The Effect of Normobaric Hypoxia on Power Output During Multiple Wingate Anaerobic Tests

A thesis submitted to the Kent State University College of Education, Health, and Human Services in partial fulfillment of the requirements for the degree of Master of Science

Corey M Nielsen

May 2017

Thesis written by

Corey Nielsen

B.S., West Virginia University, 2011

Approved by

______, Director, Master’s Thesis Committee J. Derek Kingsley, Ph.D.

______, Member, Master’s Thesis Committee Ellen Glickman, Ph.D.

______, Member, Master’s Thesis Committee John McDaniel, Ph.D.

Accepted by

______, Director, School of Health Sciences Lynne Rowan, Ph.D.

______, Interim Dean, College of Education, Health, Mark Kretovics, Ph.D. and Human Services

NIELSEN, COREY M., B.S., May 2017 EXERCISE PHYSIOLOGY

THE EFFECT OF NORMOBARIC HYPOXIA ON POWER OUTPUT DURING MULTIPLE WINGATE ANAEROBIC TESTS (62 pp.)

Director of Master’s Thesis: J. Derek Kingsley, Ph.D.

The purpose of this study was to determine the impact of altitude on power output and blood lactate, following repeated 30-s high-intensity exercise compared to sea level in anaerobically trained individuals. Seven resistance-trained men with a minimum of 6 months of resistance training volunteered and performed three 30-s Wingate Anaerobic

Tests (WATs) with 7.5% of bodyweight as the load on a cycle ergometer in both simulated altitude and sea level. Altitude was simulated using a normobaric hypoxic chamber with partial pressure of oxygen set at 13%. Performance and physiological outcomes were measured following each WAT. Three minutes of active recovery were performed with no load on the cycle ergometer following each WAT. Data were analyzed with a repeated measures ANOVA to examine the effects of power by condition. Paired t-tests were used for post-hoc testing. There were no significant interactions for any variable. There were also no main effects of condition. There were significant main effects of time for absolute and relative peak power such that they decreased over the 3 WATs. There were also main effects of time for average power and

average RPM such that both significantly dropped by 18% after the first WAT and by

12% after the second. Blood lactate levels were significantly augmented after each

WAT. These data suggest that performing repeated high-intensity exercise utilizing 3- minute rest periods in hypoxia has no impact on power output when compared to normoxia in resistance-trained men.

ACKNOWLEDGMENTS

I would like to thank my thesis director, Dr. J. Derek Kingsley, Ph.D. as well as everyone in the Department of Exercise Physiology for their continued efforts in helping me attain this distinguished degree. I would also like to thank my family for their continued support as I worked on, and completed this endeavor.

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TABLE OF CONTENTS

Page ACKNOWLEDGMENTS………………………………………………………………. iii

LIST OF FIGURES………...….……………………………………………………...… vi

LIST OF TABLES……...……….…………….…………………………………...…… vii

CHAPTER I. INTRODUCTION ………….……....………………………………………………… 1 Statement of Problem………….……………………………………………………… 3 Purpose Statement…………….………………………………………………...... 3 Research Hypothesis………….…….………………………...……………….……… 3 Operational Definitions……….………………………………………………………. 3 Assumptions………………….…………………………………….……………...... 4 Delimitations………………….…………………………………...... 5 Significance of Study………….………………………………...... 5

II. REVIEW OF RELATED LITERATURE….………………...………...... 6 Anaerobic Metabolism………………….……………………………….…………..... 6 Aerobic Metabolism……………….…………………….……………………………. 7 Hypoxia…………………………….…………….…………………………………… 8 Defined……………………….……………………...…………………………...... 8 Effect of Hypoxia on Oxygen Saturation……………….…...…….……..……….. 10 Effect of Hypoxia on Repeated Sprint Performance…….…………….………….. 11 Power Output……………………………………………..…………...…………...... 12 Defined………………………………………………….………….…………...... 12 Effect of Hypoxia on Power Output ……………………..……….………………. 12 Wingate Anaerobic Test……………………………………..…………...………….. 13 Defined…………………………………………………….………….…………... 13 Energy Contribution During Wingate Anaerobic Test………..…………….……….. 13

III. METHODOLOGY…………………………………………….……………..……… 15 Study Design……………….……………..…………….…………………………… 15 Participant Population....…………………………………………………………...... 15 Instruments/Apparatus..……….………………………………..……………………. 16 Procedures…………………...………………………………….…………………… 17 Outcome Measures…………………….………………..……….…………………... 18 Statistical Analysis…………………………………………………………………... 18

IV. RESULTS…………………………………………………………………...……….. 20 Demographics…………………………...... …………………………………..…….. 20

Outcome Measures……………………………………...………………………….... 20

V. DISCUSSION……………………………………………………………………...… 25 Limitations………………………………………………………..…………...……... 29

VI. RECOMMENDATIONS & FUTURE RESEARCH……………………...………… 31 Conclusion……………………………..………..………………….………………... 31

APPENDICES ...………………...……………………………………………………... 33 APPENDIX A. SAMPLE SIZE CALCULATION………………………….…….… 34 APPENDIX B. CHECKLIST OF INCLUSION/EXCLUSION CRITERIA………... 36 APPENDIX C. ESQ III SHORTENED QUESTIONNAIRE...……………………... 38 APPENDIX D. BORG RATING OF PERCEIVED EXERTION SCALE……..…... 40 APPENDIX E. PHYSICAL ACTIVITY READINESS QUESTIONNAIRE….…… 42 APPENDIX F. DATA COLLECTION SHEET…....………………….……………. 44 APPENDIX G. BASELINE DATA COLLECTION SHEET…...………………….. 46 APPENDIX H. LIPID RESEARCH QUESTIONNAIRE…..…………….………… 48

REFERENCES……………………………………………………………………….… 50

LIST OF FIGURES

Figure Page

1. Oxygen saturation measured at rest and following 3 WATs

in men (N=7) in hypoxia and normoxia ……………………..………………………. 22

2. The main effect of time on lactate measured at baseline and after 3 WATs

in men (N=7) in hypoxia and normoxia ………………....………...... 23

3. The main effect of time on average peak power measured 3 WATs

in men (N=7) in hypoxia and normoxia.………………….………………...... 23

LIST OF TABLES

Table Page

1. Demographic characteristics of participants (N=7)...…...……………………...... 20

2. Physiological variables during repeated Wingate Anaerobic Tests

in Hypoxia and Normoxia (N=7)….…...…………………...……..…………………. 22

3. Performance variables during repeated Wingate Anaerobic Tests

in Hypoxia and Normoxia (N=7)…………...…………………....……...... 24

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CHAPTER I

INTRODUCTION

High-altitude training is a set of parameters which can cause various physiological changes pre-, peri-, and post-exercise (Ainslie et al., 2007; Amann et al.,

