Western Washington University

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Fall 2019

Effects of Deep Slow Breath Training on

Performance and Recovery During High Intensity
Interval Cycling
Andrew D. (Andrew David) Brown
Western Washington University, [email protected]

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Recommended Citation
Brown, Andrew D. (Andrew David), "Effects of Deep Slow Breath Training on Performance and Recovery During High Intensity
Interval Cycling" (2019). WWU Graduate School Collection. 885.
https://cedar.wwu.edu/wwuet/885

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EFFECTS OF DEEP SLOW BREATH TRAINING ON PERFORMANCE AND

RECOVERY DURING HIGH INTENSITY INTERVAL CYCLING

By

Andrew David Brown

Accepted in Partial Completion

of the Requirements for the Degree
Master of Science

ADVISORY COMMITTEE

Chair, Dr. Lorrie R. Brilla

Dr. Harsh H. Buddhadev

Dr. David N. Suprak

GRADUATE SCHOOL

Kathleen L. Kitto, Acting Dean

Master’s Thesis

In presenting this thesis in partial fulfillment of the requirements for a master’s degree at
Western Washington University, I grant to Western Washington University the non-exclusive
royalty-free right to archive, reproduce, distribute, and display the thesis in any and all forms,
including electronic format, via any digital library mechanisms maintained by WWU.

I represent and warrant this is my original work, and does not infringe or violate any rights of
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copyrighted material included in these files.

I acknowledge that I retain ownership rights to the copyright of this work, including but not
limited to the right to use all or part of this work in future works, such as articles or books.

Library users are granted permission for individual, research and non-commercial reproduction
of this work for educational purposes only. Any further digital posting of this document requires
specific permission from the author.

Any copying or publication of this thesis for commercial purposes, or for financial gain, is not
allowed without my written permission.

Signature: Andrew David Brown

Date: 27 May, 2019

i
Effects of Deep Slow Breath Training on Performance and Recovery During High Intensity

Interval Cycling

A Thesis
Presented to
The Faculty of
Western Washington University

In Partial Fulfilment
Of the Requirements for the Degree
Master of Science

by
Andrew David Brown
May 27, 2019
Abstract:

The present investigation sought to delineate the effects of a six-week deep slow breathing

(DSB) program on measures of cycling performance (mean power: MP), recovery (heart rate

recovery: HRR, and expired carbon dioxide: VCO2), and pulmonary capacities (vital capacity:

VC, forced expiratory volume: FEV1, and maximum voluntary ventilation: MVV). Twenty male

cyclists were divided into training (n=10) and control (n=10) groups, where the training group

completed a six-week DSB program in addition to their own training while the control group

completed no breathe training. Participants completed two testing sessions, one before and one

after the six-week period. Testing sessions involved three repeated Wingate Anaerobic Tests

(WAnT) with three minutes of passive recovery between each interval. MP was recorded for

each WAnT while measures of VCO2 and HRR were taken immediately following each WAnT.

No significant (p < 0.05) differences were found between groups for any of the variables

measured, while both groups exhibited increase MP in the second WAnT (T2) following the six-

week training period (Treatment: pre: 516.30 ± 20.82 W versus post: 536.38 ± 20.62 W; p =

0.010; Control: pre: 549.93 ± 18.66 W versus post: 567.83 ± 18.44 W; p = 0.010). The results

presented here suggest DSB provides no performance benefit relevant to recovery or pulmonary

capabilities during high intensity interval cycling, beyond those which are incurred via

endurance training.

iv
 Acknowledgements

First and foremost I would like to thank my mother and father, David and Leigh Ann

Brown, for their continued support, guidance, and love. I would also like to thank Dr. Lorrie Brilla

for her unwavering persistence that pushed me to excel in this program. Suffice to say, you have

catalyzed my self-actualization and I am forever grateful for your keen ability to push me outside

of my comfort zone. I would also like to thank the other members of my thesis committee, Dr.

Harsh Buddhadev and Dr. Dave Suprak, for their mentorship and instruction during the completion

of this work. Thank you also, to the participcants who volunteered their time and comfort. Finally,

I would like to thank Amber Machado for her patience during my time at Western Washington

University. You are stronger than you will ever know.

v
 Table of Contents

Abstract .......................................................................................................................................... iv

Acknowledgements ......................................................................................................................... v

List of Tables and Figures.............................................................................................................. ix

Introduction ..................................................................................................................................... 1

Introduction ......................................................................................................................... 1

Methods........................................................................................................................................... 3

Participants .......................................................................................................................... 4

Procedure ............................................................................................................................ 4

High Intensity Interval Cycling (HIIC)............................................................................... 5

Carbon Dioxide Output (VCO2) ......................................................................................... 5

Heart Rate Recovery (HRR) ............................................................................................... 6

Deep Slow Breathing Procedure ..........................................................................................6

Statistical Analysis .............................................................................................................. 7

Results ............................................................................................................................................. 8

Discussion ..................................................................................................................................... 10

References ..................................................................................................................................... 20

Review of Pertinent Literature ...................................................................................................... 26

Introduction ....................................................................................................................... 29

Physiological mechanisms to explain increased performance .......................................... 27

Vagal Tone ............................................................................................................ 27

Sympathetic Tone ................................................................................................. 29

Chemo-sensitivity and energy systems ................................................................. 31

Nociception ........................................................................................................... 34

vi
Breath training for athletic performance ........................................................................... 36

Breath frequency training, deep slow breathing, and apnea ................................. 36

Device Guided Breathing ...................................................................................... 38

Considerations for study design and potential limitations ................................................ 40

Dependent variables .............................................................................................. 40

Heart Rate Recovery (HRR) ................................................................................. 41

Buffering: CO2 and Lactate ..................................................................................41

Wingate Anaerobic Test (WAnT) ..........................................................................43

Inclusion and exclusion criteria ........................................................................................ 47

Summary .......................................................................................................................... 48

References ......................................................................................................................... 50

vii
 List of Appendices

Appendix A: Journal of Sport Science and Medicine Guidelines ............................................... 65

Appendix B: Raw Data ................................................................................................................ 66

Appendix C: Statistical Analysis ................................................................................................. 72

viii
 Figures and Tables

Table 1. Deep Slow Breathing Training Progressions ................................................................. 7

Table 2. Participant Demographics .............................................................................................. 8

Table 3. Mean Power for each Wingate Test (T1-3) before and after the training period ............ 9

Table 4. VCO2 during and after each Wingate Test (T1-3) before and after training period ....... 9

Table 5. Heart Rate Recovery, Vital Capacity, Forced Expiratory Volume, and Maximum
Voluntary Ventilation. .................................................................................................................... 9

Table 6. Pearson correlations between MP and VCO2 before six-week intervention ................ 10

ix
INTRODUCTION

Voluntary alterations in breath frequency, tidal volume, and lengths of the inhalation and

exhalation components of the respiratory cycle have been utilized for centuries in yogic, qigong, and

other meditative practices (Danucalov, Simões, Kozasa, & Leite, 2008; Goyal, Lata, Walia, &

Narula, 2014; Pal, Velkumary, & Madanmohan, 2004b; Vinay, Venkatesh, & Ambarish, 2016).

While an abundance of data supports their use in cardiovascular, mental, and autonomic nervous

system health contexts, the potential benefit of these practices for the goal of enhanced sport

performance is unclear. The reported benefits of apnea and deep slow breathing (DSB) include anti-

nociceptive effects (Reyes del Paso, Muñoz Ladrón de Guevara, & Montoro, 2015; Ryan & Kovacic,

1966), increased vital capacity (VC) (Zelenkova & Chomahidze, 2016), hypercapnic and hypoxic

tolerance (Bernardi, Gabutti, Porta, & Spicuzza, 2001; Lavin, Guenette, Smoliga, & Zavorsky, 2015;

Roecker et al., 2014; Smith et al., 2014), buffering capacity (Joulia et al., 2003; Woorons et al.,

2008), cardiac vagal tone (Bhargava, Gogate, & Mascarenhas, n.d.; Eckberg, 2003; Jerath, Edry,

Barnes, & Jerath, 2006; Pal, Velkumary, & Madanmohan, 2004a; Telles, Nagarathna, & Nagendra,

1996; Vinay et al., 2016), work capacity (Hepburn, Fletcher, Rosengarten, & Coote, 2005; Porcari et

al., 2016), enhanced blood pressure response (Anderson, McNeely, & Windham, 2009; Goyal et al.,

2014; Monnazzi, Leri, Guizzardi, Mattioli, & Patacchioli, 2002), endogenous antioxidant defense

(Joulia et al., 2003), reduced oxidative stress (Joulia et al., 2003), and altered endocrine profiles

(Djarova, Ilkov, Varbanova, Nikiforova, & Mateev, 1986; Kox et al., 2014; Monnazzi et al., 2002).

Support for the use of breath training programs to enhance recovery and performance is provided

by Woorons et al. (2008). These researchers observed attenuated exercise induced acidosis and

increased HCO3- concentrations during running at 90% of predicted heart rate max following a four–

week dynamic hypoventilation program. Maintenance of acid-base balance was paralleled by an

increase of maximum velocity of 0.5 km/hr in their breath-training group. Given the greater relative

contribution of anaerobic energy systems in attaining maximum velocity, their results reflect that

glycolytic metabolism may have been altered by their breath program and that anaerobic tests (i.e.

400m sprint or Wingate tests) would better elucidate augmented buffering capacities following

breath training compared to exercise during which oxidative systems are dominant.

Another mechanism by which long DSB may enhance recovery during high intensity exercise

(HIE) is modified glycolytic metabolism subsequent to repeated hypoxic and hypercapnic stress

(Joulia et al., 2003; Lemaître, Joulia, & Chollet, 2010). Joulia et al. (2003) described attenuated

rises in blood lactate, oxidative stress, decreased heart rate during static and dynamic apneas, and

increased apnea durations following breath training in eight triathletes. These researchers suggest

that increased mobilization and use of free fatty acids following breath hold training may reduce

glycolytic energy production and subsequently decrease lactate concentrations during exercise.

However, these researchers did not address adaptations to hypercapnic tolerance or buffering

systems as potential mechanisms for improved apneic durations or attenuated increases in lactate

production.

Tests of anaerobic capacity have been utilized as measures of athletic performance (Bogdanis,

Nevill, Lakmoy, & Boobis, 1998; Hawley, Williams, Hamling, & Walsh, 1989; Rindom et al.,

2016). Of these tests, the Wingate anaerobic test (WAnT) has been routinely used, given its ability to

produce reliable and valid results and their correlative strength to sporting performance (Hachana,

Attia, Nassib, Shephard, & Chelly, 2012; Langfort, Zarzeczny, Pilis, Nazar, & Kaciuba-Uscitko,

1997; MacDougall et al., 1998; Masterson, 1999; Richard Davison, Swan, Coleman, & Bird, 2000).

Given the levels of metabolic acidosis that occur during WAnTs, they are also a useful method to

test endogenous buffering capacities. As such, the WAnT is a suitable test that may elucidate the

2
effects of breath training on performance and recovery during interval exercise with a large

anaerobic contribution.

