Statistical analysis of the effect of fatigue on the MPF of each of the four muscles examined bilaterally was done using RM-ANOVAs. This set of RM-ANOVAs consisted of factor: Time. A qualitative set of analysis was performed as well. Together with the results from the EMG amplitude analysis, the method of Joint analysis of EMG spectrum and amplitude (JASA) was used. This allowed for a combined assessment of the EMG signal which gave further insight than either data set alone.

43 Chapter 3: RESULTS

To determine subject fatigue while testing the Borg CR10 scale was used. While this

information was not utilized to address any specific hypothesis it was a vital measure to

ensure subjects experienced fatigue.

Baseline First Second 4- Min Range 0-2 0.5-5 2-10 0.5-8 Average 0.84 1.91 5.09 3.5 STD 0.64 1.14 2.24 2.13

Table 3.1: Subject Demographics: Borg Scores

3.1 Hypothesis 1: Alterations in scapular muscle fatigue will be incon- sistent between the dominant and non-dominant arms of subjects. This will result in differing kinematic and fatigue profiles between the dominant and non-dominant arms of subjects

3.1.1 Hypothesis 1.1: Kinematic alteration of the scapula, relative to the thorax, will vary across fatigue conditions between the dom- inant and non-dominant arm as the arms are elevated in flexion and the scapular plane.

In all of the rotations of the scapula examined arm dominance significantly (p ≤ .05) affected the resulting motions. In the case of IR for the Waving task there was an interaction

44 effect of Side and Fatigue Condition (p= 0.028444*). This effect was further examined using Bonferroni post-hoc tests, which showed fatigue conditions one and two, of the non- dominant scapula, to have significantly different motions. Table 3.2 summarizes the P- values for arm dominance as a factor for each scapular rotation.

Scapular Rotation Wave Task: P = Lift Task: P = IR 0.044815* 0.002500* UR 0.003100* 0.017833* Tilt 0.005594* 0.001670*

Table 3.2: Summary of Arm Dominance P-Values

3.1.2 Hypothesis 1.2: Patterns of normalized EMG activation levels for the dominant and non-dominant arms will be different and vary across condition, phase of motion, and humeral elevation.

Phase of humeral motion was examined but was not found to have a significant effect on the EMG signal. As can be seen in table (3.3), the normalized EMG amplitude of

Lower Trapezius and Pectoralis Major were significantly affected by side (p= 0.023150* and p= 0.027607*). In light of this result a set of RM-ANOVAs was performed separating sides, however, no further significant differences were found. Upper Trapezius was the only other muscle to show a significant factor in the Lifting task. At 110◦ of humeral elevation normalized UT EMG activation was significantly higher than those of 30◦ to

70◦. Originally, Humeral elevation angle violated the covariance matrix circularity (CMC), therefore the reported p-value was calculated using Geisser Greenhouse Epsilon (GGE).

45 Humeral elevation angle was more often a significant factor in the Waving task. Table

(3.5) shows that humeral elevation angle significantly effected the normalized EMG ampli-

tudes of SA, UT, LT, and nearly Pec. In each of the muscles the CMC was violated for all

factors except side and the p-values were all calculated using GGE. In these muscles, nor-

malized EMG amplitude significantly increased from the lower humeral elevation angles

to the higher elevation angles. Table (3.6) summarizes this result from Bonferroni post-

hoc tests. Lower Trapezius was the only muscle to show significant differences between

the dominant and non-dominant side. Follow up RM-ANOVA showed, on the dominant

side, that humeral elevation angle significantly effected the normalized EMG amplitude (p

= 0.015484*). Bonferroni post-hoc tests show that EMG amplitude increases with humeral

elevation across the whole range of motion in the scapular plane (30◦-120◦). Specifically,

30◦ had a lower amplitude than all angles greater than 60◦ and 40◦ and 50◦ had lower am-

plitudes than 100◦ and beyond. Again CMC was violated and this p-value was calculated

using GGE.

Muscle SA UT LT Pec P-Value P-Value P-Value P-Value Side 0.471568 0.279203 0.023150* 0.027607* Condition 0.871012 0.299723 0.305794 0.967365 Humeral 0.220153 0.033560* 0.831581 0.480026 Elevation

Table 3.3: Summary of P-Values for Normalized EMG During Lifting Task

Results from the analysis of the EMG amplitudes from the two fatigue tasks, give more information as to the effect of arm dominance on the amplitude of the EMG signal. These results can be found in table (3.7). The effect of arm dominance on the percent change of

46 Mean % of MVC Dominant Non-Dominant LT 47.4787 27.40451 Pec 518.0037 388.1823

Table 3.4: Summary of % Change for Normalized EMG During Lifting Task by Side

Muscle SA UT LT Pec P-Value P-Value P-Value P-Value Side 0.25743 0.206195 0.011347* 0.153415 Condition 0.475331 0.937149 0.318466 0.177139 Humeral 0.021367* 0.023176* 0.034313* 0.083513 Elevation

Table 3.5: Summary of P-Values for Normalized EMG During Waving Task

the EMG amplitudes measured from the Serratus Anterior, Pectoralis Major, and the Upper

and Lower Trapezius was not significant.

3.1.3 Hypothesis 1.3: Median power frequency (MPF) of EMG activa- tion levels for the dominant and non-dominant arms will differ across conditions.

None of the muscles examined showed significant differences in MPF between arms except for the Lower Trapezius (p= 0.040363*). This was confirmed using a Bonferroni post-hoc test.

47 Humeral Different From Elevation Angles SA UT LT 30◦ 90◦, 100◦, 110◦, 120◦ 80◦, 90◦, 100◦, 110◦, 120◦ 100◦, 110◦, 120◦ 40◦ 100◦, 110◦, 120◦ 90◦, 100◦, 110◦ 100◦, 110◦, 120◦ 50◦ 100◦, 110◦, 120◦ 100◦ 100◦, 110◦, 120◦

Table 3.6: Summary of Humeral Elevation Differences for Normalized EMG During Wav- ing Task

Muscle First Fatigue Second Fatigue P = Power P = Power SA 0.332013 0.155090 0.469968 0.106878 UT 0.280734 0.181761 0.446479 0.113423 LT 0.973168 0.050117 0.323216 0.159745 Pec 0.376825 0.136271 0.545368 0.089346

Table 3.7: EMG Amplitude: Summary of Arm Dominance P-Values

3.2 Hypothesis 2: Serratus anterior fatigue will lead to a decrease in scapular upward rotation, posterior tilting, and scapular internal rotation

3.2.1 Hypothesis 2.1: Scapular upward rotation, internal rotation, and posterior tilting will decrease progressively across fatigue condi- tions

An original series of RM-ANOVAs was run that demonstrated a lack of significance between conditions for each of the three scapular rotations. However, the levels of proba- bility were greatly increased when the data was filtered by arm dominance. Furthermore,

48 Muscle First Fatigue Second Fatigue P = Power P = Power SA 0.408002 0.125499 0.683251 0.067709 UT 0.312914 0.164820 0.277059 0.184986 LT 0.391651 0.131208 0.040363* 0.554088 Pec 0.941266 0.050566 0.091756 0.392312

Table 3.8: EMG MPF: Summary of Arm Dominance P-Values

Muscle First Fatigue Second Fatigue Dominant Non-Dominant Dominant Non-Dominant SA -1.571184 -4.251236 -3.183189 -1.342995 UT -8.387948 -11.76105 -4.104836 2.334536 LT 6.616344 10.42459 0.620167* -7.918277* Pec 3.352685 2.820829 2.261713 -7.453649

Table 3.9: EMG MPF: Summary of Arm Dominance Mean Percent Change

the data was then assessed qualitatively, which lead to a method of grouping subjects previ- ously not considered or reported in literature. Figures (3.1,3.2,3.3,3.4,3.5,3.6) demonstrate the variability of the data.

Unweighed Humeral Elevations in the Scapular Plane

By separating the data based on side and running a new series of RM-ANOVAs the effect of fatigue condition was better isolated. These significance of these effects can be found in table (3.10). As can be seen in this table, internal rotation of the non-dominant scapula was the only motion of the scapula to show significant changes in scapular rotation between fatigue conditions (p= 0.008652*). A set of Bonferroni post-hoc tests reveal this difference to be between fatigue conditions one and two.

49 P-Value of Fatigue Condition Scapular Non-Dominant Dominant Rotation Side Side IR 0.008652* 0.468281 UR 0.134294 0.143656 Tilt 0.222596 0.145047

Table 3.10: General P-Values of Condition

Internal rotation on the non-dominant side resulted in 11 subjects with a positive

mean change and 4 subjects with a negative mean change. This can be seen in plot (3.1).

Running RM-ANOVA on the positive group showed a significant difference in the motion

between conditions (p=0.027396*). Bonferroni post-hoc tests demonstrated that conditions

one and two had significantly different scapular internal rotations. Because the CMC was

violated for Condition as a factor, the reported p-value was calculated using GGE. The

negative group was also run but did not show significance.

