pre -conditioning with peristaltic external pneumatic...draft 1 1 word count (text and references):...

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Pre-Conditioning with Peristaltic External Pneumatic

Compression Does Not Acutely Improve Repeated Wingate Performance nor Alter Blood Lactate Concentrations During

Passive Recovery Compared to Sham

Journal: Applied Physiology, Nutrition, and Metabolism

Manuscript ID apnm-2015-0247.R1

Manuscript Type: Brief communication

Date Submitted by the Author: 15-Jul-2015

Complete List of Authors: Martin, Jeffrey; Edward Via College of Osteopathic Medicine - Auburn Campus, Cell Biology and Physiology Friedenreich, Zachary; Quinnipiac University, Physical Therapy Borges, Alexandra; Quinnipiac University, Biomedical Sciences Roberts, Michael; Auburn University, Kinesiology

Keyword: athlete performance < athlete performance, physiology < physiology, exercise performance < exercise, recovery < exercise, massage therapy < therapy

https://mc06.manuscriptcentral.com/apnm-pubs

Applied Physiology, Nutrition, and Metabolism

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Word Count (Text and References): 2706 1

Abstract Word Count: 69 2

References: 14 3

Table Count: 0 4

Figure Count: 1 5

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Pre-Conditioning with Peristaltic External Pneumatic Compression Does Not Acutely 8

Improve Repeated Wingate Performance nor Alter Blood Lactate Concentrations 9

During Passive Recovery Compared to Sham 10

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Running Head: Pre-conditioning with Peristaltic Pneumatic Compression and Repeated 13

Anaerobic Exercise Performance 14

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Jeffrey S. Martin1,3*

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Zachary D. Friedenreich2 18

Alexandra R. Borges2

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Michael D. Roberts1,3

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22 1 Department of Cell Biology and Physiology, Edward Via College of Osteopathic Medicine – 23

Auburn Campus, Auburn AL USA 36832. 24 2 Department of Biomedical Sciences, Quinnipiac University, Hamden, CT USA 06518. 25

3 School of Kinesiology, Auburn University, Auburn, AL USA 36849. 26

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E-mail addresses 29

Jeffrey S. Martin: [email protected] 30

Zachary D. Friedenreich: [email protected] 31

Alexandra R. Borges: [email protected] 32

Michael D. Roberts: [email protected] 33

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*Corresponding Author: 36

Jeffrey S. Martin, Ph.D. 37

Edward Via College of Osteopathic Medicine – Auburn Campus 38

Department of Cell Biology and Physiology 39

910 S. Donahue Dr. 40

Auburn, AL USA 36832 41

Tel: (334) 442-4007 42

Email: [email protected] 43

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Disclosures: Funding was provided, in part, by NormaTec USA (Newton, MA) for this study. 46

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ABSTRACT 1

Application of dynamic external pneumatic compression (EPC) during recovery from 2

athletic activities has demonstrated favorable effects on flexibility, soreness, swelling and blood 3

lactate (BLa) concentrations. However, the effects of “pre-conditioning” with a peristaltic pulse 4

EPC device on subsequent performance and BLa concentrations have not been characterized. 5

Herein, we demonstrate that pre-treatment for 30-min with EPC has no effect on subsequent 6

supramaximal exercise performance or BLa concentrations during passive recovery. 7

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Keywords: Intermittent Pneumatic Compression Devices; Athletic Performance; Lactic Acid; 9

Devices; Exercise Therapy; Sports Medicine; Exercise; Regional Blood Flow; Nitric Oxide; 10

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INTRODUCTION 1

Dynamic external pneumatic compression (EPC) use in athletic recovery paradigms has 2

demonstrated favorable effects on flexibility (Sands et al. 2014b), muscle soreness (Sands et al. 3

2014a), and muscle swelling (Chleboun et al. 1995). Moreover, dynamic EPC has been shown 4

to improve local contractile capacity in a model of acute recovery from a fatigue protocol 5

(Wiener et al. 2001). We recently demonstrated that 30 minutes of dynamic EPC during 6

recovery from repeated Wingate Anaerobic Tests (WAnT) significantly lowered blood lactate 7

(BLa) concentrations compared to passive recovery (Martin et al. 2015b). We also recently 8

found that vascular reactivity was improved systemically in the muscular conduit arteries and 9

locally in the resistance arteries of healthy subjects following 1 hour of dynamic EPC (Martin et 10

al. 2015a). Given the role of vascular reactivity and nitric oxide (NO) bioavailability in exercise 11

induced hyperemia and metabolite clearance (Maiorana et al. 2012), it follows that “pre-12

conditioning” with EPC may also improve BLa clearance following an intense exercise effort. 13