While there is certainly heterogeneity within the literature, much of the data supports the use of

hypercapnic or controlled frequency breathing conditions to enhance performance and potentially

recovery, though few studies have specifically investigated its potential efficacy during exercise with

primarily glycolytic energy contribution (Busch et al., 2012; Jerath et al., 2006; Joulia et al., 2003;

Kox et al., 2014; Lavin et al., 2015; Lemaître et al., 2010; Woorons et al., 2008). Further, the

specific effects of deep slow breath training on athletic performance have yet to be clearly

elucidated. The aim of the present study was to address the research hypothesis that a DSB program

would positively influence measures of cycling performance (mean power; MP), recovery (heart rate

recovery: HRR, and expired carbon dioxide: VCO2), and lung function (vital capacity: VC, forced

expiratory volume: FEV1, and maximum voluntary ventilation: MVV). A secondary purpose to the

present work was to explore the relationship between VCO2 and MP, with the hypothesis that VCO2

would show a positive relationship with MP and partly explain the ability to maintain performance

across repeated cycling sprints.

METHODS

Experimental approach to the problem

The study was a randomized control intervention where differences in interval sprint cycling

performance were examined pre- and post-six-week DSB or no training intervention. Pre-training

(PRE) testing was followed by a six-week intervention period. Subjects then completed post-training

(POST) testing during which the pre-training tests were repeated.

3
Participants

The participants included 20 young, trained cyclists from Western Washington University

(Bellingham, WA, USA) and training facilities in the surrounding area. Participants were selected

randomly from those who respond to flyers posted in training facilities in Bellingham and social

media posts (Facebook). Those selected for participation were divided evenly into to either training

(n=10) or control (n=10) groups by age and cycling experience matching.

Exclusion criteria included previous lower-extremity injury within six months, the use of anti-

inflammatory medication within the last six weeks, or cardiac or respiratory abnormalities.

Participants were excluded from the study if they had consumed creatine, beta alanine, or citrulline

malate within six months prior to the intervention (Crisafulli et al., 2018; Pérez-Guisado & Jakeman,

2010; Trexler et al., 2015). Participants were prohibited from consuming caffeine before testing

sessions. Prior to participation in the current study, all subjects received and signed an informed

consent form, which had been previously approved by the Western Washington University’s

Institutional Review Board, in accordance with the Department of Health and Human Services

guidelines.

Procedure

Baseline measurements of height (cm), mass (kg) and pulmonary measures of VC, FEV1, and

MVV were taken upon arrival to the laboratory with a Pneumoscan S-301 (Vacumed, Ventura, CA).

Participants changed into cycling clothing and were fit to the cycle ergometer. Seat height was

individually adjusted to achieve a knee flexion angle of 25-30° for all participants and recorded for

consistency between measures (Bini, Hume, & Croft, 2011). Handlebar height was adjusted to

4
achieve a trunk flexion angle of 30° (Ericson, Bratt, Nisell, Arborelius, & Ekholm, 1986).

Measurements of bike fit were recorded for future testing. Participants were fit with an electric heart

rate monitor and gas sampling mask for gas analysis throughout the test duration.

High-intensity Interval Exercise Procedure (HIE)

A Monark 894E cycle ergometer outfitted with accompanying software (Monark, Vansbro,

Sweden), toe-clips, and heel straps was used for all WAnT tests. The participants completed a five-

minute warm-up on the Monark cycle ergometer at self-selected cadence and resistance. Following

warm up, peak cadence (rev/min) was established during a five second effort during which the

participants pedaled as fast as possible. Following a 5-minute rest, subjects were then instructed to

begin cycling at maximal intent to attain 80% of peak cadence. When 80% of peak cadence was

achieved, a predetermined load equal to 0.075 kp per kg body mass was applied to the flywheel and

the participant cycled at maximal effort for 30-seconds. The participants completed a total of three,

30-second Wingate (WAnT) sprints, each interspersed with 3 minutes of passive recovery (Francois

Billaut, Giacomoni, & Falgairette, 2003; Bogdanis, Nevill, Boobis, Lakomy, & Nevill, 1995;

Bogdanis et al., 1998; Bogdanis, Nevill, Lakomy, Graham, & Louis, 1996).Verbal encouragement

was provided to all participants during each sprint. The Monark Wingate software was used to

measure and record MP performed during each sprint.

Carbon Dioxide Output (VCO2)

Gas exchange was measured for two minutes immediately following each WAnT and recovery

interval with a Parvo Medics TrueOne 2400 metabolic cart (Parvo Medics, Sandy, UT, USA). Given

the relationship between bicarbonate buffering and endogenous CO2 production , VCO2 was taken as

5
a proxy for buffering capacity (Böning, Klarholz, Himmelsbach, Hütler, & Maassen, 2007;

McGinley & Bishop, 2016; Röcker, Striegel, Freund, & Dickhuth, 1994).

Heart Rate Recovery

Heart Rate Recovery (HRR) was taken as the change in heart rate within the first minute

immediately following each WAnT, and is associated with vagal tone and autonomic function in

athletic and general populations (Goulopoulou et al., 2006; Halson, 2014; Hepburn et al., 2005;

Seiler, Haugen, & Kuffel, 2007; Wyatt, Donaldson, & Brown, 2013). Heart rate monitors (Polar T31

Heart Rate Monitor, Polar Electro, Kempele, FI) were secured around the ribcage at the level of the

xiphoid process and conducting surfaces were moistened. Heart rate recovery was tracked following

the bout of exercise with a Polar FT4 training watch (Polar Electro, Kempele, FI).

Deep Slow Breathing Procedure

The DSB utilized was validated in a pilot study conducted by the researchers. The DSB program

aimed to increase parasympathetic nervous system activity and buffering capacity via prolonged

exhalation and post expiration apnea durations (Hepburn et al., 2005; Reyes del Paso et al., 2015;

Vinay et al., 2016). The breath exhalation and hold durations were constructed progressively to

allow familiarization to extended exhalation and breath hold while potentially maintaining

parasympathetic stimulation. DSB progressions are presented in Table 1. During the first week,

participants inhaled for a count of four, held breath for a count of four, exhaled for a count of four,

and held breath for another count of four before repeating the breath cycle. One second was added to

the inspiratory pause and expiration components of the breath cycle every week while 2 seconds

were added to the expiratory pause every week to provide progressive overload. Following each 10-

6
minute training session, the participants completed three maximal post-expiratory breath holds with

recovery durations indicated by return to normal breathing frequency. Participants were asked to use

diaphragmatic breaths for all inhalations and exhalations. Instructional videos were included with

written instructions for diaphragmatic breathing and breath holding techniques (Bruton et al., 2018).

The Breath + Relaxation and Breath Training application (Dynamic App Design LLC) was utilized

as a visual tool for tracking intended for weekly breathing progressions. Post-expiration breath holds

were timed by the participants on self-selected timing devices (i.e. smartphone timers) and recorded.

Participants were required to complete 10 minutes of DSB every day for six weeks. A maximum of 4

missed sessions was allowed across the six-week training period, after which the participant was

dropped from the study.

Table 1. Deep Slow Breathing Progressions

Week 1 2 3 4 5 6
Inhalation (sec) 4 4 4 4 4 4
Hold (sec) 4 5 6 7 8 9
Exhalation (sec) 4 5 6 7 8 9
Hold (sec) 4 6 8 10 12 14
Three maximal post expiratory breath holds after each session

STATISTICAL ANALYSIS

All data analyses were completed with SPSS (SPSS; V. 25.0; SPSS, Inc., Chicago, IL, USA).

Descriptive data were generated for each outcome measure and reported as mean ± SD. Separate

(time X experimental group X test) mixed model ANOVAs with a priori significance set to p ≤ 0.05

were utilized to determine pre-to-post differences across and within DSB and control groups for

measures of MP and VCO2. Paired t-tests were conducted to determine pre-to-post differences in

measures of HRR and pulmonary measures (VC, FEV1, and MVV). Tukey post-hoc tests were

7
performed if significant group X time interactions were observed. Calculations of partial eta squared

(ηp2) were included for effect size analysis. Pearson correlations were conducted between the MP of

each WAnT (interval 1= T1, Interval 2 = T2, and interval 3 = T3) and the VCO2 of the subsequent

recovery interval, and for the MP recorded in WAnTs T2 and T3 and the VCO2 of the previous

recovery interval.

RESULTS

Participant demographics are presented in Table 2. No significant differences were found

between groups for age, mass, or height. Specifically, the sample consisted of recreational mountain

bike (n=9), recreationally aerobically trained (n=4), road bike (n=3), professional mountain bike

(n=2), cyclocross (n=1), and track cycling (n=1) athletes. All participants in the control group were

able to complete the prescribed testing before and after the tests while one participant in the training

group was unable to complete the third interval in pre-testing, while another was unable to complete

the third interval in post-testing.

Table 2. Participant Demographics (Mean ± SD).

Control Treatment
Age (yrs) 24.50 ± 4.50 26.1 ± 2.81
Height (cm) 181.73 ± 5.81 178.96 ± 7.15
Mass (kg) 80.47 ± 8.84 79.25 ± 10.09

Descriptive statistics for MP and VCO2 are presented in Table 3-4. MP decreased significantly

across each WAnT (p<0.001; ηp2= 0.857) for both pre and post testing conditions. No 3-way

interaction (group X time X test) was found for either MP or VCO2. A significant time X test

interaction was found (p =0.010) in which post testing MP was greater than pre in test 2 for both

groups. There was a systematic decline in VCO2 across each recovery interval for both groups (p

8
<0.001; ηp2=0.797). No significant differences were found between groups for either MP (p =0.336;

ηp2= 0.058) or VCO2 (p =0.10; ηp2= 0.170) during any WAnT or recovery interval.

Table 3. Mean Power for each Wingate Test (T1-3) before and after the training period

Control Treatment

Test 1 Test 2 Test 3 Test 1 Test 2 Test 3

Pre-training Mean
Power (W) 622.34± 54.68 549.93 ± 61.46 507.75 ± 83.87 622.44 ± 80.10 516.3 ± 88.50 449.81 ± 82.38
Post-training Mean 624.96 ±
Power (W) 52.49 567.83 ± 61.83* 511.30± 72.60 618.24 ± 83.41 536.37 ± 53.44* 475.18 ± 61.86

* Significant differences between pre- and post-training mean power for test 2

Table 4. VCO2 (Mean ± SD) during and after each Wingate Test (T1-3) before and after training period.

Control Treatment
Recovery Recovery Recovery Recovery Recovery Recovery
Interval 1 Interval 2 Interval 3 Interval 1 Interval 2 Interval 3
Pre-training VCO2
(L/min) 2.66 ± 0.24 2.27 ± 0.26 2.23 ± 0.33 2.51 ± 0.34 2.09 ± 0.26 1.94 ± 0.32
Post-training VCO2
(L/min) 2.73 ± 0.26 2.33 ± 0.24 2.08 ± 0.27 2.45 ± 0.24 2.19 ± 0.32 2.05 ± 0.33

Descriptive statistics for HRR, VC, FEV1, and MVV are presented in Table 5. No significant

differences were found between groups for values of HRR (p =0.331; ηp2= 0.059), VC (p =0.336;

ηp2= 0.058), FEV1 (p =0.414; ηp2= 0.037), and MVV (p =0.211; ηp2= 0.086).