2007; Dekerle et al., 2012). Depending on the training status and acclimatization of an individual, outcomes of aerobic and anaerobic training at an increased altitude can vary

(Billaut et al., 2013; Blegen et al., 2008; Dekerle et al., 2012; Fukuda et al., 2010; Hamlin et al., 2007; Pesta et al., 2011). Due to the decrease in atmospheric pressure as altitude increases, the amount of oxygen inspired in each breath is reduced, and has been known to cause a multitude of symptoms (Muza et al., 2004; Sampson et al., 1983; Beidleman et al., 2007) including fatigue and lethargy. Acute Mountain Sickness (AMS) is the onset of these symptoms due to altitude changes greater than 2400 m when all other normal vectors are ruled out (Sampson et al., 1983; Beidleman et al., 2007; Muza et al., 2004).

This has implications for performing exercise at high altitudes.

Ever since the decision was made by the International Olympic Committee to host the 1968 Summer Olympic Games in Mexico City, high-altitude training has been a point of great interest. It was during these Olympic Games that aerobic, endurance-based races saw an underwhelming performance and anaerobic, sprint-based races saw record- breaking results compared to previous Olympic Games (Olympic.org). It was speculated by the International Olympics Committee that it was the altitude that hindered the endurance athletes’ performances due to the oxygen dependent nature of those events, but that it was the decreased air resistance which caused the sprint-based athletes’

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performances to be so tremendous (Olympic.org). Endurance training effects at differing altitudes have since then been studied and adaptive protocols developed in order to better prepare these athletes for peak performance during events at high altitudes (Dufour et al.,

2006; Fukuda et al., 2010; Jensen et al., 1993; Millet et al., 2010; Ponsot et al., 2006;

Rusko et al., 2004; Wilber, 2001; Zoll et al., 2006).

Because there were no significant differences in sprint-based events due to decreased oxygen, not much effort was given to studying performance changes with anaerobic exercise at high altitude. A possible reason behind the lack of focused efforts on sprint-based, anaerobic exercise performance outcomes was the decision never to host an Olympic games at an elevation of such magnitude again, or perhaps the magnitude of increased performance outcomes from these events, which may have led to a false sense of training supremacy (Olympic.org). Despite this initial oversight, researchers have shown the deleterious effects of a decreased fraction of inspired oxygen (FiO2) on supramaximal exercise performed for periods lasting longer than ~60s (Calbet et al.,

2003; Weyand et al., 1999). Therefore, moderate hypoxia (FiO2 = ~0.15) has been shown to exacerbate the development of fatigue (Amann et al., 2007).

Current studies into the effects of hypoxia on repeated sprint-based performance have been inconsistent in their methods when performing repeated sprint-based exercises

(Dekerle et al., 2012; Ogura et al., 2006; Oguri et al., 2008). Few studies have been performed using the Wingate Anaerobic Test (WAT) as the testing protocol, and those which do vary the load on the flywheel, the duration, and the number of WATs performed in a single testing session (Dekerle et al., 2012). Despite the various testing

methods and protocols, there is a clear effect of condition of hypoxia on supramaximal performance (Dekerle et al., 2012; Ogura et al., 2006; Oguri et al., 2008; Morales-Alamo et al., 2012; Galvin et al., 2013).

Statement of Problem

High altitudes cause a variety of physiological changes. Athletes who live and compete in these hypoxic environments are affected by the surroundings in their anaerobic performance. This is problematic for those athletes trying to improve their power output and performance through multiple bouts of supramaximal exercise. There is currently very limited knowledge of the effects of hypoxia on anaerobic performance.

The WAT is a standard for safely measuring anaerobic power output and performance.

However, the effects of hypoxia on power output while performing multiple WATs are currently unknown.

Purpose Statement

The purpose of this study was to determine the degree of change in power output caused by performing multiple WATs in hypoxia when compared to normoxia.

Research Hypothesis

If hypoxia reduces blood oxygen which in turn limits peak and mean power, then performing multiple Wingate Anaerobic Tests in hypoxia should reduce peak/mean power and increase power drop.

Operational Definitions

Wingate Anaerobic Test (WAT): A clinical test, performed on a cycle ergometer, of

various factors related to anaerobic or supramaximal exercise.

Hypoxia: A physiological state of the body where there is decreased oxygen saturation in

the body’s soft tissue. Also a physical state of a defined area. For this study, we

will be using a normobaric hypoxic chamber similar to that used by Dekerle et al.

(2012) to simulate hypoxia similar to that of 10,000 ft.

Normoxia: A physiological state of the body where there is normal oxygen saturation in

the body’s soft tissue. Also a physical state of a defined area. For this study, we

will be using within 320m of sea-level as our basis for normoxia.

Acute Mountain Sickness (AMS): a subjective experience of feeling “ill” when exposed

to high altitudes of approximately 2400m or more, where other attributable causes of

illness are ruled out (Sampson et al., 1983).

Shortened Environmental Symptoms Questionnaire III (ESQ-III) – a list of 11 questions

used to measure the effects of low oxygen conditions on a person.

Assumptions

The following assumptions were made for the purpose of this study:

1. All participants will honestly report their health and exercise history.

2. All participants will refrain from using nutritional supplements, including caffeine

intake in excess of 100 mg/day for the duration of their testing cycle

3. All participants will refrain from intense exercising during the course of the study.

4. All participants will provide maximum effort when performing multiple WATs.

5. All participants will refrain from travelling to altitudes in excess of 500m above

sea level.

Delimitations

1. The participants will be limited to healthy physically active males aged 18-30

years.

2. The fraction of inspired oxygen (FiO2) will be set at 13%.

3. The load used during the WATs will be measured at 7.5% of participant’s initial

bodyweight.