All Subjects Positive Group P-Value 0.008652* 0.027396* Condition Mean Change Mean Change 2 6.371679* 7.765205* 3 3.20853 4.502536

Table 3.11: Comparison of Mean IR Change: Non-Dominant

Internal rotation on the dominant side resulted in 8 subjects in the positive group and

7 in the negative. Statistical inspection of the positive group showed a significant change in internal rotation between conditions (p=0.033029*). Because the CMC was violated for

Condition as a factor, the reported p-value was calculated using GGE.The same analysis

50 Figure 3.1: Plot of IR Mean Differences From Condition One

of the negative group also showed a significant change (p=0.021252*) and an interaction effect between humeral elevation and condition (p=0.008931*). Bonferroni post-hoc tests were run for both groups showing significant changes in internal rotation between condition one and conditions two and three in the positive group and between condition one and three in the negative group.

Further Bonferroni and statistics were run to examine the interaction effect of humeral elevation and condition present in the negative group. The results of these tests show that condition three was different than both conditions one and two for all humeral elevation angles and that condition two was different than condition one for humeral elevation angles of 120◦, 110◦, and 100◦.

51 Negative Group Positive Group P-Value 0.021252* 0.033029* Condition Mean Change Mean Change 2 -3.039841 3.232646* 3 -8.520404* 4.163414*

Table 3.12: Comparison of Mean IR Change: Dominant

Figure 3.2: Plot of UR Mean Differences From Condition One

52 Upward rotation on the non-dominant side had 12 subjects in the positive mean change group and 4 subjects in the negative mean change group. The positive group had a significant difference between condition one and both conditions two and three(p=

0.000385*). This was found by Bonferroni post-hoc tests. The negative group did not show significant results.

Negative Group Positive Group P-Value NT 0.000385* Condition Mean Change Mean Change 2 NT 4.953595* 3 NT 4.367876*

Table 3.13: Comparison of Mean UR Change: Non-Dominant

Upward rotation on the dominant side had 11 positive and 5 negative subjects. Sta- tistical analysis of the positive and negative groups showed significant changes in upward rotation between condition one and both conditions two and three, for both groups(p=

0.008271* and p= 0.007106* respectively). This was determined using Bonferroni post- hoc tests. The positive group violated CMC for Condition as a factor, therefor the reported p-value was calculated using GGE.

Negative Group Positive Group P-Value 0.007106* 0.008271* Condition Mean Change Mean Change 2 -5.777808* 4.82594* 3 -6.40674* 4.348943*

Table 3.14: Comparison of Mean UR Change: Dominant

53 Figure 3.3: Plot of Tilt Mean Differences From Condition One

Tilting on the non-dominant side demonstrated groups of almost equal size. There

were 8 subjects in the positive group and 7 in the negative. Though a significant difference

between conditions was found for the positive group (p=0.009424*) the negative group

did not give a significant difference between conditions (p=0.105958) but instead showed

significant tilting changes between humeral elevation angles(p=0.00) and for an interaction

between condition and humeral elevation angle(p=0.00). Bonferroni post-hoc tests showed

the high humeral elevation angles to be significantly different from the lower angles and

that condition two was significantly different from condition one for humeral elevation

angles larger than 60◦. Condition three was also significantly different from condition one but for only humeral elevation angles larger than 100◦.

54 Negative Group Positive Group P-Value 0.105958 0.009424* Condition Mean Change Mean Change 2 -3.405593 2.114117 3 -1.99078 4.477422*

Table 3.15: Comparison of Mean Tilt Change: Non-Dominant

Tilting on the dominant side had 3 subjects in the positive mean change group and 12 subjects in the negative group. The positive group did not yield any statistical significance.

The negative group showed a significant difference between conditions (p=0.015347*).

Bonferroni post-hoc tests showed the significants was between condition 1 and conditions two and three.

Negative Group Positive Group P-Value 0.015347* 0.186804 Condition Mean Change Mean Change 2 -3.562621* 3.825746 3 -3.896236* 3.461227

Table 3.16: Comparison of Mean Tilt Change: Dominant

Lift Task:

As in the analysis of the Wave task the Lift task data was separated based on side and a new series of RM-ANOVAs was run to better isolate the effect of fatigue condition on the three scapular rotations. The significance of these effects can be found in table 3.18. In this table it can be noted that scapular upward rotations of the non-dominant scapula had significant differences between conditions (p= 0.040932*). A set of Bonferroni post-hoc

55 Scapular Mean Change Mean Change Rotation Side Group N P-Value of of Condition 2 Condition 3 Positive 8 0.033029* 3.232642* 4.163414* Dom. Negative 7 0.021252* -3.039841 -8.520404* IR Positive 11 0.027396* 7.765205* 4.502536 Non-Dom. Negative 4 NT NT NT Positive 11 0.008271* 4.82594* 4.348943* Dom. Negative 5 0.007106* -5.777808* -6.40674* UR Positive 12 0.000385* 4.953595* 4.367876* Non-Dom. Negative 4 NT NT NT Positive 3 0.186804 3.825746 3.461227 Dom. Negative 12 0.015347* -3.562621* -3.896236* Tilt Positive 8 0.009424* 2.114117 4.477422* Non-Dom. Negative 7 0.105958 -3.405593 -1.99078

Table 3.17: Summary of Wave Task Results

tests reveal this difference to be between fatigue conditions one and two. Data from both scapular upward rotation on the non-dominant side and scapular tilting on the dominant side violated CMC. The reported p-value for the scapular upward rotation was found using

Huynh Feldt Epsilon (HFE) and the reported p-value for the scapular tilting was found using GGE. Qualitative inspection of the data reveled variability in the direction subjects moved between fatigue conditions.

P-Value of Fatigue Condition Scapular Non-Dominant Dominant Rotation Side Side IR 0.078442 0.937110 UR 0.040932* 0.066980 Tilt 0.075127 0.554699

Table 3.18: General P-Values of Condition

56 Figure 3.4: Plot of IR Mean Differences From Condition One

Internal rotation of the scapula of the dominant side had a positive group of 5 sub- jects and a negative group of 9 subjects. The positive group had significant motion changes between conditions (p= 0.042821*) and humeral elevations (p= 0.042020*). Bonferroni post-hoc tests showed these differences to be between condition one and three and were not specific for differences in scapular internal rotation between humeral elevation angles.

The negative group originally had no significant results, however visual inspection of in- dividual subject data revealed an oddity in subject 13. Subject 13 had a positive trend however, due to an oddity in the subject’s condition two data, had a negative mean change in scapular internal rotation. When subject 13 was removed from the negative group and added to the positive group both groups showed significant differences in scapular internal

57 rotation (p= 0.045000* p= 0.037284*). Bonferroni post-hoc tests on the positive group were non-specific however the same tests on the negative group showed a difference be- tween conditions one and three. See table 3.19 for a summary of these results. The negative group violated CMC for Condition as a factor, therefore the reported p-value was calculated using GGE.

Negative Group Positive Group Original Without # 13 Original With # 13 P-Value 0.116341 0.037284* 0.042821* 0.045000* Condition Mean Change Mean Change Mean Change Mean Change 2 -3.038871 -1.865482 3.651038 0.667877 3 -5.224407 -6.478837* 8.649551* 7.847165

Table 3.19: Comparison of IR Scenarios: Dominant

Internal rotation of the scapula of the non-dominant side had 10 subjects in the positive group and 4 in the negative group. The positive group showed a significant change in scapular motion between conditions (p= 0.001227*). Specifically, condition one had significantly different motions than both conditions two and three according to Bonferroni post-hoc tests. The negative group appeared to have significant changes between conditions

(p= 0.047463*), however violated CMC for Condition and the GGE probability level was not significant for Condition (p= 0.105075).

Upward rotation of the scapula of the dominant side had 8 subjects in the positive group and 7 subjects in the negative. Statistical analysis of the positive group showed that upward scapular rotation changes between fatigue conditions approached significance (p=

0.056417). The negative group had significant changes in the rotation between conditions

(p= 0.003782*) as well as an interaction between humeral elevation angle and condition(p=

58 Negative Group Positive Group P-Value 0.105075 0.001227* Condition Mean Change Mean Change 2 1.763296 6.537471* 3 -8.415662 8.286619*

Table 3.20: Comparison of IR Scenarios: Non-Dominant

Figure 3.5: Plot of UR Mean Differences From Condition One

59 0.000012*). Post-hoc Bonferroni tests showed the significance was between condition

three and both conditions one and two. Also the Bonferroni tests showed that upward

rotation of condition one was different than that of condition three for humeral elevation

angles of 50◦ and above and that upward rotation of condition two was different than that of condition three for humeral elevation angles of 80◦ and above.

Negative Group Positive Group P-Value 0.003782* 0.056417 Condition Mean Change Mean Change 2 -1.977065 3.369016 3 -6.78436* 1.844592

Table 3.21: Comparison of UR Groups: Dominant

Upward rotation of the scapula of the non-dominant side had 10 positive subjects and 5 negative. Both groups had significant changes in scapular upward rotations between conditions (p= 0.000037* and p= 0.001264* respectively). From Bonferroni post-hoc tests, we found significant motion differences between condition one and both conditions two and three in the positive group and differences between condition 3 and both conditions one and two in the negative group.