Table 5. Heart Rate Recovery, Vital Capacity, Forced Expiratory Volume, and Maximum
Voluntary Ventilation.
Control Treatment
Pre Post Pre Post
HRR
(bpm) 31.56 ± 11.10 31.56 ± 10.79 42.88 ± 18.89 34.13 ± 17.96
VC (L) 5.30 ± 0.74 5.49 ± 0.90 5.45 ± 0.90 5.53 ± 0.88
FEV1 (L) 4.39 ± 0.43 4.36 ± 0.36 4.18 ± 0.45 4.25 ± 0.56
MVV
(L/min) 182.70 ± 19.38 183.80 ± 23.03 168 ± 32.69 168.30 ± 34.88

9
 Pearson correlations and p-values are presented in tables 6 and 7. Significant correlations were

observed between the MP of each WAnT and the VCO2 of the subsequent recovery interval before

(T1: p<0.001, T2: p =0.001, T3: p =0.001) and after (T1: p =0.005, T2: p < 0.001, T3: p =0.002) the

six-week training period for both groups. Significant correlations were also observed for the MP

recorded in WanTs T2-3 and the VCO2 of the previous recovery interval before (T2 / Recovery 1: p

=0.014, T3 / Recovery 2; p =0.003) and after (T2 / Recovery 1: p =0.010, T3 / Recovery 2: p

=0.017) the six-week training period for both groups.

Table 6. Pearson correlations between MP and VCO2 before six-week intervention

r-value.
VCO2
R1 R2 R3
T1 r-value 0.725 * - -
p-value <0.001 - -
T2 r-value 0.54* 0.704* -
p-value 0.014 0.001 -
T3 r-value - 0.642* 0.69*
p-value - 0.003 0.001
R1= Recovery interval 1, R2= Recovery Interval 2, R3= Recovery interval 3;
*Significantly different from pre (p< 0.05)

DISCUSSION

The aim of the present investigation was to examine the effects of a DSB program on

measures of cycling performance, recovery, and pulmonary capacities. No significant differences

were found between the training and control groups for any of the variables measured.

Systematic decreases in both MP and VCO2 were found across successive WAnT and recovery

period, respectively, for both groups before and after the 6-week experimental period. These

systematic changes in MP and VCO2 were accompanied by large effect sizes. To the researchers’

knowledge, this is the first investigation to address the effects of breath training on recovery

10
from high intensity anaerobic intervals, though numerous studies have sought to elucidate the

relevance of breath training to sporting performance (Joulia et al., 2003; Lavin et al., 2015;

Lemaître et al., 2010; Woorons et al., 2008).

Mean Power and VCO2

The primary finding of the present study was the hypothesis that a DSB protocol would

result in maintenance of MP across repeated WAnTs was not supported (Table 2). Moreover, the

results demonstrated systematic reductions in MP and VCO2 across the testing conditions, as

would be expected due to increasing metabolic acidosis, reduction in endogenous buffering

capacity, and subsequent reductions in glycolytic energy transfer (Baker, McCormick, &

Robergs, 2010; Péronnet & Aguilaniu, 2006). The large effect sizes that accompany these data

further illustrate the degree of change between intervals and indicate the cycling protocol elicited

substantial reductions in the ability of the participants to maintain power production. A

secondary finding of this investigation was that VCO2 was unchanged in both groups but

mirrored the systematic decrement in MP across each subsequent WAnT in both pre and post-

testing conditions. Lemaitre, Joulia, and Chollet (2010) hypothesized that a primary potential

benefit of apneic training may be improvements in muscle buffering capacity and subsequent

reduction in acidosis. Given the relationship between HCO3- buffering systems and endogenous

CO2 production, it was expected that an increase in buffering capacity via HCO3- could be

estimated utilizing measurements of VCO2. However, the results did not demonstrate an increase

in VCO2 and thus it is likely that the DSB protocol did not augment HCO3- buffering systems.

However, biochemical analyses (pH, HCO3-, and blood lactate) were not included in the design,

so to state potential changes in any of these variables would be erroneous.

11
 A second finding was that the hypothesis that MP and VCO2 would display a significant

positive relationship was supported. Pearson correlational analysis revealed significant positive

relationships between the MP across the WAnTs and the VCO2 in the subsequent recovery

interval, as well as the MP recorded in WAnTs T2-3 and the VCO2 of the previous recovery

interval. These findings are in line with what is currently understood regarding the production of

non-metabolic CO2, with respect to HCO3- buffering, and suggest that MP is at least in part

explained by the ability to produce greater CO2 (Böning et al., 2007; Chicharro et al., 2000;

McGinley & Bishop, 2016). These relationships suggest VCO2 may be useful as a performance

indicator to consider for athletes whose sport requires a significant proportion of energy transfer

from glycolysis. Further research should investigate the efficacy of VCO2 production as a

predictive measure of exercise performance during endurance sport. Within the context of breath

training, these relationships support the goals of breath training to increase levels of endogenous

CO2 production. As such, this measure should be utilized to determine the efficacy of future

breath training programs, in addition to measures of exercise performance.

A factor that would largely influence CO2 kinetics in a breath training protocol is

manipulating respiratory dead space. Koppers, Vos, and Folgering (2006) elucidated the efficacy

of tube breathing in eliciting hypercapnia in healthy subjects. In a training context, Smolka,

Borkowski, and Zaton (2014) described increased arterial CO2 and decreased blood pH during

exercise at 60% VO2max with an additional 1200 mL of respiratory dead space. Their results

reflect those presented in the current study, in that their six-week training with additional dead

space had no effect on VCO2 or respiratory exchange ratio (RER) values in a cohort of healthy

males, though the exercise conditions were not similar to the present study. Arterial CO2

concentrations were not measured, so whether the degree of hypercapnia elicited in the protocol

12
used was similar to that of Smolka et al. (2014) is unclear. Additionally, the results presented

here, in tandem with those described by Smolka et al. (2014), suggest that hypercapnic breath

training does not alter carbohydrate metabolism, as proposed by Woorons (2008) and Joulia

(2003).

While the protocol did not result in improvements in VCO2 or measures of interval

cycling performance, previous literature has revealed alternative findings for various

physiological and performance measures. Lavin et al. (2015) reported decreases in 150m swim

times and increases in running economy in their group of 18 recreational swimmers following a

controlled breath-frequency program, while Porcari et al. (2016) demonstrated improvements in

power at ventilatory threshold and power at respiratory compensation point following a program

utilizing device guided breathing. However, the design of the training program presented by

these authors differs significantly from that of the present investigation, so drawing definitive

comparisons is difficult.

Fabrice et al. (2003) noted improvements in lactate kinetics, reduced oxidative stress, and

changes in arterial concentrations of oxygen and CO2 following their 12-week dynamic apnea

program. These researchers reported increased arterial CO2 and decreased lactate concentrations

at the break point of maximal apneas following their program. These results may suggest that

increased carbon dioxide production is an adaptation incurred via breath training. It is possible

the increases in arterial CO2 are explained by longer maximal apnea durations and greater

hypercapnic tolerance, though they did not address these questions in their discussion.

Additionally, the apneic conditions utilized by these researchers included dynamic apnea, in

which the participants were actively exercising during the breath holds while the protocol in the

present investigation utilized apneic durations at rest.

13
 Woorons et al. (2008) demonstrated the efficacy of a 4-week hypoventilation protocol in

eliciting maintenance of pH and HCO3- in a group of 15 male runners at 90% of maximum heart

rate, though they did not report any significant changes in exercise performance during VO2max

and time to exhaustion tests. In their study, these researchers note while enhanced buffering

subsequent to breath training may delay the onset of metabolic acidosis, it may not reduce it at

maximal intensities, as their results showed no changes in pH or HCO3- in the recovery following

their measurements of VO2max. Given these findings, it is possible that the benefit of DSB

training may be most apparent at sub-maximal intensities near lactate threshold. As such, future

research on this topic should investigate the use of sub-maximal exercise intensities slightly

above lactate threshold to further discriminate the potential for performance enhancement

following DSB training (Röcker et al., 1994).

Previous researchers have utilized measurements of relative buffering capacity as a

function of workload at ventilatory threshold and workload at respiratory compensation point

during incremental ramp exercise (Chicharro, Hoyos, & Lucía, 2000; Röcker et al., 1994).

Specifically, Chicharro, Hoyos, and Lucía (2000) calculated functional relative buffering

capacity as the difference in workload at lactate threshold and respiratory compensation point in

of group professional cyclists to elucidate the effects of endurance training on isocapnic

buffering and hypocapnic hyperventilation. Their data demonstrated that endurance training had

no effect on isocapnic buffering while the phase of hypocapnic hyperventilation decreased

significantly. These findings suggest a viable methodology to quantify buffering at sub-maximal

intensities that may be useful in later investigations on the effects of breath training

Another potential explanation for a lack of significant findings with respect to values of

VCO2, is that DSB training may augment intramuscular buffering via mechanisms distinct from

14
HCO3-. As noted by Péronnet and Aguilaniu, HCO3- buffering represents only a portion of

intramuscular pH balance, and may only buffer ~25% of H+ load during anaerobic exercise

(Péronnet & Aguilaniu, 2006). If what these researchers argue is correct, total buffering capacity,

as represented by HCO3-, histidine, carnosine, phosphocreatine, and ammonia, would need to be

measured to capture a holistic representation of the effects of a training program that aims to

maintain acid-base homeostasis.

An unexpected finding was an increase in MP in T2 for both groups. A learning effect for

WAnTs has been described previously (Barfield, Sells, Rowe, & Hannigan-Downs, 2002).

However, if a learning effect had occurred it would be expected to improve the MP values in T1

during the post testing as well. A likely scenario is that both groups experienced improvements

in T2 due to improved pacing strategies (François Billaut, Bishop, Schaerz, & Noakes, 2011).

Despite the prescribed maximal intensity, it is possible that the participants were able to attain

more optimal pacing strategies in the second round of testing. However, one would expect a

decrement in MP during T1 in combination with an increase in MP during T2, which was not

observed. Another potential explanation is that the physiological readiness of all participants

improved enough to result in an improvement in T2 but was not substantial enough to affect the

values for MP achieved in T3.

Another interpretation of the results may suggest that training status across the annual

training calendar may have influenced the values, given some data were collected during times

of the year that may correspond to varying training volumes and intensities and subsequent

physiological readiness (Manunzio, Mester, Kaiser, & Wahl, 2016). However, pre and post

testing were completed within an 8-week period for each subject, so decrements or

improvements in performance would have been relative to their current state of training,

15
regardless of season. Another potential factor that likely influenced the data were the

heterogeneity in the discipline of cycling or training across the sample population (Craig &

Norton, 2001; Hays, Devys, Bertin, Marquet, & Brisswalter, 2018; Richard Davison et al., 2000).

However, it would appear efforts to homogenize the treatment and control groups were effective,

as no differences were found in any of the measured variables before the 6-week training period.

Heart Rate Recovery

The results showed that six weeks of DSB training resulted in no change in HRR. Jerath

et al. (2006) explain deep slow breathing results in parasympathetic dominance through

activation of mechanosensitive tissues and subsequent hyperpolarization of lung tissue, which

induces synchronicity between the brainstem and hypothalamus. Eckberg (2003) provides further

elucidation for the mechanisms responsible for an increase in parasympathetic dominance

through elongation of the exhalation component of the respiratory cycle. Given the ability of

slow breathing to elicit acute and chronic changes in vagal tone, HRR were utilized as a measure

of parasympathetic activity and reactivation (Bhargava et al., 1988.; Eckberg, 2003; Jerath et al.,

2006; Pal et al., 2004; Telles et al., 1996; Vinay et al., 2016). Unfortunately, technical failures

resulted in the reduction of the sample in the training group (n=8) so only HRR data for the first

interval was analyzed. No significant differences were found between or within groups for HRR

following this DSB protocol.