4. All participants will reside in Northeast Ohio.

Significance of the Study

All individuals experience some effects of hypoxia when training in high altitude.

Currently there are no data focused on power output changes during multiple WATs in hypoxia. While many studies have been performed testing performance changes in aerobic exercise when performed in hypoxia, a minimal number of studies have looked at the performance changes in anaerobic exercise when performed in hypoxia. It is important to know these differences in order to better instruct active individuals who perform anaerobic exercise at high altitudes. The changes in performance could prove dangerous when an individual tries to perform anaerobic exercise with the same intensity and load at high altitude as they do closer to sea-level. If performance changes were determined to be present in hypoxia, athletes and other active individuals who perform anaerobic and supramaximal exercise would be able to decrease risk of injury, alter training protocols appropriately and achieve heightened levels of performance at altitude.

CHAPTER II

REVIEW OF RELATED LITERATURE

Anaerobic Metabolism

There are two forms of anaerobic metabolism, or metabolism which does not use oxygen to provide energy; the Phosphagen system and the Glycolytic system. The

Phosphagen system serves as the immediate source of energy for the regeneration of

ATP. Also known as the ATP-PCR system, the Phosphagen system has three different components. The first component is the ATP itself. ATP is broken down into ADP, inorganic phosphate and energy by ATPase.

퐴푇푃푎푠푒 퐴푇푃 → 퐴퐷푃 + 푃푖 + 푒푛푒푟푔푦

The next component is phosphocreatine (PCr) which is broken down by creatine kinase into creatine and inorganic phosphate, which then binds with ADP to form ATP.

푐푟푒푎푡푖푛푒 푘푖푛푎푠푒 푃퐶푟 + 퐴퐷푃 → 퐴푇푃 + 퐶푟

The third and final component is the formation of ATP through the combination of two

ADP molecules, which then forms ATP and adenosine monophosphate (AMP).

푎푑푒푛푦푙푎푡푒 푘푖푛푎푠푒 퐴퐷푃 + 퐴퐷푃 → 퐴푇푃 + 퐴푀푃

These components comprise the entirety of the ATP-PCr system. All three components and their respective enzymes are water soluble and reside in the cytosol portion of cells, outside of the mitochondria. This system is responsible for ATP resynthesis for the first

5-10 seconds of maximal and supramaximal exercise (Kang, 2008; Baker et al., 2010;

McArdle et al., 2006). If supramaximal/maximal exercise continues for longer than 10s,

ATP resynthesis must be continued by the Glycolytic system.

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The Glycolytic system, or glycolysis, replenishes ATP through the enzymatic breakdown of glucose and glycogen in the muscle and blood. Through the process of 11 enzymatic reactions glycogen is broken down into ATP and pyruvate. If oxygen is not present, then the pyruvate is then converted into lactic acid in the final enzyme reaction.

Anaerobic Glycolysis can be summarized with the following equation:

퐺푙푢푐표푠푒 → 2 퐴푇푃 + 2 퐿푎푐푡푎푡푒−1 + 2퐻+1

Because of the complex nature of glycolysis the production of ATP is significantly slower than that of the ATP-PCr system. Glycolysis can fuel supramaximal/maximal exercise from 30s to up to 2 minutes. If maximal effort is continued longer than that, then aerobic metabolism, i.e. beta oxidation, becomes the primary source of ATP resynthesis. (Kang, 2008; Baker et al., 2010; McArdle et al.,

2006).

Aerobic Metabolism

Aerobic metabolism, i.e. beta oxidation is the process of resynthesizing ATP through a three step process called oxidative phosphorylation. The first step in the process is the production of acetyl-CoA from the conversion of pyruvate, derived from the last steps of glycolysis.

The second step is the oxidation of acetyl-CoA in the citric acid cycle, or the

Krebs cycle. During this process, acetyl-CoA is combined with oxaloacetate to form

Citrate. What then occurs is a set of reactions which will regenerate oxaloacetate and form two molecules of CO2. The main purpose of the Krebs cycle is to remove hydrogen ions and the associated energy from the various intermediates which are involved in the

Krebs cycle using nicotinamide adenine dinucleotide (NAD) and Flavin adenine dinucleotide (FAD) as hydrogen transporters. The hydrogen removal during the Krebs cycle is imperative in that the hydrogen contains the majority of the potential energy stored in food molecule. When NAD and FAD combine with hydrogen ions they form

NADH and FADH, respectively. Both of these molecules will then proceed to the final step of oxidative phosphorylation, the electron transport chain.

Within the electron transport chain NADH and FADH use the energy stored in the hydrogen bonds to combine ADP and inorganic phosphate to form ATP. Although oxygen is not used during the Krebs cycle, it is the final hydrogen acceptor at the end of the electron transport chain. The entire oxidative system can be summarized with the following equation, using a glucose molecule as an example (Kang, 2008; Baker et al.,

2010; McArdle et al., 2006):

퐶6퐻12푂6 + 푂2 → 32 퐴푇푃 + 6퐶푂2 + 6퐻2푂

Hypoxia

Defined

Hypoxia is a physiologic state of deoxygenation in the body’s tissues caused by either environmental factors, such as increased elevation, or intrinsic factors, such as

COPD or congenital defects (Mayoclinic.org; Ainslie et al., 2007; Muza et al., 2004;

Amann et alk., 2007; Baker-Fulco et al., 2006; Billaut et al., 2013; Dekerle et al., 2012;

Dufour et al., 2006; Fukuda et al., 2010; Galvin et al., 2013; Hamlin et al., 2007;

Hoppeler et al., 2001; Ogura et al., 2006; Oguri et al., 2008; Millet et al., 2010; Pesta et al., 2011; Ponsot et al., 2006; Rupp et al., 2013). Chronic Obstructive Pulmonary

Disorder, or COPD, is a category of chronic inflammatory lung diseases which cause obstructed airflow in the lungs. Emphysema, chronic bronchitis and asthma are all forms of COPD (Mayoclinic.org). Hypoxia is also defined as the decreased availability of oxygen in the ambient air and/or the fraction of inspired oxygen (FiO2) (Muza et al.,

2004). Definitions of hypoxia vary depending on their severity and range from moderate hypoxia (FiO2 = ~0.15) to severe hypoxia (FiO2 = ~0.10) (Amann et al., 2007; Billaut et al., 2013; Ogura et al., 2006).