Negative Group Positive Group P-Value 0.001264* 0.000037* Condition Mean Change Mean Change 2 -2.036114 8.243572* 3 -9.0267686* 6.171483*

Table 3.22: Comparison of UR Groups: Non-Dominant

60 Figure 3.6: Plot of Tilt Mean Differences From Condition One

Scapular tilting of the dominant side had an almost even distribution of subjects be- tween groups. There were 6 positive and 7 negative. Both groups had significant changes in scapular tilting between conditions (p= 0.004004* and p= 0.019542* respectively). Bon- ferroni post-hoc tests on each group showed this difference to be between fatigue conditions one and three in both groups and between fatigue conditions two and three in the positive group. The negative group violated CMC for Condition as a factor, therefor the reported p-value was calculated using GGE.

Scapular tilting of the non-dominant side was more one-sided as 10 subjects had positive mean changes to their motion, while only 3 subjects had negative. The subjects of the positive group had significant differences in their scapular tilting between fatigue

61 Negative Group Positive Group P-Value 0.019542* 0.004004* Condition Mean Change Mean Change 2 -2.576086 1.260846 3 -6.095736* 5.053535*

Table 3.23: Comparison of Tilt Groups: Dominant

conditions (p= 0.022958*). The data for the positive group violated CMC for Condition as a factor, therefor the reported p-value was calculated using GGE. Bonferroni post-hoc tests on the positive group showed this difference was between fatigue conditions one and three. Statistical analysis was also performed for the negative group however no significant results were found.

Positive Group P-Value 0.022958* Condition Mean Change 2 2.215558 3 4.476803*

Table 3.24: Summary of Tilt Results: Non-Dominant

3.2.2 Hypothesis 2.2: Normalized EMG activation levels of the ser- ratus anterior muscle will rise between fatigue conditions at a great rate than those of the upper and lower trapezius muscles

This original series of analysis gave insufficient information to make claims about the fatigue status of the muscles. The reported values are of mean percentage change from the start of the task to the end in set intervals. This form of analysis did not give statistically significant results but qualitative inspection gives insight into the status of muscle fatigue.

62 Scapular Mean Change Mean Change Rotation Side Group N P-Value of of Condition 2 Condition 3 Positive 6 0.045000* 0.667877 7.847165 Dom.** Negative 8 0.037284* -1.865482 -6.478837* Positive 10 0.001227* 6.537471* 8.286619* IR Non-Dom. Negative 4 0.105075 1.763296 -8.415662 Positive 8 0.056417 3.369016 1.844592 Dom. Negative 7 0.003782* -1.977065 -6.78436* UR Positive 10 0.000037* 8.243572* 6.171483* Non-Dom. Negative 5 0.001264* -2.036114 -9.0267686* Positive 6 0.004004* 1.260846 5.053535* Dom. Negative 7 0.019542* -2.576086 -6.095736* Tilt Positive 10 0.022958* 2.215558 4.476803* Non-Dom. Negative 3 NT NT NT **The values reported are with subject # 13 moved

Table 3.25: Summary of Lift Task Results

Figures (3.7) and (3.8) show the mean percentage change in the EMG amplitudes during

the first and second fatigue tasks respectively.

3.2.3 Hypothesis 2.3: Median power frequency of EMG activation lev- els of the serratus anterior muscle will have a higher percent de- cline across fatigue conditions than those of the upper and lower trapezius muscles

In the first task only Serratus Anterior was shown to have significantly changed in MPF with Time (p = 0.040331). This data violated CMC and HFE was used to calculate the reported p-value. The set of Bonferroni post-hoc tests used to find which time point had significant differences showed that MPF had a mean decrease between 20 seconds and 70 seconds of the fatigue task.

63 Figure 3.7: First fatigue task mean EMG amplitude changes over time

Muscle First Fatigue % Change Overall Dominant Non-Dominant SEM SA 4.05 0.2315 7.87 5.37 UT -3.37 -1.293 -5.45 2.62 LT -12.72 -12.80 -12.63 3.38 Pec 2.83 0.7371 4.93 3.25 Second Fatigue % Change Overall Dominant Non-Dominant SEM SA 10.44 4.255 16.64 11.81 UT 2.02 3.90 0.1414 3.40 LT 4.47 -0.4953 9.43 6.87 Pec 13.81 11.16 16.46 6.05

Table 3.26: EMG Amplitude: Summary of Arm Dominance Average Mean Percent Change

64 Figure 3.8: Second fatigue task mean EMG amplitude changes over time

65 In the second fatigue task only the Lower Trapezius showed statistically significant changes. LT originally had significant MPF decline between the second and fourth quartile

(p = 0.049214*), however the data violated CMC and the p-value increased above 0.05 after being recalculated using HFE. None the less the decline in MPF over time approached significance for the Lower Trapezius (p = 0.059159). In table (3.8) it can be seen that

LT had differences in MPF changes between the dominant and non-dominant sides. RM-

ANOVAs were run for the dominant and non-dominant LT in hopes that variability of the data would decrease and reveal significant results. Neither Lower Trapezius yielded a significant change in MPF over time, but the change in the left LT approached significance

(p = 0.066419).

Qualitative inspection gives insight into the status of muscle fatigue. Figures (3.9) and

(3.10) show the mean percentage change in the MPF during the first and second fatigue tasks respectively. Figures (3.11) and (3.12) demonstrate the method of JASA using time point 6 of the first fatigue and the fourth quartile of the second fatigue. These time points were chosen because they represent the end of each task. Time point 7 was not chosen even though it was the final 10 seconds of the first fatigue as subjects tended need encourage- ment around one minute into the task. Tables (3.29) and (3.30) show a subject by subject distinction for the JASA plots.

Fatigue Recovery Force Increase Fatigue Force Decrease SA 1 2 5 7 UT 3 2 3 7 LT 8 1 1 5 Pec 0 4 5 6

Table 3.27: Summary of Task 1 JASA Chart

66 Figure 3.9: First fatigue task mean MPF changes over time

67 Figure 3.10: Second fatigue task mean MPF changes over time

68 Figure 3.11: First Fatigue Task: Mean MPF change is plotted on the vertical axis and mean EMG change is plotted on the horizontal axis.

69 Figure 3.12: Second Fatigue Task: Mean MPF change is plotted on the vertical axis and mean EMG change is plotted on the horizontal axis.

70 Fatigue Recovery Force Increase Fatigue Force Decrease SA 2 3 2 9 UT 3 1 8 4 LT 3 0 8 5 Pec 1 2 6 7

Table 3.28: Summary of Task 2 JASA Chart

SA UT LT Pec N Subjects N Subjects N Subjects N Subjects Recovery 1 12 3 3,10,11 8 3,7,10,11,13 0 ,14,16,17 Force Increase 2 8,10 2 14,7 1 12 4 7,8,10,16 Fatigue 5 1,4,7,14,15 3 1,8,12 1 8 5 1,5,11,12,14 Force 7 3,5,9,11,13 7 4,5,9,13,15 5 1,4,5,9,15 6 3,4,9,13,15, Decrease ,16,17 ,16,17 17

Table 3.29: Task 1 JASA Results by Subject

71 SA UT LT Pec N Subjects N Subjects N Subjects N Subjects Recovery 2 5,14 3 11,13,14 2 7,11 1 13 Force 2 12,15 1 8 0 2 12,15 Increase Fatigue 2 7,9 8 2,4,7,10,12 9 1,2,8,10,12 6 2,4,7,10,11 ,15,16,17 13,14,15,16 ,16 Force 9 1,2,3,4,8 4 1,3,5,9 5 3,4,5,9,17 7 1,3,5,8,9 Decrease ,11,13,16,17 ,14,17

Table 3.30: Task 2 JASA Results by Subject

72 Chapter 4: DISCUSSION

4.1 Primary Kinematic Findings

Scapular Motion Direction of Change Effect Positive Increase in IR IR Negative Decrease in IR Positive Decrease in UR UR Negative Increase in UR Positive Anterior Change Tilt Negative Posterior Change

Table 4.1: Key to Direction of Change for Each Scapular Rotation

In order to validate the motions of this study, normal motion of the scapula as the arm is elevated is compared against the reported values of McClure et al.[42]. Table(4.2) shows the comparison in the scapular plane and table(4.3) shows the comparison in flexion. Some differences between the studies need to be addressed. First, McClure et al. had a larger range of humeral elevation measured in both tasks. The current study measured a 57◦ smaller range of humeral elevation in flexion and a 46◦ smaller range in scapular plane abduction. In an attempt to better compare the results of the current study to those of

McClure et al., range of motion for each of the scapular rotations was interpolated from the reported graphs[42]. Second, the current study used a weighted flexion task and the motion

73 was not of pure flexion. Subjects were asked to move as if to place the bottle on a high shelf and not simply raise their rigid arm.