A potential reason for a lack of significant findings for changes in HRR may be

attributable to the trained state of the participants, as chronic endurance training results in

increases in parasympathetic activity and decreases in sympathetic activity at rest (Carter,

Banister, & Blaber, 2003). It is possible that the stimulus incurred from the DSB program was

16
not sufficient to drive adaptations that would further increase vagal tone. Had the participants

been of a lesser trained state, it is possible that larger changes in HRR would have been

observed, though contradictory data have been published elsewhere (Michaelson et al., 2019) . It

is important to note that while the statistical analyses revealed no significant differences between

groups with respect to HRR, a substantial decrease in HRR (-8.75 bpm) was recorded in the

experimental group while minimal change was recorded in the control group. It is possible the

variability in HRR response to training was large (shown by large standard deviations) in this

group may have masked any potential effect of training.

Pulmonary Measures

No differences were noted between groups for any of the measurements of lung volumes.

Previous research has demonstrated the efficacy of breath-hold and diaphragmatic breath training

in eliciting increases in VC (Ferretti, 2001; Walterspacher et al., 2011; Yong, Lee, & Lee, 2017).

The pretraining values of VC provided by Yong et al. (pre=5.32 ± 1.4 L, post = 6.05 ± 1.3 L) are

similar to those reported in the current work, while those reported by Walterspacher et al. in their

sample of breath-hold divers are larger (6.2 ± 0.6 L) (Walterspacher et al., 2011; Yong et al.,

2017). Greater ventilatory function has been reported in endurance athletes compared to power

trained and sedentary individuals (Durmic et al., 2017). The values of VC (5.37 ± 0.80 L), FEV1

(4.59 ± 0.69 L), and MVV (160.72 ± 35.41) provided by Durmic et al. (2017) are similar to those

reported here. Given their findings that endurance athletes exhibited significantly larger values

for VC and MVV compared to sedentary individuals, it is possible the breath training stimulus

was not sufficient to elicit further adaptations that would improve ventilatory function beyond

those incurred by endurance training.

17
LIMITATIONS

While attempts to homogenize the sample appeared to be effective, greater specificity

could be utilized in recruiting a cycling cohort. Recruiting from a single discipline (mountain,

road, cyclo-cross, etc.) would further reduce the potential for the confounding factors of the

adaptations specific to each of these sub-categories of cycling. Another factor that was not

controlled was the effect of season. Data collections were completed over the course of a nine-

month period, during which the training volumes of those who completed the training in the late

summer and early fall may have been larger than those completed in the winter. By requiring a

minimum volume of cycling training, an attempt was made to mitigate this effect. The chosen

testing methodology was based on the work of previous researchers who suggested

investigation on the effects of breath training at intensities and time domains during which the

proportion of energy transfer from glycolysis is relatively larger than those of PCr or oxidative

systems (Woorons et al., 2008). Future investigations should utilize sub-maximal protocols that

may more accurately quantify the potential effects of breath training.

Conclusions

The results presented here suggest DSB training provides no performance benefit during

high intensity interval cycling beyond those which are already stimulated by endurance training,

considering the measures of exercise performance utilized. Similarly, the results demonstrate no

benefit during the recovery from sprint efforts, with respect to parasympathetic reactivation.

While these results are most clearly relevant to repeated sprint efforts with a significant

contribution from glycolytic energy systems, their relation to sustained efforts near lactate

threshold remain unclear. Given these results, use of DSB training as an effective mode of

18
preparation for athletes who compete at intensities which correspond to single or repeated

glycolytic efforts (400m run, 50m swim, etc) is not warranted.

It would appear DSB training appears to provide no performance or recovery

enhancement in trained male cyclists during repeated WAnTs, while further research utilizing

ramp exercise testing procedures may more accurately represent the potential effects of DSB

training at varying levels of exercise intensity. These findings add to the existing body of

knowledge regarding the relationship between anaerobic performance and CO2 production

during high-intensity interval exercise and provide a basis for further research on the efficacy of

breath training in the context of sporting performance.

19
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Review of literature: Effects of breath training on exercise recovery

Introduction

Voluntary alterations in breath frequency, tidal volume, and lengths of the inhalation and

exhalation components of the respiratory cycle have been utilized for centuries in yogic, qigong,

and other meditative practices (35,62,79). While an abundance of data supports their use in

cardiovascular, mental, and autonomic nervous system health contexts, the potential benefit of

these practices for the goal of enhanced recovery and subsequent athletic performance is unclear

(1,27,42,45,56,62,82,90).

The reported benefits of apnea and deep slow breathing (DSB) include anti-nociceptive

effects (Reyes del Paso et al., 2015; Ryan & Kovacic, 1966), increased vital capacity (VC)

(Ferretti et al., 2012), hypercapnic and hypoxic tolerance (Bernardi et al., 2001; Lavin et al.,

2015; Roecker et al., 2014; Smith et al., 2014), buffering capacity (Joulia et al., 2003; Woorons

et al., 2008), cardiac vagal tone (Bhargava et al., n.d.; Eckberg, 2003; Jerath et al., 2006; Pal et

al., 2004a; Telles et al., 1996; Vinay et al., 2016), work capacity (Hepburn et al., 2005; Porcari et

al., 2016), enhanced blood pressure response (Anderson et al., 2009; Goyal et al., 2014;

Monnazzi et al., 2002), endogenous antioxidant defense (Joulia et al., 2003), reduced oxidative

stress (Joulia et al., 2003), and altered endocrine profiles (Djarova et al., 1986; Kox et al., 2014;

Monnazzi et al., 2002). While there is certainly heterogeneity within the literature, much of the

research supports the use of hypercapnic or controlled frequency conditions to enhance

performance and potentially recovery during or between training or competition efforts (Engan,

Richardson, Lodin-Sundström, van Beekvelt, & Schagatay, 2013; Joulia et al., 2003; Lemaître et

al., 2010; Schagatay, van Kampen, Emanuelsson, & Holm, 2000).

26
 The aim of the present review is to explore the primary physiological mechanisms

relevant to potential adaptations following DSB and apnea-training including increased vagal

tone, decreased chemosensitivity, anti-nociception, and endocrine responses. Applied training

studies utilizing breathing within the context of sport performance are evaluated. Methodical

considerations for future studies regarding the efficacy of breath training on sport performance

are presented given the specificity of adaptations purported across the literature.

Physiological mechanisms to explain increased performance

Vagal Tone. The relationships between vagal tone, heart rate, and exercise capacity are

well documented (Anderson, 1998; Anderson et al., 2009; Delapille et al., 2001; Hepburn et al.,

2005; Jerath et al., 2006; Kiviniemi et al., 2014; Machhada et al., 2017; Monnazzi et al., 2002;

Pal et al., 2004b; Vinay et al., 2016; Walterspacher et al., 2011; Wang et al., 2016; Zelenkova &

Chomahidze, 2016). One early study that illustrates the chronic effects of breath training on

cardiac activity is presented by Bhargahva et al. (Bhargava et al., n.d.). These researchers

investigated the effects of a four-week pranayama breath-training program on indices of heart

rate and blood pressure during rest and extended breath holding in ten young male volunteers.

Following their program, they reported decreases in inspiratory (p<0.05) and expiratory (p

<0.001) heart rates, systolic and diastolic blood pressure (p <0.01), and differential changes in

galvanic skin resistance, a measure of sympathetic activity. These researchers explain the

attenuated tachycardia during extended breath holding was likely subsequent to enhanced

parasympathetic vagal tone given the findings of previous research, though their disparate results

for galvanic skin resistance make it difficult to make this conclusion.

27
 The findings of the previous study are reflected in a more recent investigation presented

by Pal et al. (Pal et al., 2004b). The researchers describe enhanced parasympathetic activity as

measured by significantly lower resting heart rates (pre 73.61±10.69 versus post 65.02±8.02;

p<0.05) in 30 male graduate students. These researchers also report lower heart rates

immediately following standing (pre 108.28±9.36 vs. post 101.18±8.45; p<0.05), and conclude

their results demonstrate enhanced vagal tone, given previous findings that the rise in heart rate

immediately following standing is an indication of autonomic nervous system activity. However,

this work only addresses acute modulations in vagal dominance and thus its relevance to chronic

adaptations may be limited.

Further support for the relationship between long slow breathing and enhanced

sympathovagal balance is provided by Santaella et al. (Santaella et al., 2011) in their

investigation of a four-week yogic breathing program in 19 (14 control, 15 training) elderly

patients. The primary findings of their study revealed the yoga-breathing group had significant

decreases in low frequency component of heart rate variability (control: pre 40 ± 13 v vs. post 41

± 13 v; yoga breathing: pre 40 ± 11 v vs. 27 ± 8 v; p=0.001). These results demonstrate a shift

towards parasympathetic dominance in autonomic modulation of cardiac rhythmicity. Given the

population sampled in this study, replication of the efficacy of their breath-program may be

limited to elderly populations.

One comprehensive theory that aims to describe the autonomic alterations is provided by

Ravinder et al. (Jerath et al., 2006) who describe that deep breathing induces a shift of the

autonomic nervous system towards parasympathetic dominance via stretch induced activation of

the slow adapting mechanoreceptors and generation of hyperpolarization currents from stretch of

lung tissue, which result in synchronization of the brainstem and hypothalamus. These alterations

28
result in parasympathetic dominance causing decreased heart rate, blood pressure, and oxygen

consumption. Further elucidation of this phenomena is provided by Eckberg (Eckberg, 2003)

who describes that respiratory activity modifies preganglionic vagal and sympathetic

motoneuron membrane potentials. As such, elongation of the expiratory portion of the breath

cycle results in vagal dominance and sympathetic withdrawal while the opposite occurs during

inspiration. A simple example of such phenomena is respiratory sinus arrhythmia, during which

heart rate accelerates during inspiration and decelerates during expiration (Yasuma & Hayano,

2004). The role of this interaction between the cardiovascular and respiratory systems may be

explained by potential energy conservation during expiration when gas diffusion across alveolar

membranes decreases, thus negating the necessity for increased perfusion to the pulmonary

capillary bed (Yasuma & Hayano, 2004).

Sympathetic Tone. While decreasing breath frequency and elongation of the expiratory

component of the respiratory cycle may increase vagal dominance, increasing breath frequency

through hyperventilation elicits an acute increase in sympathetic nervous system activity.

Läderach and Straub (Läderach & Straub, 2001) investigated the effects of voluntary

hyperventilation on glucostatic hormones in eight healthy males. During the 20 minutes of

hyperventilation, these researchers observed significant (p<0.05) increases in plasma free fatty

acids (0.35 ± 0.18 mmol/ L vs. 0.345 ± 0.18 mmol/ L; p=0.01), insulin (5.5 ± 2.4 mU/ L vs. 8.7 ±

2.7 mU/ L; p=0.03), cortisol (350.6 ± 65.4 nmol/ l vs. 429.5 ± 109.7 nmol/ l; p=0.01), glucagon

(91.0 ± 33.3 pg/ml vs. 100.9 ± 28.8 pg/ml; p=0.02), adrenaline (123.0 ± 63.6 pmol/l vs. 194.0 ±

88.9 pmol/l; p=0.01), noradrenaline (557.2 ± 256.9 pmol/l vs. 480.6 ± 201.1 pmol/l; p=0.01), and

heart rate (58 ± 6 bpm vs. 60 ± 6; p=0.01). While these authors do not address sympathetic

activation specifically, elevations of catecholamine concentrations would be indicative of

29
increased sympathetic activation. However, these results reflect only acute modulation of these

hormones, and consequently their role in chronic adaption is unclear.