Therefore, the purpose of this study was to evaluate the effects of a single 30 min EPC bout on 14

subsequent repeated bouts of supramaximal exercise and BLa concentrations during passive 15

recovery. 16

MATERIALS AND METHODS 17

Subjects 18

Ten (n=10) Division I men’s college hockey players were recruited for participation in 19

this crossover design study during their off-season. Subject characteristics were as follows 20

(mean ± SD): age, 22.8 ± 1.1 years; body mass, 84.7 ± 3.9 kg; height, 181.4 ± 4.9 cm; and body 21

fat, 12.7 ± 1.3%. This study was approved by the Quinnipiac University Institutional Review 22

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Board and written informed consent was obtained from all participants prior to their 1

participation. 2

Procedures 3

All participants reported for a total of 3 visits: (a) familiarization session, (b) testing 4

session 1, and (c) testing session 2. Visits were separated by 3-7 days. At study entry, each 5

subject was randomly assigned to 1 of 2 groups: EPC at testing session 1 and sham at session 2, 6

or vice versa. 7

For all sessions, subjects reported to the Quinnipiac University Cardiovascular 8

Laboratory in a rested, hydrated, post-prandial state (> 2 hours) and had abstained from caffeine, 9

alcohol and strenuous exercise for at least 48 hours. Participants were also instructed to maintain 10

normal dietary habits throughout the study and replicate their 24-hour diet for subsequent visits. 11

All testing was performed at the same time of day for each subject to control for diurnal 12

variation. 13

Familiarization Session 14

At least 72-hours prior to the first testing session, all participants reported to laboratory to 15

become familiarized with the WAnT and expectations for the protocol. At this time, the 16

investigator explained and demonstrated the procedures and instructed the subject through a 30-17

second WAnT, 3 minutes of active rest (pedaling at 70 rpm against minimal resistance), and 18

initiation of a second WAnT. All subjects were instructed, on the investigators verbal command, 19

to maximally accelerate at the start of the WAnT and maintain a maximal effort throughout the 20

30-second test. 21

Testing Sessions 22

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Upon reporting to the laboratory, adherence with dietary and physical activity guidelines 1

was confirmed with each subject. Thereafter, height and body mass (weigh beam scale with 2

height rod; Detecto 439, Webb City, MO USA), body fat (bioelectrical impedance analysis; 3

OMRON HBF306C, Kyoto, Japan), and heart rate (HR; Polar FT1, Polar Electro, Kempele, 4

Finland) were measured. In addition, resting BLa was evaluated via fingertip blood sample 5

collected with a single-use contact-activated lancet. A Lactate Scout portable lactate analyzer 6

(EKF Diagnostics, Cardiff, Wales, UK) was used for BLa measurement. Fingertip capillary 7

blood sampling was performed following cleaning and drying of the site with sterile techniques, 8

using an alcohol swab and gauze pad, respectively. 9

Following baseline measurements, subjects were treated with EPC or sham for 30 10

minutes. Thereafter, the cycle ergometer (894E Peak Test Cycle, Monark Exercise AB, 11

Vansbro, Sweden) seat height and position were adjusted for the subject, BLa was measured 12

again, and a 5-minute warm-up period began by pedaling against minimal resistance at ~70rpm. 13

Following the warm-up, subjects were instructed to start the WAnT as described in the 14

familiarization test and the brake weight resistance (7.5% of subject’s body mass) was applied 15

automatically when the subject reached 100 rpm. Immediately following the completion of the 16

first 30-second WAnT (WAnT1), brake weight resistance was removed and the subject was 17

instructed to pedal at ~70 rpm until the second WAnT (WAnT2) commenced 3 minutes 18

following WAnT1. The same procedure was employed following WAnT2 for transition to 19

WAnT3. After completion of WAnT3, subjects were instructed to pedal at ~70 rpm for 1 minute 20

followed by dismount from the bike and translocation to a treatment table for a 30 minute 21

passive rest recovery period. 22

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At exactly 5 minutes following WAnT3, BLa concentration was measured. Moreover, 1

BLa concentration was evaluated 10 and 15 minutes thereafter (15, 30 minutes post-WAnT3). 2

HR was recorded prior to and immediately following each of the WAnTs, as well as at 5 minute 3

intervals throughout the recovery period. Peak power, mean power, and the fatigue index were 4

measured as parameters of anaerobic cycling performance and recorded through a PC interface. 5

Peak power was calculated as the highest running average of 1 second (Watts), average power 6

was calculated as the mean power of the entire 30-second test (Watts), and the fatigue index was 7

calculated as the percentage change in power output between the first and last five seconds of the 8