There are a variety of central and peripheral physiological effects in response to moderate to severe hypoxia; some effects include but are not limited to increased cardiac output, elevated heart rate, decreased cerebral oxygenation, increased cerebral blood flow velocity, decreased cerebrovascular autoregulation, increased muscle sympathetic discharge, increased skeletal blood flow, decreased peripheral blood oxygenation (SpO2), decreased skeletal muscle oxygenation, and reduced muscle force-generating capacity

(Beidleman et al., 2007; Fukuda et al., 2010; Hoppeler et al., 2001; Muza et al., Sampson et al., 1983). Some individuals may have an extreme adverse reaction to being exposed to this level of decrease in FiO2, which can be categorized as Acute Mountain Sickness

(AMS). AMS is characterized by many symptoms including but not limited to headache, insomnia, anorexia, nausea, dizziness, and fatigue without abnormal neurological findings (Beidleman et al., 2007; Fukuda et al., 2010; Hoppeler et al., 2001; Mairer et al.,

2013Muza et al., Sampson et al., 1983). The severity of AMS can be assessed using an

11 question test administered either verbally or electronically. This test, known as the shortened ESQ-III, is a validated substitution for the standard 67 question pencil-and-

paper ESQ-III. Factors which can exacerbate the incidence and severity of AMS include initial altitude, rate of ascent, altitude reached, duration of exposure, degree of hypoxemia, level of physical exertion performed, inherent individual predisposition, and previous altitude acclimatization (Beidleman et al., 2007).

Effect of Hypoxia on Oxygen Saturation

As previously stated, hypoxia decreases oxygen saturation in the bloodstream and in tissues across the body. The main tissues affected by hypoxia are the brain and the muscles. During the first hour of hypoxic exposure cerebral and arterial oxygenation is significantly decreased (Ainslie et al., 2007; Subudhi et al., 2007). It takes ~10 minutes for the deoxygenation of SpO2 to stabilize, while cerebral deoxygenation does not plateau until ~20 minutes to a maximum of 40 minutes (Ainslie et al., 2007; Hamlin et al., 2007; Rupp et al., 2013; Subudhi et al., 2007). Cerebral [HHb] does not plateau until

~30 – 40 minutes of exposure (Rupp et al., 2013). When examined with near-infrared spectroscopy (NIRS), cerebral [HHb] are more than 10 times the concentrations in hypoxia as compared to normoxia. In the muscles, the concentration of deoxygenated hemoglobin ([HHb]) is significantly increased after ~10 minutes of hypoxic exposure and remains steady for the duration of the first hour. Muscle [HHb] are more than two times the concentrations in hypoxia as compared to normoxia (Subudhi et al., 2007).

Prolonged hypoxic exposure (>60 min) can start to elicit varied skeletal muscle deoxygenation hemodynamics (Rupp et al., 2013). These variables are tissue-specific and inter-individual in nature, because of which this study has limited itself to <60 min hypoxic exposure. Due to the time delayed nature of the effects of hypoxic exposure and

deoxygenation, Rupp et al., (2013) and Subudhi et al., (2007) both recommend a wash-in period of hypoxic exposure of ~30 minutes, hence the 30 minute quiet rest period of subjects upon entrance to the hypoxic chamber.

Effect of Hypoxia on Repeated Sprint Performance

Due to hypoxia’s deoxygenating effect during rest, one can assume that the effects would be magnified during exercise, especially supramaximal exercise and

Repeated Sprint Performance (RSP). Subudhi et al., (2007) demonstrated that even incremental exercise up to maximal effort can cause a larger degree of cerebral deoxygenation when compared with normoxia. Many of the same effects of hypoxia on oxygen saturation are present during RSPs. Initial performance is not affected, due mostly to the PCr storage being at capacity during rest (Baker et al., 2010; Baker-Fulco et al., 2006; Billaut et al., 2013; Galvin et al., 2013; Ogura et al., 2006; Smith et al., 1991;

Vianna et al., 2011). It is during the subsequent trials and sprints that increased effects and decreased performances are elicited (Amann et al., 2007; Billaut et al., Dekerle et al.,

2012; Galvin et al., 2013; Gastin, 2001; Kurobe et al., 2014; Morales-Alamo et al., 2012;

Ogura et al., 2006; Oguri et al., 2008; Ratamess et al., 2007). Baker-Fulco et al. (2006) tested repeated maximum voluntary contraction (MVC) in normoxia and then hypoxia and found that there was no difference between the two starting MVCs, but the volitional cessation of the trials was much more abrupt in hypoxia than normoxia which leads to the conclusion that hypoxia and the deoxygenation it induces may lead to decreased repeated sprint ability.

Power Output

Defined

Power output is measured in many different ways but the unit of measurement is always Watts (W). Many different measures are assessed when testing power output.

The primary measurement is the peak power output in W. Peak power is defined as the highest power produced in a 5 s segment of a WAT (Smith et al., 1991).

Effect of Hypoxia on Power Output

Peak power output is one of the many power related variables affected by hypoxia which include but are not limited to peak power output, average power output and power output relative to mass. Dekerle et al. (2012) found that power output and peak power are both significantly affected by hypoxia (p<0.001 and p<0.05, respectively). A lowering of FiO2 can change the exercise tolerance levels for supramaximal exercise by increasing the reliance on anaerobic metabolic pathways, which has been shown to exacerbate peripheral levels of fatigue (Dekerle et al., 2012; Billaut et al., 2013).

While power output was shown to not be affected initially (Baker-Fulco et al.,

2006; Jensen et al., 2007; Levine et al., 2002; Richardson et al., 2014), Dekerle et al.

(2012) were also able to show a decrease in power-based variables with repeated WATs.

While the WATs varied in duration, the results suggested that there is an interaction between hypoxia and multiple WATs on power output. A possible explanation for this effect would be the decreased aerobic function caused by hypoxia due to the decreased levels of available oxygen. This in turn limits the aerobic energy reconstitution capacity and limits the PCr resynthesis necessary to provide energy for the first third of the WAT.

Because one single 6 s maximal cycle sprint can decrease PCr levels to ~35-55% resting levels (Galvin et al., 2013) and only recovers to ~69% after 30 s, as well as the normal decrease in anaerobic glycolytic contribution to ATP generation (Galvin et al., 2013), it is not a far reach to hypothesize an exacerbated decrease in power output due to hypoxia when compared to normoxia.