Similarly, Telles et al. (Telles et al., 1996) noted increased sympathetic activation in 12

participants (four males, eight females) following 45 minutes of rapid yogic breathing. These

researchers observed significant (p<0.01) increases in sympathetic tone as measured by

decreased skin resistance (treatment: 461.3 ± 312.0 kohms to 183.0 ± 159.2 kohms; control: 440.

± 328.0 kohms to 306.0 ± 205.7 kohms), increased systolic blood pressure (treatment: 100.6 ±

9.8 mmHg to 110 ± 9.6 mmHg; control: 104.5 ± 10.1 mmHg to 101.7 ± 10.9 mmHg), oxygen

consumption (treatment: 257.4 ± 54.0 mL/min to 301.1 ± 51.1 mL/min; control: 251.65 ± 40.0

mL/min to 205.3 ± 59.2 mL/min), and digital pulse volume (treatment: 7.0 ± 2.0 mm to 3.8 ± 1.8

mm; control: 6.6 ± 4.6 mm to 6.7 ± 5.0 mm). However, these authors do not mention potential

chronic adaptations to this style of breathing, nor do they give implications for populations

outside obese and hypertensive populations. Consequently, the relevance of these data to athletic

performance is unclear.

Further demonstration of voluntary sympathetic activation through hyperventilation is

provided by Kox et al. (Kox et al., 2014). These researchers subjected participants to mild

endotoxemia following 5-9 days of voluntary hyperventilation, cold baths, and meditation to

address the effects of these modalities on sympathetic activation and attenuation of the innate

immune response. Their results demonstrate significantly larger basal epinephrine in their

training group (1.02 ± 0.22 vs. 0.35 ± 0.06 nmol/L, p = 0.007) and a rise in epinephrine during

hyperventilation (up to 5.3 nmol/L). These observations were paralleled with a significant

enhancement of immune function and attenuation of the immune response of endotoxin, as

measured my increased leukocytes, neutrophils, and monocytes, decreased TNF-α (53% lower),

30
IL-6 (57% lower) and IL-8 (51% lower) levels, and increased IL-10 (194% higher). While the

immune response described by these researchers is beyond the scope of the present review, their

findings regarding the trainable activation of the sympathetic nervous system are intriguing and

potentially relevant to athletic performance given the inflammatory and immune processes in

muscle remodeling (Aoi et al., 2004; Peake, Neubauer, Gatta, & Nosaka, 2016; Weisleder et al.,

2014). There are, however, methodical issues to consider in reviewing this article given their

training protocol was not comprised only of hyperventilation training, but also included cold

bathing and meditation. Consequently, the relative roles of these other factors on their findings

are potentially limiting to their application.

While the bulk of these studies do not address the effect of enhanced vagal or

sympathetic tone on exercise per se, the roles of each during sporting performance have been

clearly elucidated (Coote, 2010; Machhada et al., 2017). However, further research is warranted

to determine whether the vagal or sympathetic adaptations subsequent to breath training may be

beneficial to performance in athletic and performance contexts.

Chemosensitivity and energy systems

Another mechanism by which breath training may influence sport performance is via

altered chemo-sensitivity to hypoxia, hypercapnia, and maintenance of acid-base balance, given

repeated reductions in arterial oxygen and increases in arterial CO2 and acidosis. The effects of

breath holding, hyperventilation, and a combination of the two on endocrine response and acid-

base balance have been described (Djarova et al., 1986). Djarova et al. (Djarova et al., 1986)

found three maximal duration breath holds significantly (p < 0.05) decreased PO2 (81.1± 6.6

mmHg to 58.00±5.1 mmHg) and raised PCO2 (39.04 ± 1.76 mmHg to 45.7 ± 3.70 mmHg) while

hyperventilation raised PO2 (66.48 ± 14.4 mmHg to 89.40 ± 16.2 mmHg) and decreased PCO2

31
(36.27± 2.24 mmHg to 19.60 ± 1.6 mmHg). These researchers also describe elevated cortisol

(12.77 ± 5.87 ng / mL to 28.0 ±7.59 ng/ mL; p < 0.05) and human growth hormone (2.13 ± 2.10

ng / mL to 10.35 ± 8.28 ng / dL; p < 0.05) in the breath holding condition. While these data are

relevant to potentially enhanced recovery and sport performance, few studies have directly

investigated the effects of breath holding or breath patterns on similar endocrine parameters.

However, these data clearly demonstrate the effects of breathing or apnea on arterial gas

concentrations.

Bernardi et al. (Bernardi et al., 2001) investigated the effects of slow-breathing on the

chemoreflex response to both hypercapnia and hypoxia in 15 healthy participants (seven men,

eight women). Participants underwent either spontaneous or fixed frequency breathing (6 or 15

breaths per minute) in hypoxic and hypercapnic conditions. Their results demonstrated a blunted

chemoreflex to both hypoxia (-0.14 ± 0.03 l/min per % SaO2 vs. -0.46 ± 0.09 l/min per % SaO2;

p < 0.01) and hypercapnia (0.32 ± 0.07 l/min per % SaO2 vs. 1.38 ± 0.29 l/min per % SaO2; p

<0.001) during breathing at six breaths per minute compared to spontaneous breathing. These

researchers also describe preserved heart rate variability as measured by electrocardiogram in

their six breaths per minute condition compared to spontaneous breathing (713 ± 35 ms versus

680 ± 18ms; p<0.001). These researchers indicate that altered baroreflex activity may have been

the primary mechanism for their findings, but that altered vagal activity may have also played a

role in altered chemo-sensitivity to both hypoxia and hypercapnia. A primary limitation of this

study is these data represent only acute modulations in chemo-sensitivity and do not reflect

chronic adaptations that may arise following breath training.

Chronic adaptations to hypercapnia and hypoxia are reported consistently in breath-hold

divers (BHDs). In their investigation on the chronic respiratory adaptations in BHDs,

32
Walterspacher et al. (Walterspacher et al., 2011) performed lung function assessments in 12 elite

BHDs. Their results demonstrated increased mean pulmonary volumes (FEV1: 4.5 ± 0.02 L vs.

4.7 0.03 L; total lung capacity: 8.1 ± 0.8 L vs. 8.5 0.7 L; VC: 6.2 ± 0.6 L vs. 6.5 ± 0.5 L)

attenuated respiratory drive in response to 6 and 9% CO2 concentrations in ambient air.

However, these authors present only graphical representation of the ventilatory drive measures.

These researchers conclude that CO2 tolerance is likely a training adaptation as opposed to a

genetically inherited trait, given comparison of their results to their previous work. These results

are representative of the literature on BHDs, as similar chronic adaptations in breath hold divers

have been reported consistently (Andersson, Linér, Rünow, & Schagatay, 2002; Delapille et al.,

2001; Ferretti, 2001; Smith et al., 2014; Zelenkova & Chomahidze, 2016).

Another area in which breath training may significantly affect sporting performance is

through adaptations of respiratory musculature, namely, through attenuation of the respiratory

metaboreflex. This phenomenon is best illustrated in the work presented by Witt et al. (Witt,

Guenette, Rupert, McKenzie, & Sheel, 2007), who investigated the effects of a six-week

respiratory musculature training program on the sympathetically mediated increases in heart rate

(HR) and mean arterial pressure (MAP) during fatiguing respiratory work in sixteen healthy

men. Following training, participants in the training group demonstrated significantly (p < 0.05)

increased maximum inspiratory pressure (training: −125 ± 10 to −146 ± 12 cm H2O; sham: −141

± 11 to −148 ± 11 cm H2O) and attenuated rises in MAP and HR during their respiratory work

task (HR: 59 ± 3 to 74 ± 2 beats min−1; MAP: 84 ± 1 to 89 ± 2 mm Hg). These researchers

hypothesize that improved fiber type composition and enzyme profile likely improved the

aerobic capacity of the respiratory musculature, which aided in a decrease in metabolite

accumulation and subsequent attenuation of sympathetic mediated metaboreflex. Moreover,

33
these researchers conclude that their results have direct implications on athletic performance

given high work demands of the respiratory musculature during endurance and high-intensity

training.

Nociception

Anti-nociception presents another mechanism by which breath training may enhance

physical performance and athletic capacities (Birrer & Morgan, 2010; Ryan & Kovacic, 1966;

Walker, 1971). Paso et al. (Reyes del Paso et al., 2015) demonstrated anti-nociceptive effects in

their group of 38 healthy men and women in a breath hold condition during varying pain

intensities elicited with progressive algometric fingernail loading. Their data demonstrated

smaller increases in pain intensity (slow inhale: p<0.001, η2= 0.708 vs. breath hold: p= 0.018,

η2= 0.141), unpleasantness (slow inhale: p <0.001, η2= 0.141 vs. breath hold: p = 0.006, η2=

0.708), and greater heart rate deceleration (p = 0.047) in the breath holding condition. These

researchers suggest the anti-nociceptive effects may have been elicited by increased activity of

baroreceptors in the aortic arch and lungs implicated by a bi-phasic systolic blood pressure

response during the breath hold condition (p < 0.001) for all pain intensities during which blood

pressure initially rose in the first one to three seconds and decreased in seconds seven and eight

(pain intensity 1: p < 0.005; pain intensity 2-3: p < 0.007). These researchers suggest clinical

relevance for these results and do not mention implications for athletic performance, nor do they

indicate the potential for chronic adaption subsequent to breathing interventions.

Further support for the role of breathing on anti-nociception and cardiac-modulation is

provided by Chalaye et al. (Chalaye, Goffaux, Lafrenaye, & Marchand, 2009) in their

investigation of varying breathing conditions on thermal pain threshold and tolerance in 20

healthy adults (11 men, nine women). Their results demonstrated significantly (p<0.005) higher

34
pain threshold (1.0 ± 0.3 DS vs. -0.2 ± 0.3 DS; p = 0.002) and pain tolerance (0.5 ± 0.2 DS vs.

0.0 ± 0.1 DS; p = 0.003) in their slow breathing intervention during which participants breathed

at six breaths pre minute while measures of cardiac rhythmicity revealed significantly (p<0.005)

greater vagal tone as measured by peak-to-valley amplitude (0.296 ± 0.021 vs. 0.079 ± 0.008; p

< 0.001) and low frequency power heart rate variability (9,194 ±1433 ms2 vs. 751 ± 229 ms2; p

< 0.001). Peak-to-valley units of amplitude were not provided.