30-second test. 9

Treatments (EPC and Sham) 10

A dynamic, sequential pulse EPC device (NormaTec, Newton Center, MA, USA) was 11

used for treatments. Briefly, the EPC device consists of two separate “leg sleeves” which 12

contain five circumferential inflatable chambers (arranged linearly along the limb) encompassing 13

the leg from the feet to the hip/groin. The “leg sleeves” are connected to an automated 14

pneumatic pump at which target inflation pressures for each zone and the duty cycle can be 15

controlled. However, the unit is commercially marketed with pre-programmed defaults for the 16

duty cycle and recommended inflation pressure settings. In this study, we chose to use the 17

recovery protocol recommended by the manufacturer which consists of target inflation pressures 18

of ~70mmHg for each chamber. The device and compression protocol has been described in 19

detail previously (Martin et al. 2015b). 20

The sham treatment condition consisted of 30 minute application of the EPC “leg 21

sleeves” and connection to the pneumatic pump, without actual compression. This protocol was 22

employed to control for any thermogenic effect as heat loss from the legs is likely affected. A 23

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lower pressure treatment was not employed for the sham treatment given the potential for even 1

very low pressures having an effect on the study outcomes. 2

Statistical Analysis 3

Subject HR and BLa concentrations at baseline between treatment conditions were 4

evaluated using paired t-tests. Continuous primary outcome variables were analyzed by two-way 5

repeated measures ANOVA and partial eta squared (��) values were calculated as estimates of 6

effect size using Cohen’s guidelines of small, medium and large effects (��=0.01, 0.09 and 0.25, 7

respectively) (Cohen 1992). When a significant main effect of time was observed, between time 8

point differences, on average (i.e. collapsing across treatments), were evaluated using paired t-9

tests with Bonferroni correction for multiple comparisons. Bonferroni corrected p-values are 10

presented in these instances. Paired t-tests and Cohen’s d effect sizes were also used to analyze 11

treatment effects on the overall fatigue index and BLa concentration area under the curve (AUC) 12

with d values of 0.2, 0.5, and 0.8 corresponding to small, moderate and large effect sizes, 13

respectively. AUC analysis using the trapezoidal method was performed for BLa from 5 to 35 14

minutes of recovery. An alpha level of P < 0.05 was required for statistical significance. Data 15

are presented as mean ± SD and [brackets] indicate 95% confidence intervals around the mean. 16

All statistical analyses were performed using SPSS version 23.0 for Windows (SPSS, Chicago, 17

IL, USA). 18

RESULTS 19

All subjects completed the entire study protocol without incident. No significant 20

differences between trials were observed for HR (66 ± 11 bpm vs. 64 ± 12 bpm, for EPC and 21

sham, respectively; P=0.597), or BLa concentrations at baseline (2.0 ± 0.9 mmol/L vs. 1.7 ± 0.8 22

mmol/L for EPC and sham, respectively; P=0.529). 23

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Parameters of anaerobic cycling performance are shown in Figure 1 (panels A-C). A 1

main effect of time (P<0.001, ��=0.884), but no main effect of treatment (P=0.309, ��

�=0.114) or 2

time*treatment interaction (P=0.928, ��=0.008) was observed for peak power with the 3

consecutive WAnTs. Similarly, a main effect of time (P<0.001, ��=0.944) but no main effect of 4

treatment (P=0.217, ��=0.164) or time*treatment interaction (P=0.600, ��

�=0.055) was observed 5

for average power. Between time point differences, on average, illustrating the main effect of 6

time for peak power and average power are presented in Figures 1A and 1B, respectively 7

(P<0.002 for all significant differences). No main effect of time (P=0.093, ��=0.469), treatment 8

(P=0.889, ��=0.052) or time*treatment interaction (P=0.908, ��

�=0.063) was observed for the 9

fatigue index during consecutive WAnTs (Figure 1C). Moreover, the overall fatigue index (ratio 10

of peak power during the first 5 seconds of WAnT1 and last 5 seconds of WAnT3; 57.6 ± 9.4% 11

vs. 58.1 ± 6.3% for EPC and sham, respectively) was not different between treatments (-0.51 ± 12

9.06% [-7.00, 5.97]; P=0.862; d=0.07) 13

For HR measured immediately before and following the consecutive WAnTs, a main 14

effect of time (P<0.001; ��=0.957), but no main effect of treatment (P=0.475; ��

�=0.058) or 15

time*treatment interaction (P=0.647; ��=0.041) was observed (Figure 1D). HR responses 16

during 30 minutes of passive recovery demonstrated a main effect of time (P<0.001; ��=0.975), 17

but no main effect of treatment (P=0.141; ��=0.225) or time*treatment interaction (P=0.180; 18