Posterior Tilting UR IR Right 6◦ ** 34◦ -2◦ Current Study Left -1◦ 30◦ ** -2◦ ** Literature (Reported) 30◦ 50◦ -24◦ Literature (Approx. From Graphs) 12◦ 31◦ -9◦ ** denotes data calculated from the most prominent directional group

Table 4.2: Comparison of Kinematics to Literature: Scapular Plane

Posterior Tilting UR IR Right 10◦ 24◦ -10◦ Current Study Left 4◦ ** 29◦ -5◦ ** Literature (Reported) 31◦ 46◦ -26◦ Literature (Approx. From Graphs) 9◦ 26◦ -4◦ ** denotes data calculated from the most prominent directional group

Table 4.3: Comparison of Kinematics to Literature: Flexion

4.1.1 Hypothesis: 1.1

Arm dominance was shown to significantly effect all three of the scapular rotations in both the Lifting and Waving tasks. P-Values for each of the motions, separated by task, can be found in table (3.2). Considering these results it is reasonable to conclude that each scapula is moved in a different way and that either side show be examined separately. This supports Hypothesis 1.1. While this is not an entirely unexpected result, as the effect of

74 dominance is a commonly assumed, its verification is important. This is especially true considering the lack of significance seen between sides the EMG analysis.

4.1.2 Hypothesis: 2.1 Discussion of Variations Between Tasks

The results found in the frontal lifting task were more varied than those of the scapular plane abduction task. The most probable explanations for these differences are the stan- dardized height of the lift, the addition of weight, and duration from the fatigue tasks.

Lifting was always performed after scapular plane abduction and the subjects had resting time on the order minutes since being fatigued. As seen from the fourth time point Borg scores, subjects recovered quickly from fatigue. The extent of fatigue is not clear in this study.

The decision to separate subjects based on direction of movement divided the subjects into groups far smaller than that calculated for the power analysis of this study. By doing this the significance of the results was greatly affected and analysis was made more diffi- cult. However, based on the significance of the results obtained and the variations found in the literature for the direction of altered motion in patients with SIS[19, 37, 39, 41], this novel form of analysis may helpful in the analysis of a larger population. McCully et al.[43] reported a similar variation in the direction of altered scapular kinematic. They note that if magnitude of the directional change is measured statistically, all three rotations of the scapula show significant changes in the absence of the supraspinatus and infraspina- tus muscles. This suggests compensation strategies are acquired and therefore vary from subject to subject.

75 Scapular Plane Abduction Task:

After the fatigue conditions most subjects gained IR and lost UR on both sides. While the non-dominant side was more consistent in this trend the dominant tended to be more variable for these motions. Scapular tilting showed the dominant side to have more consis- tent trends of motion. The dominant scapula tended to posteriorly tilt as fatigue conditions progressed while the non-dominant scapula tended to anteriorly tilt. With more subjects, it is possible that a significant change in the posterior direction could be found across fatigue conditions as nearly half of the subjects tilted their non-dominant scapula posteriorly and the effect was near significant (p = 0.11). Our hypothesis that UR would diminish was supported by the majority of subjects however the hypothesis that fatigue would result in a decrease in IR opposed. Scapular motions of the dominant scapula that ran contrary to the majority were found to be significant in UR and IR. This suggests that subjects do not re- spond to fatigue in a uniform fashion. Also the anterior tilting of the non-dominant scapula supports the hypothesis that tilting would become less posterior and shows that different responses to fatigue are experienced by the dominant scapula. The gain of IR and loss of UR in this motion agree with the findings presented in the literature for subjects with

SIS[19, 37]. The results for the non-dominate arm fit the reported literature for all motions.

Frontal Lifting Task:

The results of the frontal lifting task were more varied than those of the scapular plane task. While the majority of scapular motion changes of the non-dominant scapula sup- ported the UR and Posterior tilting portions of the hypothesis by decreasing, the change in

IR of the non-dominant scapula increased as seen in the scapular plane task. The dominant scapula was less definitive in its results as the positive and negative groups tended to both

76 show significant changes and were of similar size. The reported statistics make the results more hazy. Originally, in IR, the negative group did not show significant results because subject # 13 gave an unexpected pattern of motion. Subject # 13 was moved into the posi- tive group because this motion fit a more positive changing pattern and the result was that both groups showed significant changes in scapular internal rotation. If the original results were reported the dominant scapula would only show significant increases in scapular IR, opposing the hypothesis that IR would decrease. This was not the case in UR, where the significant change as fatigue progressed was to increase UR. Though the negative group was smaller than the positive, its data was more consistent. Had more subjects participated, it is possible that significant UR decreases could be found significant, as the current data approaches p≤0.05 (p = 0.06). Scapular tilting on the dominant side showed significant changes in both the anterior and posterior directions therefor no conclusion about the hy- pothesis that posterior tilting would decrease. Again the data from this studies coincides well with that of the reported literature for SIS, especially for the non-dominant arm.

4.2 Primary Fatigue Findings

4.2.1 Hypothesis: 1.2

Differences in the normalized amplitudes of the EMG signal during the kinematic tasks showed significant changes across the dominant and non-dominant sides consistently for only the LT. Though insight into this muscle ended with this difference in the Lifting task, the waving task was able to show how the LT was activated over the range of humeral el- evation angles between 30◦ and 120◦. LT was activated significantly more in the highest

30◦ of humeral elevation angles than it was in the lower 30◦. This was an expected result, as this pattern of activation was described by Bragg and Forest in 1987, and it helped to

77 validate the method used to obtain this data. UT and SA also showed expected results for differences over humeral elevation in the wave task. As Bragg and Forest described, initial scapular UR is initiated by the UT and SA who are joined in the middle range of UR by LT.

As UR progresses LT activation increases with that of SA to stabilize the scapula in the end ranges of humeral elevations. While this profile of the UT is also demonstrated in the lift- ing task, the lack of significant differences found in the other two muscles detract from the claim that the lifting task elicited the same pattern of motion. Still, the significant increase in normalized EMG amplitude of UT only between the most extreme humeral elevation an- gle (110◦) and 30◦ to 70◦ demonstrates the increased utilization of UT in order to maintain a load overhead while fully extended. Another interesting finding was the large activation differences between the dominant and non-dominant Pec and LT. Considering both hands were clutching the bottle for the full duration of the task, this was a non-obvious result.

It suggests that, despite the load being shared, subjects were more likely to activate their dominant sided muscles. If this is true, it would give credence to the notion that compen- sation strategies for fatigue may also differ between sides. Unfortunately, the results of the dynamic EMG amplitude data provide no information describing the fatigue and no more conclusions can be drawn from the data at this time. A more conclusive set of results may have been obtained if more subjects were tested.

4.2.2 Hypothesis: 1.3

Again only the LT showed a significant difference between the dominant and non- dominant sides. The repeated occurrence of LT being statistically different may suggest that LT either has the most consistent activation pattern across subjects or that subjects uti- lize the non-dominant LT earlier in compensation or to a higher degree than the dominant

78 LT. The logic behind first suggestion would be that, due to the generally large amounts of variability in the EMG data which subsequently effected the calculated MPFs, the LT would have to consistently give non-overlapping values for each side. To give such con- sistent data, it can easily be inferred, that the LT has a more consistent activation pattern across the subjects than the other muscles examined. The other suggestion is based on the possibility that the difference in magnitude of MPF change is so large between sides that, even with highly varied data, the difference was significant. If this is the case, then subjects must utilize their LT differently between sides, thereby giving support to the hypothesis that the dominant and non-dominant scapulae are controlled differently. However, at this time a claim like this cannot be concluded as more information would be needed.

4.2.3 Hypothesis: 2.2

The amplitude of the EMG signal was not significantly different between the fatigue conditions in neither the static nor th dynamic EMG amplitude analysis. This may be due to a low number of subjects for this type of analysis. Originally, only the analysis of the dynamic tasks were planned. When the results from those proved to be inconclusive, expla- nations were explored. One of these explanations was that EMG signals are small and the sensors used are highly susceptible to motion artifact[12, 27], whether is be from the motion of the sensor itself or the skin over the underlying tissues[16]. For this reason the results derived from kinematic EMG amplitude analysis may have been masked and an analysis of the EMG amplitudes of the fatigue tasks was attempted. Subjects were in an isometric static hold throughout both fatigue tasks making meaningful results more likely to be found. This was not the case when this data was examined statistically, however, the qualitative analysis allowed for a description of the fatigue profile of the muscles. All meaningful qualitative

79 analysis presented was performed on the static EMG amplitude data. The qualitative re- sults of the EMG amplitude changes across time first fatigue task show that SA and Pec progressively rise in magnitude, seemingly together, as UT and LT decline. This suggests, based on commonly the common interpretation of this form of analysis[29, 27, 17, 12], that

SA and Pec are either increasing in force production or fatiguing. The interpretation for

UT and LT, whose amplitudes decline from the start of the task, is that they are lowering their force production. As the load being applied is not changing[59], either there is some form of compensation the subject is using or the SA and Pec are fatiguing. In the second fatigue all muscles show a progressively increasing percentage amplitude gain from the

first quartile across the duration of the task. This suggests that all of the muscles are either producing more force or fatiguing. As before the loading did not change. Any information drawn from these results assumes that the qualitative mean data is representative of the subjects.