Busch et al. (Busch et al., 2012) also reported altered thermal pain perception following

six-weeks of attentive or relaxed deep slow breathing in 15 young (13 female, three male)

undergraduate students. In the attentive intervention (aDSB), participants were asked to breathe

according to biofeedback and external pacing, while in the relaxed intervention (rDSB) attention

was directed on each breath and was intended to induce a meditative state. In both interventions,

respiratory frequency was held at seven breaths per minute. Their results demonstrated that

stimulus detection (p = < 0.001; Cohen’s d = .88) and pain threshold (p = < 0.001; Cohen’s d =

1.01) were significantly increased only in their rDSB (aDSB: 37.86° C ± 2.87, 39.97 ± 3.35° C,

40.19 ± 3.22° C vs. rDSB: 39.76 ± 4.0° C, 40.23 ± 3.39° C, 41.36 ± 3.72° C). Similarly, skin

conductance (a measure of sympathetic activity) was decreased significantly (p = 0.002; Cohen's

d = 1.35) by 18% in their rDSB group only. While these data are not presented within the context

of athletic performance per se, they certainly illustrate the potential for chronic adaptations for

nociception following breath training, and potentially enhanced athletic performance. Further

research is warranted to investigate these findings in a sport or training specific environments.

35
Breath-training for athletic performance.

As described by Joulia et al. (Lemaître et al., 2010), apnea and breath training represents

a fertile area of research given the potential of these modalities to induce sporting relevant

physiological adaptions. While the potential of these modalities have yet to be fully understood,

many studies demonstrate the efficacy of breath training in improving athletic performance.

Studies utilizing breath frequency, apnea, and device guided breathing are presented.

Breath frequency training, deep slow breathing, and apnea. Lavin et al. (Lavin et al.,

2015) explored the effects of controlled-frequency breathing (CFB) on swimming performance

and running economy in 18 recreational swimmers. The CFB group demonstrated greater

decreases in 150 m swim time (CFB: -13 ± 9 s vs. control: 8 ± 19 s) and increases in running

economy (CFB: −15mL/kg/km vs. Control: −8 mL/kg/km). Kapus et al. (Kapus, Ušaj, &

Lomax, 2013) explored the effects of reduced breathing frequency on vital capacity and the

ventilatory response to hypercapnia. Their training protocol consisted of a progressive six-week

high-intensity interval program utilizing a fixed breathing frequency of 10 breathes per minute

during training sessions. Their results demonstrated reduced ventilatory sensitivity to

hypercapnia (experimental group: 31.46 ± 21.56 L / min/ kPa to 18.16 ± 13.23 L / min/ kPa vs.

control: 38.34 ±28.22 L / min/ kPa to 29.00 ± 10.10 L / min/ kPa; p = 0.03), and increased vital

capacity (CFB: 5.53 ± 1.16 L to 5.88 ± 0.96 L vs. control: 5.95 ± .4 L to 6.0 ± 0.32; p = .02) in

their controlled frequency breathing group.

Chronic adaptations to repeated exposures to hypoxia and hypercapnia are well

documented in elite breath hold divers. Roecker et al. (Roecker et al., 2014) investigated the

ventilatory responses to a graded exercise test in 24 male participants (8 breath hold divers, 8

scuba divers, 8 non-divers). The breath hold divers illustrated distinct ventilatory reactions to

36
maximal exercise in tandem with significantly (p < 0.01) lower lactate threshold, higher blood

lactate concentrations at respiratory compensation point (RCP), greater power output at RCP,

and lower end tidal CO2 and estimated arterial CO2 at lactate threshold, RCP, and VO2peak. The

region between lactate threshold and RCP took 43% ± 10% of VO2peak in the BHDs while the

same region was 23% ± 7% for the scuba divers and 24% ± 11% for their control group.

While the primary indication of this study is decreased chemo-sensitivity to hypercapnia

in the breath hold divers as noted by the delayed onset of RCP, their findings indicate a myriad

of chronic adaptations to repeated hypoxia and hypercapnia. These researchers explain increased

lactate load and delayed RCP would indicate enhanced anaerobic energy production in tandem

with increased buffering capacities, while the earlier onset of lactate threshold likely illustrates

the relative decrease in aerobic function in their breath hold divers. While the results presented in

this study are clearly relevant to the chronic adaptations of breath training and sporting contexts,

it must be noted that this is a cross-sectional examination and its relevancy across populations

may be limited.

Fabrice et al. (Joulia et al., 2003) investigated the effects of a 12-week apnea training

program on measures of blood acidosis and oxidative stress following dynamic handgrip

resistance exercise in eight well trained triathletes. The training protocol consisted of three

sessions per week of one-hour cycle efforts at predetermined 30% VO2max interspersed with 20

seconds of breath holding followed by 40 seconds of spontaneous breathing. Following their

program, the researchers noted an attenuated maximal rise in blood lactate (pre: +2.8± 0.34

mmol/L vs. post: 1.99 ± 0.22 mmol/L), reduced oxidative stress as measured by decreased

thiobarbituric acid reactive substance (pre: + 35± 10 mg/mL vs. post: +12± 4 mg/mL) and

erythrocyte reduced glutathione (pre: -2.82 ± 4 mg/100 mL vs. post: -1.16± 0.3 mg/100 mL)

37
responses, increased partial pressure of alveolar O2 (pre: 72 ± 3 mmHg vs. post: 79 ± 3 mmHg),

and decreased partial pressure of alveolar CO2 (pre: 46 ± 1 mmHg vs. post: 42 ± 1 mmHg).

These researchers purport their intervention attenuated oxidative stress, and sensitivity to

hypercapnia and hypoxemia during the handgrip exercise in tandem with enhanced buffering

capacity as noted by lower rises in lactate concentrations and decrease alveolar pressures of CO2

and attenuated falls in alveolar pressure of O2 (Joulia et al., 2003).

Woorons et al. (Woorons et al., 2008) demonstrated the potential of a four-week reduced

frequency breathing training program to delay blood acidosis during exercise in 15 male runners.

While their results did not demonstrate any differences in exercise performance between control

and hypoventilation groups, higher venous pH (p < 0.05) and higher HCO3- (p < 0.05) at 90%

heart rate max were found in the hypoventilation group. However, it is difficult to comment on

the physiological relevance of these increases as they did not provide the data and only indicated

the values in the hypoventilation group were higher compared to the control. As no differences

were observed between groups with regard to exercise performance, it is possible the impact of

these effects were marginal. Their occurrence warrants further investigation

Device guided breath training. Hepburn et al. (Hepburn et al., 2005) utilized a re-

breather device which provided resistance to the respiratory musculature while simultaneously

inducing a hypercapnic breathing environment. Their data showed enhanced work capacity (+

0.031 ± 0.022 J/heartbeat), cardiac vagal tone (HF: +13.2 ± 5.7 v; LF: -10.2 ± 5.5 v), and heart

rate recovery (3.3 ± 1.5 bpm) following a six-week training period. Further support for the use of

device guided breath training is provided by Porcari et al. (Porcari et al., 2016), who investigated

the effects of the commercially popular elevation training mask on aerobic capacity, lung

function, and hematological variables following a progressive six week high intensity interval

38
program. While their data did not show improvements in vital capacity, forced expiratory

volume, hemoglobin or hematocrit concentrations, they did demonstrate increased ventilatory

threshold (VT) (mask: +14.0 % vs. control: +2.1 %), power at VT (mask: +19.0 % vs. control:

9.2 %), respiratory compensation point (mask: +10.2 % vs. control: 1.0 %), and power at

respiratory compensation point (mask: +16.4% vs. control: 4.0 %).

While device assisted and controlled frequency breath training differ in modality, the

research indicates the similarities between the adaptations following their use may be due in part

to the hypercapnic environments produced in each context. Porcari et al. (Porcari et al., 2016)

hypothesize the mask acted as respiratory resistance and effectively increased the strength and

subsequent work capacity of the respiratory musculature. They also note the training mask

induced an increased partial pressure of CO2 (32.9 ± 6.0 mmHg CO2 vs. 55.6 ± 12.4 mmHg

CO2) and that hypercapnic breathing conditions may have caused additional respiratory

adaptation and subsequent fatigue resistance, though no descriptive statistics were provided.

Further support for device guided respiratory training is provided by HajGhanbari et al.

(HajGhanbari et al., 2013) in their comprehensive review of respiratory muscle training.

Given the balance of the research presented. It is clear that breath training in its various

forms has the potential to impact athletic performance. Differential adaptations to varying

modalities of breath training may induce adaptations more relevant to sports that require greater

reliance on aerobic energy systems than anaerobic. Given the role of respiratory musculature

during aerobic sporting events, adaptations that improve the mechanical and metabolic efficiency

of inspiratory and expiratory musculature may improve aerobic performance while their

relevancy in anaerobic contexts may be limited (HajGhanbari et al., 2013). Conversely, apnea

training results in adaptations specific to anaerobic metabolism, and consequently, may be best

39
suited for sporting events during which lactic anaerobic energy production is dominant (Roecker

et al., 2014; Woorons et al., 2008). Adaptations to enhance vagal tone are largely relevant to the

broad spectrum of sport, given their function in maintaining autonomic balance and potentially

improving recovery and perception (Anderson, 1998; Anderson et al., 2009; Delapille et al.,

2001; Hepburn et al., 2005; Jerath et al., 2006; Kiviniemi et al., 2014; Machhada et al., 2017;

Monnazzi et al., 2002; Pal et al., 2004b; Vinay et al., 2016; Walterspacher et al., 2011; Wang et

al., 2016; Zelenkova & Chomahidze, 2016). Consequently, sport specific adaptations should be

addressed in developing a methodology to address the efficacy of breath training on athletic

performance.

Consideration for study design and potential limitations

Prior to designing a study to address the efficacy of deep slow breathing in augmenting

anaerobic exercise performance, dependent variables, exclusion criteria, and inclusion criteria

must be established to select sensitive and accurate measures of recovery and to control for

population homogeneity with regard to training, sex, training history, injury, and supplement use.

Dependent Variables. A multitude of measures presently exist to objectively and

subjectively quantify fatigue and recovery between and within training sessions. Tests of

anaerobic capacity (Wingate; WAnT) serve the dual purpose as a test of performance (peak

power, mean power, total work) and a method to induce metabolic acidosis. Heart rate recovery

(HRR) and respiratory exchange ratio (RER) have been effective objective methods of

measuring recovery and buffering capacity, while sessions ratings of perceived exertion (sRPE)

has been consistently used as subjective measures of perception and recovery during and

following exercise.

40
 Heart Rate Recovery (HRR). HRR is a measure of autonomic recovery

(parasympathetic reactivation) and is defined as the rate at which heart rate decreases

immediately following exercise and has been projected as a strong indicator of mortality risk and

athletic readiness (Borresen & Lambert, 2008; Halson, 2014; Lamberts, Swart, Capostagno,

Noakes, & Lambert, 2009; Mayo, Iglesias-Soler, Fariñas-Rodríguez, Fernández-del-Olmo, &

Kingsley, 2016; Nishime, Cole, Blackstone, Pashkow, & Lauer, 2000; Seiler et al., 2007).

Lamberts et al. (Lamberts et al., 2009) evaluated the efficacy of HRR in predicting athletic

performance in a group of 14 trained cyclists that participated in a 4-week high intensity interval

training program. These researchers divided the 14 cyclists into two groups based on whether

HRR increased or decreased over the 4-week HIIT protocol (HRRincrease or HRRdecrease). The

HRRincrease group improved PP more than the HRRdecrease group during a 40 km time trial ride (p=

0.010) and demonstrated a tendency for faster 40-km time trial completions, while both groups

displayed improvements in relative PP (p= 0.001). These researchers conclude that HRR is an

effective measure by which to monitor and prescribe training loads, and predict performance in

athletic populations. In their comprehensive review, Daanen et al. (Daanen, Lamberts, Kallen,

Jin, & Van Meeteren, 2012) confirm the potential efficacy of measurements of HRR in

determining the recovery status in athletes.