Wingate Anaerobic Test

Defined

The Wingate Anaerobic Test (WAT) is a valid and reliable tool commonly used to assess anaerobic power and peak power output (Lovell et al., 2013; Ogura et al., 2006;

Oguri et al., 2008; Smith et al., 1991). Although there are many different ways to perform the WAT, the form being used for this study is one in which the testing participant pedals at maximal speed for 30 s with 7.5% bodyweight used as resistance on the flywheel of a cycle ergometer (Oguri et al., 2008; Smith et al., 1991). Once the participant reaches a speed above 110 RPM the resistance is added to the flywheel.

Following the 30s supramaximal effort, a period of ~3 minutes of active recovery pedaling using no resistance on the flywheel will be performed (de Salles et al., 2009;

Ratamess et al., 2007).

Energy Contribution During Wingate Anaerobic Test

During a 30 s WAT, energy contribution is divided between the 3 energy systems.

In Smith et al. (1991), total power production peaked at 819(16) W and decreased to

450(10) W over the 30 s test. ATP-PCr contribution was assumed to have a rapid decline in energy contribution from its assumed peak at 2.5 s to the 10 s mark. Twenty-eight

percent of total energy expenditure over the 30 s test was produced through ATP-PCr system. Glycolysis contribution was assumed to increase steadily until the 10-15 s time interval. Fifty-six percent of total energy expenditure over the 30 s test was produced through glycolysis. Aerobic contribution was assumed to gradually increase throughout the test until peaking during the last 5 s time interval. Sixteen percent of total energy expenditure over the 30 s test was produced through aerobic metabolism.

As demonstrated in Smith et al. (1991), aerobic metabolism plays a very minute role in energy contribution to power output during a 30 s WAT. With the results from this study, we can assume that anaerobic metabolism will be the main source of ATP production during our 30-s multiple WATs. Because of this, we can assume any changes in power output during this study will be caused due to an effect on the anaerobic metabolic pathways and their precursors.

CHAPTER III

METHODOLOGY

Study Design

The research design was a single-blind counterbalanced control study. The investigator was aware of the participants’ group allocation and treatment prior to baseline measurements and throughout the study. The participants were blinded to if they were performing the hypoxic protocol first or the normoxic protocol first. The independent variables were the group (normoxia, hypoxia) and the WAT bout (WAT1,

WAT2, WAT3). The dependent variables were absolute peak power, relative peak power, average power, absolute power drop, relative power drop, peak RPM, average

RPM, power decline, SaO2, and ratings of perceived exertion (RPE). All tests and measurements took place in a controlled laboratory setting.

Participant Population

Twenty-five healthy participants aged 18-30 years were to be recruited from Kent

State University and the surrounding area. Based on previous work by Dekerle et al.

(2012), an effect size of 1.07 was calculated when measuring average power output.

Based on this for a power of 0.80, 12 participants would be the necessary minimum number to show significance. Twenty-five participants would have allowed for voluntary participant withdrawal from the study while maintaining statistical power. Participants were randomly allocated to perform one of two first: hypoxia, or normoxia.

Participants were included if they were free from any cardiopulmonary diseases or disorders. Participants must have had a history of performing regular resistance and

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cardiovascular exercise at least 3-4 times per week for the past 6 months as determined by the Lipid Research Questionnaire (Appendix F). Participants were excluded if they had any known contraindication to supramaximal exercise and hypoxia including but not limited to fever, pacemaker or other implanted devices, metabolic disorders, current taking of anticoagulant/anti-inflammatory medications or other medications which alter heart rate and/or blood pressure, any and all supplements including caffeine intake above

100mg per day, being diagnosed with cancer, history of smoking within the last 6 months, pulmonary disease , and uncontrolled hypertension (systolic >140 mmHg, diastolic >90 mmHg).

Participants were asked to refrain from any strenuous exercise involving the lower extremities for the duration of the study. Study methods underwent review and approval from the Institutional Review Board at Kent State University. Prior to participating in the study all participants read and signed a voluntary consent form.

Instruments/Apparatus

Instruments used for this study included a PAR-Q, bodyweight scale, Monark cycle ergometer, pulse oximeter, Borg RPE scale, Lipid Research Questionnaire and a

Normobaric hypoxic chamber. Fitness level and exercise history were assessed through use of the Lipid Research Questionnaire. The Monark cycle ergometer was situated in the middle of the hypoxic chamber. SpO2 was assessed by means of the pulse oximeter.

Fatigue and pain were verbally assessed through use of the Borg RPE scale. Hypoxic conditions were assessed and monitored by auto-regulated units. Power output variables were assessed by Monark Anaerobic Test Software.

Procedures

Following an orientation and signing of the informed consent, on the first day of testing at the Kent State Exercise Physiology Laboratory, the participants had their height and weight measured and their age recorded, as well as completing the Lipids Research

Questionnaire and the PAR-Q. After these data had been collected, the participants underwent one of two protocols; either hypoxia or normoxia. This was chosen at random and only the participant was blinded to which protocol was being performed. They performed a warmup, in the chamber, on the cycle ergometer for a total of 5 minutes at an easy pace with 1 kg load on the flywheel . After this warmup, the participant completed 3 consecutive Wingate tests, separated by 3 minutes of pedaling at an easy pace with no load on the flywheel. No encouragement was given to any participants during these tests; the only prompts given by the investigator were “Go”, signaling the start of the next WAT, and “Rest”, signaling the start of active recovery. The active rest periods of 3 minutes were completed on the cycle ergometer to allow for improved recovery. Each Wingate test required the participant to pedal as fast as possible on the cycle ergometer. When maximal speed had been met (≥110 rpm), 7.5% of the participant’s bodyweight was added to the flywheel of the cycle ergometer. The participant then pedaled for 30 seconds. The investigator used the Borg RPE scale to measure fatigue and pain, as well as monitoring SaO2. Should the participant’s SaO2 drop below 72%, previously established as the laboratory standard, they would have been removed from the chamber immediately and seated in a chair until SaO2 returns to a normal level of >97%. AMS symptoms were checked after each bout by asking if the

participant was experiencing a headache. Had the participant answered in the affirmative to the question, they would have been removed from the chamber immediately and seated in a chair until they no longer exhibited symptoms. Had a medical emergency arisen, 911 was to be called and emergency medical personnel would have been responsible for the well-being of the participant following their removal from the Kent State University

Exercise Physiology Laboratory. These test days took 45 minutes. One week after the initial testing was completed the other protocol was performed and was identical. These test days also took 45 minutes. The total time commitment was 2 hours over 2-3 test days.