4.2.4 Hypothesis: 2.3

In the first fatigue task serratus anterior was the only muscle to show significant changes in EMG MPF with time. Overall this decline was only 5.5% and did not qualify as fatigue based on the accepted standard (8%)[69, 18]. Separating the analysis by side shows an

8% decline in the non-dominant SA and a 3.2% decline in the dominant. Though side to side differences were not found to be significant, these values may provide so additional insight. No other muscles showed a significant change with time lending some credence to the hypothesis that SA EMG MPF would decline at a faster rate than the other muscles of the scapula examined. Also it can be noted the Pec showed significant changes in MPF with time (p = 0.036910* GGE) if time point 7 was not concidered. A look at figure (3.9) shows

80 that the final time point for Pec is greatly different than the others. While the clavicular portion of pectoralis major does not affect the scapula directly, it does affect the clavicle which plays a role in scapular positioning. The second bout of fatigue showed no significant changes in the MPF of any of the muscles examined. LT did approach significance when examined across sides and, when separated in to dominant and non-dominant analysis, the non-dominant LT also approached a significant change in MPF. This lack of significant results may have been due to the separation of the data by quartiles. This was done to standardize the data as subjects varied in the duration of their final fatigue task. By taking an average MPF over each quarter of the task duration the effects of fatigue may have been washed out. Wash out effects would also explain the lower percent MPF declines found than expected based on Borg scores and the task one trends.

4.3 JASA Findings

Qualitatively all the muscles examined experienced a declining trend in MPF from the baseline values in the second fatigue task. While it appears that the muscles either stagnate in MPF decline together (SA and Pec) or decline at a steady similar rate (UT and LT), the lack of time divisions must be taken into account. With only 3 points plotted, variations in the unique signals are masked and the shape of the plots should not be compared. Fatigue task one plots have more time divisions and are more representative of discrete time based trends. UT seems to have a steep initial slope that levels at mid-task. This could be inter- preted as fatigue however this was not shown to be a statistically significant decline. If UT were to be fatiguing the expectation is that the static EMG amplitude analysis would show an increasing level of activation. A similar issue could be raised with LT, who in static

EMG amplitude analysis shows large declines in amplitude but in MPF show a consistent

81 increase. A notable qualitative trend in figures (3.7) and (3.9) is the close proximity of the data for SA and Pec. The amplitude analysis would suggest that the first fatigue task had the same effect on SA as it did on Pec. This is confounded by the MPF data which shows the Pec to have MPF gains for the first half of the fatigue task and then declines. This type of issue is not new in EMG analysis and the method of JASA was developed to aid in interpreting results of this kind.

There are four general cases[12]: EMG amplitude increase and MPF increase (Muscle force increase) EMG amplitude increase and MPF decrease (Muscle Fatigue) EMG am- plitude decrease and MPF decrease (Muscle force decrease) EMG amplitude decrease and

MPF increase (Muscle recovery from fatigue). This will be the guiding principle in the analysis of the defining of the following EMG data.

MPF Increase MPF Decrease Increase Increase in Muscle Force Muscle Fatigue Present EMG Amplitude Decrease Recovery From Previous Fatigue Decrease in Muscle Force EMG Amplitude

Table 4.4: Key to JASA

The tables and figures of section (3.2.3) display the results of the JASA analysis. This method has the advantage of displaying an interpretation of each subject’s combined EMG data. The subject’s results were then compared to their grouped motion data in order to draw a correlation between scapular kinematics and muscle specific fatigue. In the first task, the majority of subjects experienced a fatigue of SA or decrease in force. This re- sponse was almost identical for the Pec, however due to the low number of subject, the

82 meaning of the Pec results can not be determined. UT had a majority of subjects expe- rience a decrease however a the other categories had an almost even distribution. As in the Pec, conclusions cannot be drawn from this information. The Lt showed the definitive results, with 8 subjects recovering from fatigue as the first fatigue task progressed. This was surprising and the best explanation for this result is that LT was not utilized in the first fatigue task and did not give meaningful results. The second fatigue task showed that the muscles of the shoulder analyzed in this all fatigued. This gives credence to this study’s incremental fatigue approach.

4.4 Limitations and Future Work

4.4.1 Subjects

Only 17 subjects were recruited into this study. While the number of subjects was suffi- cient to find significant kinematic results, there were too few for significant EMG analysis.

This is because EMG is inherently more variable. More subjects would have been recruited however timing issues presented a barrier to this goal. We had a relatively young subject pool with a mean age of 24 years. Considering all subjects reported no history of pain or pathology and were mostly college students, the results of this study express effect of fatigue on a low risk population for shoulder pathology.

4.4.2 Instrumentation EMG Limitations

Surface EMG analysis has obvious advantages that make it the best tool for our specific application. EMG is non-invasive, can be easily applied and removed, can be qualitatively assess in real time, can be specific to a single muscle, and it correlates well to biochemical and physiological changes in the muscles from fatigue[12].

83 Kinematic Limitations

Kinematic data recorded from an electromagnetic tracking system can be affected by distance from the transmitter and by surrounding metal. These effects were minimized by restricting the amount of space a subject had to travel to complete each task and by giving subjects a clearly defined set of boundaries. Because the sensors in the tracking system used in this study were affixed to the skin there is a possibility of movement artifact in the data. In a study by Karduna et al[31] the use of skin sensors was validated against bone pins, though at higher humeral elevations the sensors show a larger error. This study approached these high humeral elevations, where the errors grow larger, however the maximum elevation analyzed was 120◦ in scapular plane abduction and 110◦ in flexion.

Study Limitations

An angle of 30◦ was chosen as the inclination for the fatigue tasks of this study due to a combination of a pilot study of multiple fatigue positions and a previous attempt to base fatigue to SA in or lab[9, 69]. A second, unilateral, pilot study was done in our lab using the same fatigue task of the current study that showed kinematic alteration and increased

SA activation. A more thorough or directed validation of this fatigue task could be done to optimize its ability to bias fatigue to the SA.

The choice to use a unilateral plane during humeral elevation in the scapular plane for the guide may have influenced the data showing differences between the dominant and non-dominant sides. This plane was moved each time to an alignment with the subject’s scapular plane. Subjects were asked by the tester to maintain right hand contact with the plan for as much of the motion as possible. The tester instructed the subject to mirror this motion with the left hand arm. This resulted in interesting, while not directly analyzed

84 motions. Some subjects would stop elevation of the right arm at the superior border of the plane. It was typical in these subjects to continue elevation of the left arm through the full instructed range of elevation. Except in such cases, subjects maintained symmetry.

A second plane was not used due to issues of inconvenience and the imperative for quick testing. As noted in the post Borg assessment, made 4 minutes after the end of the final lifting task, subjects recovered quickly from the perceived effects of fatigue. This issue of symmetry was not an issue in the frontal lifting task as both hands were on the bottle being lifted.

Due to its lack of appearance in the literature, the sensor placement for the Pec Ma- jor was not obvious. A small pilot study was performed to determine the most effective placement of this sensor. This position should measure the EMG activity of the clavicular portion of the Pec major. Care was taken to avoid possible cross talk of this sensor with

EMG activity of the Pec minor, though it is a possible limitation due to its proximity. This effect was not fully explored. The clavicular portion of the Pec Major was chosen based on this muscles role in clavicular retraction. The motion of the clavicle, while not directly of concern to the present study, affects the motion of the scapula, as the clavicle attaches to the scapula via the AC joint. For the present study it was assumed that the normal motion of the clavicle would be maintained, however this was not verified. Our chosen fatigue task, based on visual inspection and result of the study, did activate the pectoralis major and fatigue it. For this reason the fatigue profile of pectoralis major was recorded.

An unforeseen limitation of our study that was the impact of the therapeutic bands on the hands of subjects. While an attempt to avoid this was made, with lifting gloves, the problem was not entirely remedied and resulted in subjects terminating the final fatigue task early. This resulted in a lowered mean fatigue time.

85 Another limitation that was unforeseen was, while rare, subjects feeling ill during the digitization process. This may have been due to an extended time standing in place. All subjects that this occurred in were approximately 6 ft and above. While subjects were in- formed that they could shift and move this event happened in a total of 3 subjects. Subjects were given a foam mat to stand on which gave them boundaries to move in and a more comfortable surface to stand on.

A limitation to the the accuracy of band weight given to subjects was availability, band lengths, tester strength, and reach of the subject. The weight of the bands given to subjects was aimed to account for 10% BW for each arm. This was chosen based on loads reported in previous studies[59]. In the case of unreported loading, estimated loading were obtained through linear interpolation of the rating data. While estimates made were close, the mean body weight achieved across fatigue tasks was 8.73% BW with a standard deviation of

1.63% BW, subjects did not all receive the same load to body weight ratio. This limit was further confounded by subjects who could not extend the bands. Most often this occurred in heavier and taller subjects. The author feels that % BW may not have been the opti- mum criteria for deciding band force. This was unforseen and, this authour feels, mostly unavoidable without curtailing the inculsion criteran and requiring subjects to perform ad- ditional task. By this time another method entirely would be preferable, therefore this was the best available option.

While it was attempted to move the subject from the fatigue task to the functional tasks as quickly as possible and then again to the fatigue task, the transition did take time on the order of minutes. Literature[2] has shown that muscles are able to recover from the perceivable effects of acute fatigue quickly. Data from the current study showed subjects to recover fatigue after 4 minutes, as reported by Borg CR10 scores, to nearly baseline levels.

86 This presents a source of error in the current study. EMG amplitudes were taken for the functional task and those are the values reported, however they proved inconclusive. An at- tempt to remedy this source of error was to analyze EMG amplitude data during the fatigue tasks. This was helpful in giving a more accurate depiction of fatigue. Unfortunately, it has been shown that the addition of pressure to EMG can alter the resulting amplitudes. For this reason the MVC values could not be confidently used and a percentage change from the initial time point was taken as the reference value.