��=0.134) (Figure 1E). Between time point differences, on average, illustrating the main effect 19

of time are presented in figures 1D and 1E (P<0.05 for all). 20

BLa concentrations following EPC and sham were 1.99 ± 0.71 and 1.94 ± 0.84 mmol/L, 21

respectively. No significant main effect of time (P=0.639; ��=0.026), main effect of treatment 22

(P=0.440; ��=0.068) or time*treatment interaction (P=0.743; ��

�=0.013) was observed for 23

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treatment-mediated changes in BLa concentrations at rest (i.e. before WAnT1). For BLa 1

concentrations during 30 minutes of recovery, a main effect of time (P<0.001; ��=0.918), but no 2

main effect of treatment (P=0.364; ��=0.092) or time*treatment interaction (P=0.271; ��

�=0.279) 3

was observed. Between time point differences, on average, illustrating the main effect of time 4

are presented in Figure 1F (P<0.003 for all). AUC for BLa concentrations during recovery (9.2 5

± 1.6 vs. 9.7 ± 2.0 mmol/L/min for EPC and sham, respectively) were not different during 6

recovery between groups (-0.4 ± 1.5 mmol/L/min [-1.48, 0.63]; P=0.250; d=0.24). 7

DISCUSSION 8

Given our prior data demonstrating that EPC increases vascular reactivity at rest (Martin 9

et al. 2015a) and significantly reduces BLa concentrations following repeated WAnTs (Martin et 10

al. 2015b), we hypothesized that EPC pre-conditioning may have potentiated greater metabolite 11

clearance during multiple WAnTs. Notwithstanding, we report that pre-conditioning with EPC 12

does not alter peak BLa concentrations observed following intense exercise, nor the subsequent 13

decline in circulating BLa concentrations during passive recovery. Granted, given the present 14

data set, we cannot determine if BLa production and/or clearance are affected by pre-15

conditioning with EPC, only that circulating concentrations do not differ between treatment 16

conditions. Ultimately, while reducing BLa concentrations during recovery may be a desired 17

effect, the fact that pre-conditioning with EPC does not alter peak BLa levels following intense 18

exercise suggest that it does not mitigate the exertion-induced increase in BLa. This is a 19

particularly important point when considering that skeletal muscle acidity has been suggested to 20

play a role in preserving and/or improving muscle force (Allen et al. 2008). 21

Recent studies in athletes have shown nitrate supplementation to increase endurance 22

performance by potentially increasing NO bioavailability and blood flow to working muscle 23

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(Cermak et al. 2012, Handzlik and Gleeson 2013). To this end, EPC has been shown to enhance 1

blood flow and skeletal muscle NO production (Martin et al. 2015a, Kephart et al. 2015). In 2

addition, multiple models of dynamic compression have been shown to acutely increase 3

intramuscular gene expression patterns related to mitochondrial biogenesis and vascular biology 4

(Sheldon et al. 2012, Kephart et al. 2015). However, herein we report that pre-conditioning with 5

EPC does not acutely improve performance and/or mitigate fatigue during subsequent, repeated 6

WAnTs tests. 7

Our null performance findings with EPC pre-conditioning may have arisen from multiple 8

factors including: a) performance during repeated WAnTs may largely hinge upon the ATP/PCr 9

bioenergy system and be less reliant on an enhancement in lower limb blood flow, and it is likely 10

that pre-conditioning with EPC does not enhance the former metabolic pathway; b) while 11

application of EPC enhances lower limb vascular reactivity and blood flow, these pre-12

conditioning effects may be largely negated at the onset of exercise during high intensity muscle 13

contractions; and c) a relatively small sample size with highly variable performance measures 14

resulting in low observed power (<0.25) to detect a treatment effect. Finally, it is important to 15

note that we only investigated peripheral fatigue and the effect of EPC on central factors (e.g. 16

descending motor drive), which may play a role in performance fatigue (Rattray et al. 2015), is 17

largely unknown. Thus, although acute pre-conditioning with EPC does not appear to be 18

effective for improving subsequent repeated supramaximal cycling efforts, future studies should 19

continue to investigate the potential ergogenic effects of EPC in acute and chronic application 20

models. 21

ACKNOWLEDGEMENTS 22

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The authors wish to thank Brian Fairbrother, ATC for his assistance with participant 1

recruitment and study organization, the study participants for their time and effort. 2

CONFLICTS OF INTEREST 3

Partial support (~50%) for consumable costs associated with this study was provided by 4