Outcome Measures

The Borg RPE scale was administered verbally. Participants were asked to give a corresponding number indicating their greatest amount of fatigue and pain following completion of each WAT. The pulse oximeter was used to assess SaO2 following completion of each WAT. The pulse oximeter was placed on their LEFT index finger.

Monark Anaerobic Test Software was used to assess all power output variables. The software was loaded onto a laptop and a cord used to connect the Monark cycle ergometer and the laptop where data are recorded continuously.

Statistical Analysis

The statistical analysis for this study included a mixed model ANOVA for group and time. To analyze power output, we used a 2x3 group (hypoxia, normoxia) by time

(Wingate Bout 1, Bout 2, Bout 3) mixed-model ANOVA. Post-hoc testing was done using paired t-tests if the ANOVA was deemed significant. Post-hoc corrections were

applied using the Benjamini Hochberg Correction if necessary. For all analyses significance was set at less than 0.05.

CHAPTER IV

RESULTS

Demographics

Demographic data for the participants are presented in Table 1.

Table 1.

Demographic characteristics of participants (N=7)

Hypoxia Normoxia (n = 6) (n = 7) Mean SD Mean SD Height (cm) 181.2 3.8 180.3 4.1 Weight (Kg) 81.8 5.3 81.1 5.2 BMI (Kg/m2) 24.9 1.8 24.9 1.7 Age (years) 23 3 23 2 Data are displayed as mean ± SD

Outcome Measures

There were no significant interactions for any variable. SaO2 was not different between the groups at any time point but did significantly decrease after each WAT for each condition (Figure 1). Post hoc tests showed that regardless of group, RPE significantly increased (p<0.0001) by the end of WAT3 when compared to baseline

(Table 2). Blood lactate levels were significantly (p=0.0001) augmented after each WAT

(WAT1: 7.2±2.1 mmol; WAT2: 12.0±3.2 mmol; WAT3: 14.0±2.9 mmol) (Figure 2).

There were significant main effects of time for absolute (WAT1: 876±1336Watts (W);

WAT2: 733±127W; WAT3: 635±117W, p=0.0001) and relative (WAT1: 10.8±1.9W;

WAT2: 9.0±1.8W; WAT 3: 7.8±1.5W, p=0.001) peak power such that they decreased over the 3 WATs (Table 3 and Figure 3). There were also main effects of time for

20 21

average power and average RPM such that they both significantly (p=0.0001) dropped by

18% after the first WAT and by 12% after the second. Post hoc tests showed that a main effect of time was present for both absolute (WAT1: 560.3±157.0W; WAT2:

463.7±154.1W; WAT3: 418.9±152.9W) and relative (WAT1: 6.9±2.0W; WAT2:

5.8±2.0W; WAT3: 5.2±1.9W) power drop (p<0.01) There was a significant (p=0.004) decrease in peak RPM over time. Power decline was found to significantly (p=0.028) decrease over time.

† † †

† †

Figure 1. Oxygen saturation measured at rest and following 3 WATs in men (N=7) in hypoxia and normoxia. †p<0.05, significantly different from rest Data are mean ± SD

Table 2.

Physiological variables during repeated Wingate Anaerobic Tests in Hypoxia and Normoxia (N=7).

Hypoxia Normoxia (n = 6) (n = 7) RPE Baseline 6 0 6 0 WAT 1 15.3 1.6 14.1 0.9 WAT 2 17.3 1.6 16.4 1.5 WAT 3 18.5 1.9 18 1.9 WAT, Wingate Anaerobic Test

20 † † Hypoxia † † Normoxia 15 † † 10

Lacate (mmol) Lacate 5

0 Baseline WAT1 WAT2 WAT3

Figure 2. The main effect of time on lactate measured at baseline and after 3 WATs in men (N=7) in hypoxia and normoxia. †p<0.05, significantly different from rest Data are mean ± SD

* * *

Figure 3. The main effect of time on average peak power measured 3 WATs in men (N=7) in hypoxia and normoxia.*p<0.05, significantly different from WAT1 Data are mean ± SD

Table 3.

Performance variables during repeated Wingate Anaerobic Tests in Hypoxia and Normoxia (N=7).

Hypoxia Normoxia (n = 6) (n = 7) Mean SD Mean SD Absolute Peak Power, W 856.7 151.1 891.2 131.8 WAT 1 WAT 2 732.1* 95.5 732.9 156.7 WAT 3 672.3* 119.5 602.2 113.5 Relative Peak Power, W/kg 10.5 2.1 11.1 1.9 WAT 1 WAT 2 8.9 1.3 9.1 2.2 WAT 3 8.3 1.5 7.5 0.6 Average Power, W 569.3 51.9 601.1 40.9 WAT 1 WAT 2 475.7 34.9 480.4 43.5 WAT 3 429.4 35.2 411.9 41.1 Average RPM WAT 1 93.9 8.4 101.3 7.3 WAT 2 78.6 3.3 81.5 7.1 WAT 3 69.6 3.2 69.8 6.7 Absolute Power Drop, W/s 560.6 178.3 560 151.1 WAT 1 WAT 2 466.2 130.9 461.5 182.3 WAT 3 474.9 169.9 370.8 129.7 Relative Power Drop, W/s/kg 6.9 2.4 6.9 1.9 WAT 1 WAT 2 5.7 1.7 5.8 2.4 WAT 3 5.8 2.1 4.6 1.7 Peak RPM 132.7 18.3 140.2 15.7 WAT 1 WAT 2 121.8 7.8 127.9 10.7 WAT 3 123.7 7.1 117.9 8.5 Power Decline, % 469.7 144.5 493.2 148.6 WAT 1 WAT 2 427.2 108.9 424.3 140.5 WAT 3 406.9 178.9 312.4 141.1 Data are displayed as mean ± SD

CHAPTER V

DISCUSSION

The aim of the present study was to determine the effects of hypoxia on power output and other performance measures in hypoxia compared to normoxia following multiple WATs. To our knowledge, this was the first study to keep WAT conditions of both duration and resistance consistent throughout each successive WAT, and to compare the results in hypoxia to normoxia. The results of this study showed no significant differences between hypoxia and normoxia for any variables after a period of high- intensity exercise.