4.5 Conclusions

Hypothesis 1: Alterations in scapular muscle fatigue will be inconsistent between the dominant and non-dominant arms of subjects. This will result in differing kinematic and fatigue profiles between the dominant and non-dominant arms of subjects

Side to side differences were consistently found for both kinematic tasks. This shows control strategies for the dominant and non-dominant side differ. This was not consistently supported by EMG data, however this result may be a product of low numbers of subjects.

Some muscles, LT and Pec, showed side to side differences which supports the claim that lack of subjects is the primary reason for inconclusive fatigue results.

Hypothesis 2: Serratus anterior fatigue will lead to a decrease in scapular upward rotation, posterior tilting, and scapular internal rotation

The fatigue task qualitatively shows that fatigue was biased to SA and Pec for the first task. The fatigue of Pec may have influenced the rotations of the scapula found, however,

Pec does not attach to the scapula and plays a secondary role in these rotations. SA fatigue was the primary goal of this task and the results suggest this was successful. The second fatigue task shows a more global fatigue of the musculature examined. This result was expected and shows that a task to failure, despite the musculature biased by the task, has

87 the potential to collaterally fatigue unintended musculature. Future studies could use this information to better study the progression of fatigue and examine compensation strategies in more detail. JASA plots and tables support these findings despite the limited subject pool.

The kinematic tasks showed altered kinematics in healthy subjects. These changes from the fatigue tasks are similar to those reported in SIS patients; increased internal rotation, de- creased upward rotation, and increased anterior tilting of the scapula. Non-dominant arms are more consistent in these changes. Dominant arms showed more variation in the altered kinematics of the scapula. Compensation strategies for fatigue may be better developed on the dominant arm, which would account for these varied results.

• Both kinematic tasks showed movement pattern changes similar to that seen in SIS

pathology. The results of this study similar to Ludwig and Cook who studies move-

ment alteration in construction workers with SIS.

• The non-dominant arm showed movement alterations closer to pathology more con-

sistently than the dominant arm.

• The dominant arm was more likely to have varied movements between subjects. This

suggests variations in movement is indicative of acquired compensation strategies,

suggesting they can be re-taught.

• While this fatigue protocol shows encouraging results, more analysis is needed to

validate it. A future study could be done with more subjects.

88 Appendix A: BI-LATERAL KINEMATIC & EMG TESTING PROTOCOL VERSION 1.3

Hints: Key FOB Flock of Birds SA Serratus Anterior UT Upper Trapezius LT Lower Trapezius ER External Rotators PEC Pectoralis Major W Wave Task L Lifting Task RHS Right Hand Side LHS Left Hand Side MM Motion Monitor PLA Posterior Lateral Angle

Lab Setup:

1. Tear out 5 pieces of carpet tape that are slightly longer than a FOB sensor.

2. Tear out 13 long pieces of skin tape and 8 longer pieces of skin tape.

3. Apply EMG sensor tape to each of the 8 EMG sensors and drape the sensors over the

sensor stand.

4. Drape the 5 FOB sensors over the sensor stand.

5. Lay out:

• Tape measure

89 • Therabands

• Force measure chart

• IRB Consent form

• Subject Data sheet

• Pillow & sheets for the table.

6. Turn on computer.

7. Load protocol file named: [OrenC]

8. Activate sensors

Subject Setup

1. Subject enters and sits down

2. Go over consent form and flow of the experiments

3. Let subject read over paperwork

4. Set up sensors with tape

5. Get organized for data collection

6. By this time subject should be done with paperwork

7. Collect consent document

8. Get subject: Age, Dominant Arm, Injury information . . .

90 9. Measure subject: Height, Weight, Arm Lengths . . .

*Note* Arm length is measured from web of the thumb to the AC joint. All mea-

surements will need to be done in BG units.

1 10. Select band weight and length based on ≈ .20BW (i.e. 10 BW for each arm)

11. Begin sensor setup by applying EMG sensors like so: EMG Sensor Key 1 Left Serratus 5 Right Serratus 2 Left Pectoralis Major 6 Right Upper Trapezius 3 Left Upper Trapezius 7 Right Pectoralis Major 4 Left Lower Trapezius 8 Right Lower Trapezius • Serratus Anterior sensor was placed on the lateral mid-line of the subject at the

6th rib anterior to Latissimus dorsi. (Fig.A.2)

• Lower Trapezius sensor was placed at the middle of the line between the root

of the spine of the scapula and T8. (Fig.A.1)

• Pectoralis Major sensor was placed 2cm below the medial convexity of the

clavicle.(Fig.A.1)

• Upper Trapezius sensor was placed at the midpoint of the line between the PLA

and C7.(Fig.A.1)

FOB Sensor Key 2 Left Scapula 4 Right Scapula 3 Left Arm 5 Right Arm • Scapular sensor is to be placed on the acromion

• Arm sensor is to be placed on the posterior of the arm at its midpoint.

12. Tape wires together with slack into RHS and LHS bundles

91 Figure A.1: EMG Sensor Placement of Upper and Lower Trapezius and of Pectoralis Major

92 Figure A.2: EMG Sensor Placement of Serratus Anterior

93 Figure A.3: EMG Sensor Placement of Ground Electrode

Setup of Subject Sensors

1. Go to setup subject sensors

2. Follow the on screen instructions using these pictures as a guide:

3. Tape Digitizer (Sensor 1) to the chest just below the Sternal notch.

Setup of Kinematic Capture Parameters in Motion Monitor:

1. Go to ’Edit Capture Parameters’ in MM

2. Un-click ’automatic termination’ & ’end with special trigger’

3. Change capture period to 120 sec.

94 Pre-Fatigue Tasks

1. Take resting EMG and Kinematics for 5 sec while the subject is standing still yet

unaware. Do not tell the subject! (Have a discussion with the subject to distract them

if need be)

2. Name of save file ’OCXXResting’

3. Do MVC tasks of each muscle we have sensors for.

4. Name of save file ’OCMXXVC’

5. Demo the Wave task and let the subject practice it. Be sure to highlight the need to

go through a full range of motion (30◦ to 120◦)

6. Demo the Lifting task and let the subject practice it.

7. Demo the Fatigue task and let the subject practice it.

8. Ask subject to preform Wave Task 5 times.

9. Name for save file ’OCXXKinPREW’

10. Ask subject to preform Lifting task 5 times.

11. Name for save file ’OCXXKinPREL’

12. Show subject the Borg sheet and describe the meaning of the numbers

13. Ask for a baseline Borg Score. Record this on the data sheet.

95 Setup of EMG Capture Parameters in Motion Monitor:

1. Go to ’Edit Capture Parameters’ in MM

2. Click ’automatic termination’ & ’end with special trigger’

3. Change capture period to 120 sec.

4. Change tigger delay to 10 sec.

5. Name for save file ’OCXXFat(First—Second)00’

6. Hit DONE when you are finished collecting.

7. Activity will not show up on screen

First Fatigue Task

This task is to be held for 1 minute. When the subject is ready to begin ask them the rest their arms on the table such that the arm is flush with the table-top. Move the stand as needed to achieve this.

Setup of Kinematic Capture Parameters in Motion Monitor:

1. Go to ’Edit Capture Parameters’ in MM

2. Un-click ’automatic termination’ & ’end with special trigger’

3. Change capture period to 120 sec.

96 Mid-Fatigue Tasks

1. Show subject the Borg sheet and describe the meaning of the numbers

2. Ask for a Borg Score. Record this on the data sheet.

3. Ask subject to preform Wave Task 5 times.

4. Name for save file ’OCXXKinMIDW’

5. Ask subject to preform Lifting task 5 times.

6. Name for save file ’OCXXKinMIDL’

Setup of EMG Capture Parameters in Motion Monitor:

1. Go to ’Edit Capture Parameters’ in MM

2. Click ’automatic termination’ & ’end with special trigger’

3. Change capture period to 120 sec.

4. Change tigger delay to 10 sec.

5. Name for save file ’OCXXFat(First—Second)00’

6. Hit DONE when you are finished collecting.

7. Activity will not show up on screen

97 Second Fatigue Task

When the subject is ready to begin ask them the rest their arms on the table such that

the arm is flush with the table-top. Move the stand as needed to achieve this.This task is to

be held until failure. Failure is when:

• Subject choses to quit.

• Subject can no longer reach their previous reach distance.

• Subject’s hand deviate from normal position.

Setup of Kinematic Capture Parameters in Motion Monitor:

1. Go to ’Edit Capture Parameters’ in MM

2. Un-click ’automatic termination’ & ’end with special trigger’

3. Change capture period to 120 sec.

Post-Fatigue Tasks

1. Show subject the Borg sheet and describe the meaning of the numbers

2. Ask for a Borg Score. Record this on the data sheet.

3. Ask subject to preform Wave Task 5 times.

4. Name for save file ’OCXXKinPOSTW’

5. Ask subject to preform Lifting task 5 times.

6. Name for save file ’OCXXKinPOSTL’

98 7. Record end time of data collection. After 4 min you will ask and recorded the sub-

ject’s final Borg score on the data sheet.