Buffering: CO2 and Lactate. Lactate is a product of glycolytic ATP production and

historically has been viewed as a potential mechanism for the occurrence of fatigue during high

intensity exercise. Contemporary models of fatigue reveal decreased pH subsequent to ion

accumulation is more likely the culprit linking lactic acidosis to the development of fatigue

during exercise (Brooks, 2001; Goodwin, Harris, Hernández, & Gladden, 2007; Sahlin, 2014).

Lactate kinetics during and following exercise have been implicated in improvements in exercise

41
performance and recovery as illustrated by measurements of anaerobic threshold, onset of blood

lactate accumulation (OBLA), and their respiratory equivalents (ventilatory threshold and

respiratory compensation point) (Sahlin, 2014; Tanaka et al., 1983). Messonnier et al.

(Messonnier, Freund, Denis, Féasson, & Lacour, 2006) investigated the effects lactate of

clearance capacity on exhaustive exercise performance in eight active participants following

endurance training. Their results demonstrated improved performance during a 5-minute cycling

test at 90% PP output by 8% for PP output (p= 0.0687) and improved lactate clearance in the

following 90-minute recovery session (p< 0.05).

Intrinsic buffer systems regulate acid-base balance to maintain homeokinesis, which is

challenged by rising H+ concentrations during high intensity exercise (Böning et al., 2007;

Sahlin, 2014; Yunoki, Horiuchi, & Yano, 2000). The bicarbonate buffering system (equation 1)

offers proton acceptors in the form of bicarbonate (HCO3-):

Equation 1. H+ + HCO3- ⇌ H2CO3 ⇌ H2O + CO2 (Yunoki et al., 2000)

HCO3- binds hydrogen protons and produces excess CO2, which can be measured by gas

exchange analysis.

Yunoki et al. (Yunoki et al., 2000) found significant correlations between CO2excess (VO2

-VCO2), and peak blood lactate concentrations (Lapeak) in six male sprinters (r = 0.920, p< 0.01)

and seven long distance runners (r = 0.588 , p < 0.05). Similar results are provided by Yano et al.

(Yano, Yunoki, Matsuura, & Arimitsu, 2009) who described a significant relationship (r = 0.845)

between CO2excess and blood lactate concentrations in their group of eight male participants

during high intensity cycling intervals.

While bicarbonate buffering (βbi) represents the primary mechanism by which blood pH

is maintained during exercise, hemoglobin, phosphates, and blood proteins offer protection

42
against rising H+ concentrations during exercise. Boning et al. (Böning et al., 2007)

demonstrated the capacity of non-bicarbonate buffering (βnbi) estimated from measures of La,

HCO3-, pH, and PCO2 in trained and untrained males derived from the relationship between their

measured variables:

Equation 2: βnbi = –Δ [La] x ΔpH-1 – Δ [HCO3-] x ΔpH-1

With regard to total buffer capacity, their data demonstrated larger βbi + βnbi for the untrained

state (78± 2 mmol x L -1 vs. 68 ± 2 mmol x L -1; p < 0.02). These data demonstrate while buffer

capacity may relate to enhanced physical performance, other factors such as increased plasma

volume, greater hemoglobin, and an increase in La efflux efficiency may present larger

determinants of pH regulation in the trained state. However, their methods do allow for a distinct

comparison of extracellular βbi versus βnbi buffering capacities.

Respiratory exchange ratio (RER; VCO2 / VO2) demonstrates skeletal muscle’s oxidative

capacity and differentiates utilization of substrates utilized for energy production. Given the

relationship between HCO3- buffering and CO2 production, respiratory exchange ratio presents

another measure that effectively quantifies the amount of HCO3- buffering occurring as values

increase beyond one and excess CO2 is expired. (Ramos-Jiménez et al., 2008).

Wingate Anaerobic Test (WAnT). The rise in H+ concentrations during anaerobic

exercise presents the ability of anaerobic exercise to act as an acid-base titration model for the

human body in vivo. The Wingate anaerobic test (WAnT) has been utilized as a standard for

testing anaerobic power production and consistently raises blood La (Gratas-Delamarche, Le

Cam, Delamarche, Monnier, & Koubi, 1994; Vandewalle, Pérès, & Monod, 1987). The WAnT

consists of a maximal effort sprint on cycle ergometer against 0.075 kg x kg bodyweight-1

typically ranging from ten to 60 seconds in duration. Given the time course of bioenergetics

43
supply of ATP from creatine phosphate, shorter WAnTs target the phosphagen system while

longer (>20 sec) WAnT involve greater contributions from glycolytic and aerobic energy

systems and subsequently greater blood lactate accumulations (Attia et al., 2014; Baker et al.,

2010; Bogdanis et al., 1998). However, instrument type, duration, and type of recovery interval

have been shown to affect measures of WAnT performance.

Mechanically and electronically braked cycle ergometers have been utilized to perform

WAnTs. The Monark Ergometer 894E cycle ergometer is a mechanically braked cycle ergometer

designed specifically for the high forces produced during WAnTs (Astorino & Cottrell, 2012;

Hachana et al., 2012; Harbili, 2015). The Velotron Racermate (Racermate Inc., Seattle, WA) is

an electronically braked cycle ergometer that has been shown to produce test-retest reliability

during 30-second WAnTs for PP (r = 0.70, p <0.05), MP (r =0.90, p <0.01), and minimum

power (r = 0.79, p<0.05). PP was significantly (p<0.05) greater on the Racermate Velotron

(9.95±1.39 W / kg) compared to the Monark Ergometer 894E utilizing automated weight

(9.13±1.26 W / kg), while significantly greater MP was displayed on the Monark (6.95 ± 0.89 W

/ kg) compared to the Racermate Velotron (6.11 ± 0.52 W / kg) (Astorino & Cottrell, 2012).

Further validation for the use of the Velotron Racermate and electronically braked cycle

ergometers is provided elsewhere, while some articles suggest specific chain ring to maintain

validity during WAnTs (Astorino & Cottrell, 2012; Clark, Wagner, & Heath, 2017;

Micklewright, Alkhatib, & Beneke, 2006; Vandewalle et al., 1987). The potential variation

between ergometers with respect to measurement of PP and MP must be taken into account when

comparing results of these measures between studies.

Aside from duration and mode of WAnT, many researchers have utilized the WAnT in a

repeated sprint format with varying recovery interval durations and active versus passive

44
recovery. Repeated 30-second WAnTs with one and two-minute recoveries resulted in

significantly lower PP (one-minute, p<0.05; two- minute p<0.05) while one, two, and three-

minute recoveries resulted in significantly lowered MP across conditions (one minute, p<0.05;

two minutes, p<0.05; three minutes, p<0.05). Billaut et al. (Francois Billaut et al., 2003) found

recovery of PP following brief cycle sprints was significantly lower after only 15 and 30 seconds

of recovery (p < 0.001 and p < 0.05, respectively) compared to 60, 120, and 240 second

recoveries. However, these sprints only lasted 8 seconds in duration and their relevance to lactate

recovery are limited. Bogdanis et al. (Bogdanis et al., 1995) investigated the effects of 1.5, three,

and six minutes recoveries between two consecutive 30-second WAnTs. Their results

demonstrated rapid recovery of PP (88.7%) and pedal speed (93.5%) during the first three

minutes of recovery, a 3% increase of the MP in the first six seconds (MP6: 30) between the

three and six minutes recoveries, while MP throughout the second test (MP30; W) followed a

slower recovery than PP and MP6 for each recovery duration. Nearly full recovery of creatine

phosphate (resting 39.0 ± 3.2 mmol / kg; after 2nd interval 19.8 ± 3.5 mmol / kg; after 1st

recovery 39.9 mmol / kg) was demonstrated in a four minute passive recovery between three

consecutive 30-second maximal isokinetic bike sprints, while total work (kJ), MP, and

glycogenolysis decreased from 78.5% and 64.5%, 15% and 20%, and 32%, respectively, across

the three intervals (Spriet, Lindinger, McKelvie, Heigenhauser, & Jones, 1989). Active recovery

allows significantly greater recovery of PP (90 ±3% active versus 87 ± 3% passive) and MP (603

± 17 W active versus 589 ± 15 W passive) during four-minute recoveries between two

consecutive WAnTs. This was due to increased blood flow and subsequent removal of H+ and

metabolites and delivery of O2 down their respective concentration gradients.

45
 The WAnT presents the dual capacities as a test of anaerobic exercise performance and as

a method by which to induce metabolic acidosis. The use of electronically and mechanically

braked cycle ergometers has been validated for WAnT use while test duration and recovery

interval duration will affect the energy system targeted (phoshpagen versus glycolytic) and the

degree to which this energy system is recovered between efforts (shorter for phosphagen

compared to glycolytic). Active recovery intervals increase recovery of PP and MP between

WAnT intervals over passive recovery.

Sessions Rating of Perceived Exertion (sRPE). The (sRPE) is a tool developed by

Foster et al. (Foster et al., 2001) to quantify perceived training stress during non-steady state

exercise. These researchers utilized a two-part design in which 12 active participants first

completed maximal, steady state, and interval exercise on cycle ergometer during which HR,

blood lactate, and Borg RPE were tracked. The second part involved basketball practice during

which only HR and practice RPE were recorded. While session RPE derived training impulse

(TRIMP) was significantly larger than HR derived TRIMP scores across all 10 exercise

durations and intensities (30-minute steady state: 110 ± 24 bpm vs. 130 ± 57 RPE; 60-minute

steady state: 216 ± 39 bpm vs. 270 ± 63 RPE; 90-minute steady state: 350 ± 44 bpm vs. 432 ± 57

RPE; 30s/30s intervals: 107 ± 14 bpm vs. 131 ± 45 RPE; 60s / 60 s intervals: 117± 18 bpm vs.

148 ± 54 RPE; 120s / 120s: 114 ± 17 bpm vs. 146 ± 47 RPE; +10% interval: 114 ± 16 bpm vs.

136 ± 60 RPE; +25% interval; 117 ± 18 bpm vs. 148 ± 54 RPE; +50% interval: 114 ± 11 bpm vs.

161 ± 46 RPE; basketball: 652 ± 59 bpm vs. 744 ± 84 RPE; p< 0.05) regression analyses

revealed the session RPE method was consistent in determining training load. The researchers

conclude sRPE is an effective, consistent, and simple method by which to quantify subjective

training stress.

46
Nutrient Intake.

Given the potential for macronutrient and total kilocalorie intake to affect indices of

mean power, controlling for these variables is crucial in investigations that aim to identify

performance increases during exercise bouts which derive a majority of energy production from

glycolytic ATP production. Langfort et al. (50 ) compared the effects of moderate carbohydrate

(130 kJ/kg of body mass daily, 50% carbohydrate, 30% fat, 20% protein) and isocaloric low

carbohydrate (up to 5% carbohydrate, 50% fat, 45% protein) diets on indices of MP during 30-

second WAnTs. Their results demonstrated significantly diminished MP (533 ± 7 W vs. 581 ± 7

W; p < 0.05) and lactate concentrations (9.5 ± 0.4 mmol x L-1 vs. 10.6 ± 0.5 mmol x L-1; p <

0.05) in the low carbohydrate group. Similar data has been presented by Simonsen et al.