There was no significant difference for SaO2 at any point between groups. This differs from the findings of Dekerle et al. (2012) who found a significant difference when comparing pre- and post-exercise SaO2 levels between groups (Resting % difference: -

6.4 ± 4.0% End-exercise % difference: 12.4 ± 7.0%). As previously stated, hypoxia decreases oxygen saturation in the bloodstream and in tissues across the body. The main tissues affected by hypoxia are the brain and the muscles. During the first hour of hypoxic exposure, cerebral and arterial oxygenation is significantly decreased (Ainslie et al., 2007; Subudhi et al., 2007). It takes ~10 minutes for the deoxygenation of SaO2 to stabilize, while cerebral deoxygenation does not plateau until ~20 minutes to a maximum of 40 minutes (Ainslie et al., 2007; Hamlin et al., 2007; Rupp et al., 2013; Subudhi et al.,

2007). The initial ‘wash-in’ period of 1 hour in hypoxia of the current study should have been long enough for SaO2 to stabilize at lower levels and could be the cause for the non- significance. Seeing as the resting levels of SaO2 were not statistically significantly

25 26

different (87.2 % at hypoxia, 98 % at normoxia) it is not surprising that the identical exercise in each condition did not change that relation, despite the main effect of time on

SaO2.

In the present study, increases in blood lactate levels were noted across time.

However, the minimal level of rest for anaerobic exercise of 3 minutes in between bouts

(Willardson et al., 2008; Ratamess et al., 2007; de Salles et al., 2009) should have been enough time for the lactate levels to sufficiently metabolize. It is plausible that the short rest breaks in the current study reduced the ability to clear lactate from the skeletal muscle. It is also feasible that the hypoxic condition limited the clearance of lactate due to the decreased availability of inspired oxygen. Therefore, these data may have direct implications on the need to evaluate work to rest ratios in order to maximize performance. Examination of acute resistance exercise demonstrates that a 2-minute rest period in between sets of moderate- to high-intensity is sufficient to process the metabolites from exercise (Willardson et al. 2008). In addition, work by Ratamess et al.

(2007) observed different rest intervals in between sets of moderate- to high-intensity.

They found that 30 s and 1-minute rest intervals showed a reduction in resistance and volume; 2-minute rest intervals allowed for performance to be maintained during the first two sets, but was significantly reduced for the 3-5 sets. Furthermore, 3-minute rest intervals allowed for maintained performance during the first three sets but decreased during sets 4 and 5. Lastly 5-minute rest intervals allowed for maintained performance up to the last set. Collectively, these data demonstrate that a work to rest ratio of at least 1:6,

which was used in the present study, should be sufficient to allow for a reduction in lactate in the normoxia condition. However, this was not the case.

The results of the present study demonstrate an increase in RPE irrespective of group when compared to baseline measures. This is not surprising as the WAT is a maximal effort test and it was performed three times for each testing protocol. No other studies have analyzed the difference in RPE following multiple WATs in hypoxia when compared to normoxia. However, previous studies using repeated bouts of high-intensity exercise have shown that RPE directly correlates to all metabolic variables (Ratamess et al. 2007; Galvin et al. 2014). Collectively, it is clear that increases in RPE after repeated bouts of high-intensity exercise, such as the WAT, are to be expected due to the exertion associated with testing at this level of intensity.

There were no significant differences between groups for absolute or relative peak power output. Our data in hypoxia differ from the findings of Dekerle et al. (2012) who found a significant difference in peak power output in hypoxia when compared to normoxia. This difference may be due to the nature of Dekerle et al.’s testing protocol.

The present study performed three constant load WATs for 30 s with identical load each time, whereas Dekerle et al.’s protocol consisted of three to four constant load tests to exhaustion with different loads each time, with peak power being measured over the first minute of a 3-minute test. A lowering of FiO2 was hypothesized to change the exercise tolerance levels for supramaximal exercise by increasing the reliance on anaerobic metabolic pathways, which had been shown to exacerbate peripheral levels of fatigue

(Dekerle et al., 2012; Billaut et al., 2013).

The data for absolute and relative peak power in the normoxia group is more congruent with previously published results. For instance, the data for absolute peak power in a study by Kingsley et al. (2016) that utilized 3 WATs with 2-minute rest breaks were 890, 757, and 685W. That is a difference of 0.1% for the first WAT, 3.3% for

WAT2, and 13.8% for WAT3. In addition, the absolute peak power for 3 WATs with 4.5 minute rest breaks reported by Rakobowchuk (2009) were 1090, 1015, and 888W.

Compared to the present, our data were attenuated by 22.3%, 38.5%, and 47.5%. This is not necessarily surprising as Rakobowchuk utilized a 66% longer rest break compared to the present study. Examination of the relative peak power to that of Kingsley et al.

(2016) are also similar. Kingsley et al. (2016) reported relative peak powers of 11.6, 9.8,

8.9W/kg, which are 4.5%, 7.7%, 18.7% greater than those from the present study. The differences here are minimal, except for perhaps WAT3. The difference here may be due to the participants training background. While both the present study, and Kingsley et al. (2009), utilized participants that had been resistance training, it is plausible that the training backgrounds (intensity, duration, frequency) were different. Our criteria was 6 months of resistance training experience whereas Kingsley et al. (2016) required at least

1 year of resistance training.

The present study demonstrates for the first time that repeated WATs with 3 minutes of recovery reduces measures of performance such as absolute and relative peak power output, average power output, average RPM, absolute and relative power drop, average RPM, and power decline similarly in both hypoxia and normoxia. Since the participants in the present study did not have statistically significant differences in SaO2,

this may explain the lack of differences. While SaO2 was lower by 10.8% in hypoxia compared to normoxia, it was not statistically different. However, while SaO2 was not statistically lower in hypoxia, it was lower than normoxia. This suggests some physiological declines in SaO2 occurred, despite no statistical differences being noted.