8. Show the subject their final task animation.

9. Offer subject to make a custom video to take home with them.

10. Label this animation ’OCXXCust’

11. THANK THE SUBJECT

99 Bibliography

[1] D.C. Ackland and M.G. Pandy. Lines of action and stabilizing potential of the shoul- der musculature. J Anat, 2009.

[2] D. G. Allen, G. D. Lamb, and H. Westerblad. fatigue: Cellular mech- anisms. Physiological Reviews, 88(1):287–332, 2008.

[3] S.D. Bagg and W.J. Forrest. A biomechanical analysis of scapular rotation during arm abduction in the scapular plane. Am J Phys Med Rehabil, 67(6):238–45, 1988.

[4] J.A. Barabas, T. Day, M.D. Bishop, S.Z. George, and T.A. Lentz. The relationship of pain intensity, physical impairment, and pain-related fear to function in patients with shoulder pathology. J Orthop Sports Phys Ther, 39:270–277, 2009.

[5] B.K. Barry and R.M. Enoka. The neurobiology of muscle fatigue: 15 years later. Integrative & Comparative Biology, 47(4):465 – 473, 2007.

[6] P.A. Borsa, K.G. Laudner, and E.L. Sauers. Mobility and stability adaptations in the shoulder of the overhead athlete: A theoretical and evidence-based perspective. Sports Medicine, 38(1):17–36, 2008.

[7] J.D. Borstad and P.M. Ludewig. Comparison of scapular kinematics between ele- vation and lowering of the arm in the scapular plane. Clinical Biomechanics, 17(9- 10):650 – 659, 2002.

[8] J.D. Borstad and P.M. Ludewig. The effect of long versus short pectoralis minor resting length on scapular kinematics in healthy individuals. J Orthop Sports Phys Ther, 35(4):227–38, 2005.

[9] J.D. Borstad, K. Szucs, and A. Navalgund. Scapula kinematic alterations following a modified push-up plus task. Human Movement Science, 28(6):738 – 751, 2009.

[10] J.N. Chopp, S.L. Fischer, and C.R. Dickerson. On the feasibility of obtaining mul- tiple muscular maximal voluntary excitation levels from test exertions: A shoulder example. Journal of Electromyography and Kinesiology, 20(5):896 – 902, 2010.

100 [11] R.S. Churchill and J.K. Ghorai. Total cost and operating room time comparison of rotator cuff repair techniques at low, intermediate, and high volume centers: Mini- open versus all-arthroscopic. Journal of Shoulder and Elbow Surgery, 19(5):716 – 721, 2010.

[12] M. Cifrek, V. Medved, S. Tonkovic’, and S. Ostojic’. Surface emg based muscle fatigue evaluation in biomechanics. Clinical Biomechanics, 24(4):327–340, 2009.

[13] A.M. Cools, E.E. Witvrouw, G.A. Declercq, L.A. Danneels, and D.C. Cambier. Scapular muscle recruitment patterns: Trapezius muscle latency with and without impingement symptoms. The American Journal of Sports Medicine, 31(4):542–549, 2003.

[14] A.M. Cools, E.E. Witvrouw, G.A. Declercq, G.G. Vanderstraeten, and D.C. Cam- bier. Evaluation of isokinetic force production and associated muscle activity in the scapular rotators during a protraction-retraction movement in overhead athletes with impingement symptoms. British Journal of Sports Medicine, 38(1):64–68, 2004.

[15] Ascension Technology Corporation. Installation and operation guide. Ascension Technology Corporation, Burlington, Vermont 05402 USA, May 2001.

[16] C.J. De-Luca. Surface electromyography: Detection and recording. DelSys Incorpo- rated, 2002.

[17] L.P. Diederichsen, J. Nrregaard, P. Dyhre-Poulsen, A. Winther, G. Tufekovic, T. Bandholm, L.R. Rasmussen, and M. Krogsgaard. The activity pattern of shoul- der muscles in subjects with and without subacromial impingement. Journal of Elec- tromyography and Kinesiology, 19(5):789 – 799, 2009.

[18] D.D. Ebaugh, P.W. McClure, and A.R. Karduna. Effects of shoulder muscle fatigue caused by repetitive overhead activities on scapulothoracic and glenohumeral kine- matics. Journal of Electromyography and Kinesiology, 16(3):224 – 235, 2006.

[19] K. Endo, T. Ikata, S. Katoh, and Y. Takeda. Radiographic assessment of scapular rotational tilt in chronic shoulder impingement syndrome. J Orthop Sci, 6(1):3–10, 2001.

[20] R.F. Escamilla and J.R. Andrews. Shoulder muscle recruitment patterns and related biomechanics during upper extremity sports. Sports Medicine, 39(7):569 – 590, 2009.

[21] K.A. Ginn and M.L. Cohen. Conservative treatment for shoulder pain: prognostic indicators of outcome. Arch Phys Med Rehabil, 85(8):1231–5, 2004.

[22] H. Graichen, H. Bonel, T. Stammberger, K-H. Englmeier, M. Reiser, and F. Eckstein. Subacromial space width changes during abduction and rotation -a 3-d mr imaging study. Surgical and Radiologic Anatomy, 21:59–64, 1999. 10.1007/BF01635055.

101 [23] H. Graichen, H. Bonel, T. Stammberger, M. Haubner, H. Rohrer, K.H. Englmeier, M. Reiser, and F. Eckstein. Three-dimensional analysis of the width of the subacro- mial space in healthy subjects and patients with impingement syndrome. AJR Am J Roentgenol, 172(4):1081–6, 1999.

[24] J.R. Grieve and C.R. Dickerson. Overhead work: identification of evidence-based exposure guidelines. Occupational Ergonomics, 8 (1):53–66, 2008.

[25] J.D. Harris, A. Pedroza, and G.L. Jones. Predictors of pain and function in patients with symptomatic, atraumatic full-thickness rotator cuff tears: A time-zero analysis of a prospective patient cohort enrolled in a structured physical therapy program. Am J Sports Med, 2011.

[26] L. Hashemi, B.S. Webbster, E.A. Clancy, and T.K. Courtney. Length of disability and cost of work related musculoskeletal disorders of the upper extremity. Journal of Occupational and Environmental Medicine, 40:261–269, 1998.

[27] G.M. Ha¨gg and M. Luttmann, A. Ja¨ger. Methodologies for evaluating electromyo- graphic field data in ergonomics. Journal of Electromyography and Kinesiology, 10(5):301 – 312, 2000.

[28] L.J. Hubert, H. Moffet, B.J. McFadyen, and Dionne C.E. Scapular behavior in shoulder impingement syndrome. Archives of Physical Medicine and Rehabilitation, 83(1):60 – 69, 2002.

[29] I. Jonkers, G. Nuyens, J. Seghers, M. Nuttin, and A. Spaepen. Muscular effort in multiple sclerosis patients during powered wheelchair manoeuvres. Clinical Biome- chanics, 19(9):929 – 938, 2004.

[30] A.R. Karduna, P.J. Kerner, and M.D. Lazarus. Contact forces in the subacromial space: Effects of scapular orientation. Journal of Shoulder and Elbow Surgery, 14(4):393 – 399, 2005.

[31] A.R. Karduna, P.W. McClure, L.A. Michener, and B. Sennett. Dynamic measure- ments of three-dimensional scapular kinematics: a validation study. J Biomech Eng, 123(2):184–90, 2001.

[32] B.W. Kibler and J. McMullen. Scapular dyskinesis and its relation to shoulder pain. Journal of the American Academy of Orthopaedic Surgeons, 11(2):142–151, March/April 2003.

[33] W.B. Kibler. The role of the scapula in athletic shoulder function. The American Journal of Sports Medicine, 26(2):325–337, 1998.

[34] W.B. Kibler and A. Sciascia. Scapular dyskinesis: current concepts. Br J Sports Med, 2009.

102 [35] P.K. Levangie and C.C. Norkin. Joint structure and function: a comprehensive anal- ysis. F.A. Davis, 2001.

[36] P.M. Ludewig and J.D. Borstad. Effects of a home exercise programme on shoulder pain and functional status in construction workers. Occup Environ Med, 60(11):841– 9, 2003.

[37] P.M. Ludewig and T.M. Cook. Alterations in shoulder kinematics and associated mus- cle activity in people with symptoms of shoulder impingement. PHYSICAL THER- APY, 80(3):276–291, MAR 2000.

[38] P.M. Ludewig, V. Phadke, J.P. Braman, D.R. Hassett, C.J. Cieminski, and R.F. LaPrade. Motion of the shoulder complex during multiplanar humeral elevation. The Journal of Bone and Joint Surgery, 91(2):378–389, 2009.

[39] A.C. Lukasiewicz, P. McClure, L. Michener, N. Pratt, and B. Sennett. Comparison of 3-dimensional scapular position and orientation between subjects with and without shoulder impingement. J Orthop Sports Phys Ther, 29(10):574–83; discussion 584–6, 1999.

[40] D.J. Magermans, E.K.J. Chadwick, H.E.J. Veeger, and F.C.T. van der Helm. Re- quirements for upper extremity motions during activities of daily living. Clinical Biomechanics, 20:591–9, 2005.