(Simonsen et al., 1991) in their investigation on the effects of moderate (5 g x kg-1 x day-
1
) versus high (10 g x kg-1 x day-1) carbohydrate diets on mean power during rowing efforts.

Their results illustrate 65% greater muscle glycogen content (p <0.05) and significantly greater

mean power output increases (10.6 % versus 1.6%; p < 0.05) in the high carbohydrate group.

These results clearly demonstrate the necessity of controlling carbohydrate intake during testing

procedures that derive a significant source of ATP production form glycolysis

Inclusion and Exclusion Criteria

Previously resistance trained individuals have shown attenuated muscle damage and

enhanced recovery following successive bouts of resistance exercise [69]. Newton et al. [69]

reported attenuated muscle function reduction following 30 eccentric elbow extensions in

resistance-trained individuals compared to the untrained group as noted by decreased rises in CK

(Trained: 2-fold increase, Untrained: 20-fold increase; p =0.007) and greater decrements in

47
isometric torque (Trained: -25%, Untrained: -47%). These results are mirrored in the data

provided by Zourdos et al. [70] which showed attenuated decrements in isometric torque at 24

hrs post exercise (Session 1: -8%, Session 2: no change from baseline) though p-values were not

provided. This protective mechanism has been previously referred to as the repeated bouts effect

(RBE) and persists for up to 6 months following a bout of resistance training [71].

Prior injury reduces skeletal muscle function. Holder-Powell et al. [72] demonstrate the

long term effects of lower extremity injury on decrements on isometric peak torque in injured

compared to uninjured limbs (p=0.001). Similar results are presented in a later study, which

demonstrated decrements in concentric isometric (Injured: Uninjured: 90.47 ± 13.7%; p=0.003),

concentric isokinetic strength (30°s-1: 84.07 ± 14.2%; p= .0001; 120°s-1: 89.37 ± 17.8%; p=

.0015), and eccentric isokinetic strength (30°s-1: 83.07 ± 15.3%; p=0 .0001) [73].

Summary

A review of the pertinent literature around breath training identifies autonomic, chemo-

sensitive, anti-nociceptive, and endocrine mechanisms that potentially explain how breath

training may augment athletic performance and recovery within or between training sessions.

Adaptations to the respiratory musculature may be more relevant to aerobic sporting efforts

while enhanced buffering and anaerobic metabolism may have greater positive effects on

sporting effects in which ATP production from anaerobic energy systems is dominant. Other

adaptations, including enhanced vagal tone and augmented endocrine profile, may have

relevance across the sporting spectrum given their role in recovery and general health contexts.

However, a large majority of this literature has not been conducted within the realm of sport

performance, so the ability to generalize the results across populations may be limited. Further

48
research is warranted to elucidate the potential of breath training on indices of performance and

recovery within athletic populations. The aim of the proposed article is to address the null

hypothesis that breath-training will have no effect on measures of performance and recovery

during anaerobic interval exercise.

49
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Appendix A: Journal of Sport Science and Medicine Guidelines

Journal of Sport Science and Medicine

Journal guidelines to authors:

https://www.jssm.org/newauthors.php

65
Appendix B: Raw Data

Subject Group Age (Years) Height (cm) Weight (kg)

1 1 24 171.45 75
5 1 23 187 92.7
6 1 27 182.88 90.11
9 1 19 187.96 80.4
10 1 19 185.42 71.36
13 1 24 181.61 73.6
17 1 24 186.69 92.3
18 1 24 184 85
19 1 26 175 72.9
20 1 35 175.26 71.36
2 2 28 175.26 72
3 2 28 170.18 70.5
4 2 28 186 96.4
7 2 26 173 67.6
8 2 21 185.42 90.68
11 2 27 190.5 84
12 2 30 181.6 80.45
14 2 26 172 66.4
15 2 22 182.88 79
16 2 25 172.72 85.45

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Subject Group MEAN PWR MEAN PWR 2 MEAN PWR 3 MEAN PWR 1 MEAN PWR 2 MEAN PWR 3
1_Pre (W) PRE (W) PRE (W) Post (W) Post (W) Post (W)
1 1 550.56 484.23 442.35 532.89 489.62 457.21
5 1 621.04 506.97 433.29 602.26 539.35 468.71
6 1 635.68 580.6 581.45 646.88 637.69 591.11
9 1 620.78 580.8 592.97 646.65 618.08 592.66
10 1 586.99 541.59 488.77 630.86 549.03 466.57
13 1 607.86 519.55 439.69 593.1 532.43 464.32
17 1 742.45 632.8 588.44 731.94 664.51 588.63
18 1 680.21 627.24 607.75 643.25 598.71 577.53
19 1 581.75 458.5 370.96 582.34 477.5 388.48
20 1 596.08 566.98 531.79 639.41 571.36 517.82
2 2 570.12 516.81 470.95 570.12 516.81 470.95
3 2 511.09 481.43 430.47 511.09 511.09 430.47
4 2 681.79 570.06 515.6 669.32 596.12 541.89
7 2 505 450.15 371.99 494.72 418.14 -
8 2 651.2 537.67 450.65 680.43 550.91 464.59
11 2 673.81 620.84 579.37 673.81 620.84 579.37
12 2 635.8 493.7 - 580.32 455.12 420.47
14 2 510.8 451.66 411.23 484.47 450.63 401.87
15 2 713.87 509.4 445.54 667.81 509.94 415.8
16 2 666.86 442.5 294.67 688.89 534.66 496.52

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Subject Group VCO2 1 Pre VCO2 2_Pre VCO2 3 Pre VCO2 _ VCO2 2 VCO2 3
(L/min) (L/min) (L/min) Post (L/min) Post (L/min) Post (L/min)
1 1 2.42 2.21 1.89 2.36 2.11 1.87

5 1 2.76 2.22 2.49 2.73 2.41 1.99

6 1 2.76 2.14 2.25 2.62 2.48 2.21

9 1 2.50 2.62 2.31 2.62 2.49 1.96

10 1 2.54 2.54 2.26 3.21 2.56 2.33

13 1 2.69 2.08 2.08 2.56 2.02 1.83

17 1 2.94 2.38 2.76 3.00 2.61 2.56

18 1 3.03 2.29 2.34 2.72 2.44 2.30

19 1 2.40 1.81 1.74 2.69 2.03 1.88

20 1 2.62 2.62 2.20 2.99 2.60 2.17

2 2 2.42 1.82 1.56 2.41 2.08 1.85

3 2 1.88 1.91 1.71 2.27 1.96 1.74

4 2 2.75 2.43 2.13 2.72 2.46 2.38

7 2 2.37 1.60 1.44 2.13 1.64 -

8 2 2.59 2.08 2.08 2.87 2.43 1.91

11 2 2.62 2.49 2.24 2.49 2.44 2.43

12 2 2.02 1.92 - 2.68 1.96 1.76

14 2 2.17 1.87 1.68 2.14 1.67 1.52

15 2 2.70 1.92 2.43 2.38 1.95 2.33

16 2 2.93 2.19 1.66 2.33 2.53 2.20

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Subject Group VE 1 Pre (L/min) VE 2 Pre (L/min) VE 3 Pre (L/min) VE 1 Post (L/min) VE 2 Post (L/min) VE 3 Post (L/min)

1 1 58.84 74.87 67.99 67.99 64.76 64.76

5 1 91.30 98.64 104.33 78.78 79.08 80.34

6 1 80.87 73.37 88.63 67.70 74.97 72.07

9 1 72.63 88.54 90.88 74.20 77.23 82.69

10 1 72.90 92.83 92.79 82.92 98.80 99.81

13 1 81.12 81.00 76.82 70.26 74.34 61.09

17 1 82.70 88.68 97.52 85.91 103.86 101.64

18 1 82.11 80.64 95.74 84.63 91.68 97.37

19 1 59.22 65.12 66.38 71.11 74.41 80.15

20 1 65.18 96.72 79.95 83.64 96.20 86.72

2 2 76.85 73.67 63.14 68.06 70.79 73.60

3 2 47.66 52.39 53.81 49.06 53.43 54.30

4 2 63.06 67.52 75.12 67.76 67.56 86.40

7 2 67.59 56.82 68.94 50.27 52.17 -

8 2 79.59 83.12 89.00 84.40 86.40 88.73

11 2 74.97 85.83 78.72 74.82 85.50 78.28

12 2 63.37 78.26 - 69.29 67.31 65.81

14 2 62.80 67.26 60.49 58.95 61.64 62.55

15 2 91.46 81.56 90.11 72.05 84.61 86.36

16 2 85.84 92.84 82.25 79.20 91.93 90.30

69
Subject Group HRR 1 HRR 2 HRR 3 HRR 1 HRR 2 HRR 3
Pre (bpm) Pre (bpm) Pre (bpm) Post (bpm) Post (bpm) Post (bpm)
1 1 41 20 29 29 27 30

5 1 28 30 25 35 34 33

6 1 34 25 26 47 37 37

9 1 55 61 46 50 43 46

10 1 20 17 16 21 17 10

13 1 24 34 40 32 32 33

17 1 20 15 14 21 12 12

18 1 30 28 27 27 32 27

19 1 32 19 16 22 18 14

20 1 37 23 20 40 34 21

2 2 46 23 30 27 - 31

3 2 73 59 50 76 51 54

4 2 31 29 35 23 23 32

7 2 32 40 48 39 24 -

8 2 23 18 16 21 14 17

11 2 30 36 37 27 31 34

12 2 70 23 - 25 4 12

14 2 38 31 28 35 29 27

15 2 - 16 26 23 19 17

16 2 16 26 49 - - -

70
 MVV Pre MVV Post
Subject Group VC PRE (L) VC Post (L) FEV1 Pre (L) FEV1 Post (L)
(L/min) (L/min)
1 1 5 4.9 4.3 4 191 152

5 1 6.1 6.2 4.8 4.3 195 187

6 1 6 5.6 3.8 4.4 202 197

9 1 4.2 5 3.8 3.7 152 171

10 1 5.3 5.1 4.3 4.5 157 166

13 1 6.2 6.1 4.8 4.9 160 201

17 1 5.9 5.9 4.5 4.7 205 214

18 1 5.3 6.8 5.1 4.7 195 216

19 1 4.2 4.8 4.1 4.2 187 155

20 1 4.8 4.5 4.4 4.2 183 179

2 2 5.2 5.1 4 3.9 155 164

3 2 4 4.2 3.5 3.4 154 122

4 2 5.2 5.2 4.1 4.3 172 198

7 2 5.1 5.1 4.3 4.5 210 205

8 2 6 6.1 4.9 5.5 190 204

11 2 7.4 7.3 4.8 4.3 160 132

12 2 5.9 6.2 4.5 4.6 191 192

14 2 4.7 4.8 3.9 4 90 114

15 2 5.3 5.3 4.1 4.1 185 189

16 2 5.7 6 3.7 3.9 173 163

71
Appendix C: Statistical Analysis

Mean Power:

72
VCO2:

73
HRR:

VC:

FEV1:

MVV:

74
Pearson Correlation between MP and VCO2:

75