Further analysis of the data demonstrated that there was an outlier in the normoxia group after WAT2, and WAT3 for SaO2. However, with such few participants, we were unable to remove this outlier from the analysis. Furthermore, decreases in these variables is in agreement with our hypothesis. Given the short rest period between bouts, 3 minutes, the ability to regenerate ATP to maximal capacity was limited and the ability to continually perform at maximal capacity was reduced. Based on our data, it is clear that short rest periods between repeated bouts of high-intensity exercise is deleterious in terms of performance.

Limitations

There are a few limitations associated with this study. The first limitation is that we only used healthy males between the ages of 18 and 30 years of age from the surrounding Kent State area. Because of this it is unknown how females or males of other ages would respond to our intervention. Another limitation of this study is the small sample size. Another limitation of this study was the limited exposure of the test prior to data collection. The WAT is a maximal effort test and participants might not have experience with maximal exertion tests, and the use of a familiarization would be warranted in future studies. Another limitation of this study is use of resistance-trained individuals without further inquiry as to their primary methods of training. Resistance

training is largely anaerobic and aerobically trained individuals may have a different reaction to performing a maximal exertion test in hypoxia than anaerobically trained individuals. This coincides with the limitation of VO2 max testing. A VO2 max test would show whether an individual was more anaerobically or aerobically trained. The last limitation of this study was the singular WAT duration and resistance. Previous research into the effects of WATs on power output in hypoxia when compared to normoxia used varied intensity protocols to elicit a significant difference between groups.

CHAPTER VI

RECOMMENDATIONS & FUTURE RESEARCH

This study examined the effects of hypoxia on SaO2, RPE, blood lactate, RPE, and multiple power output measures following multiple WATs when compared to normoxia. Although a main effect of time was observed for both hypoxia and normoxia for all variables, this study did not find a significant difference between groups. This suggests that hypoxia, when compared to normoxia, does not affect RPE, blood lactate, and measures of performance following multiple WATs in healthy, college-aged men from Kent State University and the surrounding area. Future research should explore the effect of hypoxia in other populations such as resistance-trained women, highly aerobically trained men and women, and sedentary men and women. It may be beneficial for future studies to vary the duration and intensity of the repeated WATs in a consistent manner to elicit a significant difference between groups. The present study was necessary in order to show the lack of difference of performance and biological measures in hypoxia when compared to normoxia. There are certain diseases and illnesses that symptomatically mimic high altitude exposure, yet there are no anaerobic-based exercise recommendations for those populations. The present study was a stepping-stone in the direction of being able to develop anaerobic-based exercise programs for individuals suffering from those relevant illnesses.

Conclusion

This study was, to the best of our knowledge, the first to explore the effects of hypoxia on SaO2, RPE, blood lactate, and measures of performance following multiple

31 32

WATs when compared to normoxia. Our results found that performing multiple WATs in hypoxia or normoxia had no effect on SaO2, RPE, blood lactate, and performance measures when compared to normoxia. Although there was no effect on power output or other performance measures, different levels of intensity and duration of each WAT have shown promise of creating a significant difference in hypoxia when compared to normoxia.

APPENDICES

APPENDIX A

SAMPLE SIZE CALCULATION

Appendix A

Sample Size Calculation

Sample size estimation was determined using data from “Influence of moderate hypoxia on tolerance to high intensity exercise” by Dekerle et al. (2012). The estimation was determined using the average power output measure in normoxia and hypoxia. The effect size for the published average power output data was Cohen’s d = 1.07. With an effect size of d=1.07, and an alpha of α = 0.05 and β = 0.80, the estimated number of subjects needed per group for our study is 12; 12 total due to the counterbalanced design.

Assuming a 20% attrition rate, the total number of subjects that will be recruited is 25.

APPENDIX B

CHECKLIST OF INCLUSION/EXCLUSION CRITERIA

Appendix B

Checklist of Inclusion/Exclusion Criteria

Yes No Between ages 18 and 30 Do not have pacemaker or other implanted device Do not have fever Participated in aerobic/resistance training past 6 months Do not have metabolic disease No history of smoking within last 6 months No prescription medication affecting heart or lungs Do not have high blood pressure Do not have cardiopulmonary disorder Do not have previous diagnosis of cancer Do not have heart condition

APPENDIX C

ESQ-III SHORTENED QUESTIONNAIRE

Appendix C

ESQ-III Shortened Questionnaire

1. I feel lightheaded 0 1 2 3 4 5

2. I have a headache 0 1 2 3 4 5

3. I feel dizzy 0 1 2 3 4 5

4. I feel faint 0 1 2 3 4 5

5. My vision is dim 0 1 2 3 4 5

6. My coordination is off 0 1 2 3 4 5

7. I feel weak 0 1 2 3 4 5

8. I feel sick to my stomach 0 1 2 3 4 5

9. I lost my appetite 0 1 2 3 4 5

10. I feel sick 0 1 2 3 4 5

11. I feel hung-over 0 1 2 3 4 5

APPENDIX D

BORG RATING OF PERCEIVED EXERTION SCALE

Appendix D

Borg Rating of Perceived Exertion Scale

APPENDIX E

PHYSICAL ACTIVITY READINESS QUESTIONNAIRE

Appendix E

Physical Activity Readiness Questionnaire

APPENDIX F

DATA COLLECTION SHEET

Appendix F

Data Collection Sheet

The effect of hypoxia on power output during multiple Wingate Anaerobic Tests

Participant Number ______Date ______

5-minute warm-up on cycle ergometer

Body Weight ______7.5% Body Weight ______Seat Height ______

Treatment

1 ______2______

Pre-RPE _____

Pre-SpO2 _____

Trial 1 Trial 2 Trial 3

Absolute Peak Power ______

Relative Peak Power ______

Average Power ______

Absolute Power Drop ______

Relative Power Drop ______

Peak RPM ______

Average RPM ______

Power Decline ______

SpO2 ______

RPE ______

APPENDIX G

BASELINE DATA COLLECTION SHEET

Appendix G

Baseline Data Collection Sheet

Baseline Data

The effect of hypoxia on power output during multiple Wingate Anaerobic Tests

Participant Number ______

Height ______Weight ______Age ______

APPENDIX H

LIPID RESEARCH QUESTIONNAIRE

Appendix H

Lipid Research Questionnaire

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