[41] P.W. McClure, L.A. Michener, and A.R. Karduna. Shoulder function and 3- dimensional scapular kinematics in people with and without shoulder impingement syndrome. Physical Therapy, 86(8):1075–1090, August 2006.

[42] P.W. McClure, L.A. Michener, B.J. Sennett, and A.R. Karduna. Direct 3-dimensional measurement of scapular kinematics during dynamic movements in vivo. Journal of Shoulder and Elbow Surgery, 10(3):269 – 277, 2001.

[43] S.P. McCully, D.N. Suprak, P. Kosek, and A.R. Karduna. Suprascapular nerve block disrupts the normal pattern of scapular kinematics. Clin Biomech (Bristol, Avon), 2006.

[44] K.J. McQuade, S.H. Wei, and G.L. Smidt. Effects of local muscle fatigue on three- dimensional scapulohumeral rhythm. Clinical Biomechanics, 10(3):144 – 148, 1995.

[45] L.A. Michener, P.W. McClure, and A.R. Karduna. Anatomical and biomechan- ical mechanisms of subacromial impingement syndrome. Clinical Biomechanics, 18(5):369 – 379, 2003.

[46] C. Milgrom, M. Schaffler, S. Gilbert, and M. van Holsbeeck. Rotator-cuff changes in asymptomatic adults. the effect of age, hand dominance and gender. J Bone Joint Surg Br, 77(2):296–8, 1995.

103 [47] K.L. Moore, A.F. Dalley, and A.M.R. Agur. Clinically oriented anatomy. Clinically Oriented Anatomy. Lippincott Williams & Wilkins, 2009.

[48] S.M. Moore, E.R. Bauer, and L.J. Steiner. Prevalence and cost of cumulative injuries over two decades of technological advances: A look at underground coal mining in the u.s. mining engineering. National lnstitute for Occupational Safety and Health, 60:46–60, 2008.

[49] B.F. Morrey and K.A. An. Biomechanics of the shoulder. In C.A. Rockwood and F.A. Matsen, editors, The Shoulder. Saunders, 1990.

[50] J.B. Myers, K.M. Guskiewicz, R.A. Schneider, and W.E. Prentice. Proprioception and neuromuscular control of the shoulder after muscle fatigue. J Athl Train, 34(4):362– 367, 1999.

[51] C.S. Neer 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am, 54(1):41–50, 1972.

[52] C.S. Neer 2nd. Impingement lesions. Clin Orthop, (173):70–7, 1983.

[53] G.P. Nicholson, D.A. Goodman, E.L. Flatow, and L.U. Bigliani. The acromion: mor- phologic condition and age-related changes. a study of 420 . J Shoulder Elbow Surg, 5(1):1–11, 1996.

[54] Poppen N.K. and Walker P.S. Normal and abnormal motion of the shoulder. The Journal of Bone and Joint Surgery, 58(2):195–201, 1976.

[55] W.E. Nordt 3rd, R.B. Garretson 3rd, and E. Plotkin. The measurement of subacromial contact pressure in patients with impingement syndrome. Arthroscopy, 15(2):121–5, 1999.

[56] Bureau of Labor Statistics. Number, incidence rate and median days away from work for non-fatal occupational injuries and illness involving days away from work by se- lected injury or illness characteristics and private industry, state government, and local government sectors. www.bls.gov/news.release/osh2.to3.htm, 2008.

[57] American Academy of Orthopaedic Surgeons. Research statistics on rotator cuff re- pairs, national ambulatory medical care survey, 1998-2004 , data obtained from: U.s. department of health and human services; centers for disease control and prevention; national center for health statistics.

[58] American Academy of Orthopaedic Surgeons. Research statistics on rotator cuff re- pairs, national inpatient sample, 1998-2004.

[59] P. Page, A. Labbe, and R. Topp. Clinical force production of thera-band elastic bands. J Orthop Sports Phys Ther, 2000.

104 [60] C.S. Roberts, J.N. Davila, S.G. Hushek, E.D. Tillett, and T.M. Corrigan. Magnetic resonance imaging analysis of the subacromial space in the impingement sign posi- tions. J Shoulder Elbow Surg, 11(6):595–9, 2002.

[61] C.A. Rockwood, F.A. Matsen, S.B. Lippitt, and M.A. Wirth. The Shoulder. Number v. 4 in Expert Consult. Saunders/Elsevier, 2009.

[62] N. Schibany, H. Zehetgruber, F. Kainberger, C. Wurnig, A. Ba-Ssalamah, A.M. Her- neth, T. Lang, D. Gruber, and M.J. Breitenseher. Rotator cuff tears in asymptomatic individuals: a clinical and ultrasonographic screening study. Eur J Radiol, 51(3):263– 8, 2004.

[63] W.A. Schmidt, H. Schmidt, B. Schicke, and E. Gromnica-Ihle. Standard refer- ence values for musculoskeletal ultrasonography. Annals of the Rheumatic Diseases, 63(8):988–994, 2004.

[64] A.L. Seitz, P.W. McClure, S. Finucane, N.D. Boardman III, and L.A. Michener. Mechanisms of rotator cuff tendinopathy: Intrinsic, extrinsic, or both? Clinical Biomechanics, 26(1):1 – 12, 2011.

[65] J.S. Sher, J.W. Uribe, A. Posada, B.J. Murphy, and M.B. Zlatkin. Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am, 77(1):10–5, 1995.

[66] B. Sivlerstein, E. Welp, N. Nelson, and J. Kalt. Claims incidence of work related disorders of the upper extremities: Washington state, 1987 through 1995. American Journal of Public Health, 88:1827–1833, 1998.

[67] L.J. Soslowsky, J.E. Carpenter, J.S. Bucchieri, and E.L. Flatow. Biomechanics of the rotator cuff. Orthop Clin North Am, 28(1):17–30, 1997.

[68] L.J. Soslowsky, S. Thomopoulos, A. Esmail, C.L. Flanagan, J.P. Iannotti, J.D. Williamson 3rd, and J.E. Carpenter. Rotator cuff tendinosis in an animal model: role of extrinsic and overuse factors. Ann Biomed Eng, 30(8):1057–63, 2002.

[69] K. Szucs, A. Navalgund, and J.D. Borstad. Scapular muscle activation and co- activation following a fatigue task. Medical & Biological Engineering & Computing, 47(5):487 – 495, 2009.

[70] K.A. Szucs. Capturing Three-Dimensional Clavicle Kinematics During Arm Eleva- tion: Describing the Contribution of Clavicle Motion and Associated Scapulothoracic Muscle Activation to Total Shoulder Complex Motion. PhD thesis, The Ohio State University, 2010.

[71] S. Tempelhof, S. Rupp, and R. Seil. Age-related prevalence of rotator cuff tears in asymptomatic shoulders. J Shoulder Elbow Surg, 8(4):296–9, 1999.

105 [72] Nian-Tuen Tsai, Phil W. McClure, and Andrew R. Karduna. Effects of muscle fatigue on 3-dimensional scapular kinematics. Archives of Physical Medicine and Rehabili- tation, 84(7):1000 – 1005, 2003.

[73] C.J van Andel, N. Wolterbeek, C.A.M Doorenbosch, D.H.E.J Veeger, and J. Har- laar. Complete 3d kinematics of upper extremity functional tasks. Gait & Posture, 27(1):120 – 127, 2008.

[74] D.J.S. Wadsworth and J.E. Bullock-Saxton. Recruitment patterns of the scapular rota- tor muscles in freestyle swimmers with subacromial impingement. Int J Sports Med, 18:618–624, 1997.

[75] J. Warner, L. Micheli, L. Arslanian, J. Kennedy, and R. Kennedy. Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impinge- ment syndrome. Clinical Orthopaedics and Related Research, 285:191–199, 1992.

[76] G.R. Williams Jr, C.A. Rockwood Jr, L.U. Bigliani, J.P. Iannotti, and W. Stanwood. Rotator cuff tears: why do we repair them? J Bone Joint Surg Am, 86-A(12):2764–76, 2004.

[77] G Wu, F.C.T van der Helm, H.E.J. Veeger, M Makhsous, P. Van Roy, C. Anglin, J Nagels, A.R. Karduna, K. McQuade, X Wang, F.W. Werner, and B. Buchholz. 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. Journal of Biomechanics, 38(5):981 – 992, 2005.

[78] A. Yamamoto, K. Takagishi, T. Kobayashi, H. Shitara, and T. Osawa. Factors in- volved in the presence of symptoms associated with rotator cuff tears: a compari- son of asymptomatic and symptomatic rotator cuff tears in the general population. J Shoulder Elbow Surg, 2011.

[79] A. Yamamoto, K. Takagishi, T. Osawa, T. Yanagawa, D. Nakajima, H. Shitara, and T. Kobayashi. Prevalence and risk factors of a rotator cuff tear in the general popula- tion. J Shoulder Elbow Surg, 2009.

[80] T. Yanagawa, C.J. Goodwin, K.B. Shelburne, J.E. Giphart, M.R. Torry, and M.G. Pandy. Contributions of the individual muscles of the shoulder to glenohumeral joint stability during abduction. J Biomech Eng, 130(2):021024, 2008.

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