NormaTec USA (Newton Center, MA USA) through a contract awarded to the corresponding 5

author (J.S.M.). However, the authors have no conflict of interest to disclose. 6

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REFERENCES 1

Allen, D.G., Lamb, G.D., and Westerblad, H. 2008. Skeletal Muscle Fatigue: Cellular 2

Mechanisms. Physiol. Rev. 88(1): 287–332. doi: 10.1152/physrev.00015.2007. 3

Cermak, N.M., Gibala, M.J., and van Loon, L.J.C. 2012. Nitrate supplementation’s improvement 4

of 10-km time-trial performance in trained cyclists. Int. J. Sport Nutr. Exerc. Metab. 5

22(1): 64–71. 6

Chleboun, G.S., Howell, J.N., Baker, H.L., Ballard, T.N., Graham, J.L., Hallman, H.L., Perkins, 7

L.E., Schauss, J.H., and Conatser, R.R. 1995. Intermittent pneumatic compression effect 8

on eccentric exercise-induced swelling, stiffness, and strength loss. Arch. Phys. Med. 9

Rehabil. 76(8): 744–749. doi: 10.1016/S0003-9993(95)80529-X. 10

Cohen, J. 1992. A power primer. Psychol. Bull. 112(1): 155–159. doi: 10.1037/0033-11

2909.112.1.155. 12

Handzlik, M.K., and Gleeson, M. 2013. Likely Additive Ergogenic Effects of Combined 13

Preexercise Dietary Nitrate and Caffeine Ingestion in Trained Cyclists. Int. Sch. Res. Not. 14

2013: e396581. doi: 10.5402/2013/396581. 15

Kephart, W.C., Mobley, C.B., Fox, C.D., Pascoe, D.D., Sefton, J.M., Wilson, T.J., Goodlett, 16

M.D., Kavazis, A.N., Roberts, M.D., and Martin, J.S. 2015. A single bout of whole‐leg, 17

peristaltic pulse external pneumatic compression upregulates PGC‐1α mRNA and 18

endothelial nitric oxide sythase protein in human skeletal muscle tissue. Exp. Physiol. 19

100(7): 852–864. doi: 10.1113/EP085160. 20

Maiorana, D.A., O’Driscoll, G., Taylor, R., and Green, D. 2012. Exercise and the Nitric Oxide 21

Vasodilator System. Sports Med. 33(14): 1013–1035. doi: 10.2165/00007256-22

200333140-00001. 23

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Martin, J.S., Borges, A.R., and Beck, D.T. 2015a. Peripheral Conduit and Resistance Artery 1

Function Are Improved Following a Single, 1-hour Bout of Peristaltic Pulse External 2

Pneumatic Compression. Eur. J. Appl. Physiol. Article in press. doi: 10.1007/s00421-3

015-3187-8. 4

Martin, J.S., Friedenreich, Z.D., Borges, A.R., and Roberts, M.D. 2015b. Acute Effects of 5

Peristaltic Pneumatic Compression on Repeated Anaerobic Exercise Performance and 6

Blood Lactate Clearance. J. Strength Cond. Res. Natl. Strength Cond. Assoc. Article in 7

press. doi: 10.1519/JSC.0000000000000928. 8

Rattray, B., Argus, C., Martin, K., Northey, J., and Driller, M. 2015. Is it time to turn our 9

attention toward central mechanisms for post-exertional recovery strategies and 10

performance? Front. Physiol. 6: 79. doi: 10.3389/fphys.2015.00079. 11

Sands, W.A., McNeal, J.R., Murray, S.R., and Stone, M.H. 2014a. Dynamic Compression 12

Enhances Pressure-to-Pain Threshold in Elite Athlete Recovery: Exploratory Study. J. 13

Strength Cond. Res. 29(5): 1263-1272. doi: 10.1519/JSC.0000000000000412. 14

Sands, W.A., Murray, M.B., Murray, S.R., McNeal, J.R., Mizuguchi, S., Sato, K., and Stone, 15

M.H. 2014b. Peristaltic pulse dynamic compression of the lower extremity ehances 16

flexibility. J. Strength Cond. Res. 28(4): 1058–1064. doi: 17

10.1519/JSC.0000000000000244. 18

Sheldon, R.D., Roseguini, B.T., Thyfault, J.P., Crist, B.D., Laughlin, M.H., and Newcomer, S.C. 19

2012. Acute impact of intermittent pneumatic leg compression frequency on limb 20

hemodynamics, vascular function, and skeletal muscle gene expression in humans. J. 21

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Wiener, A., Mizrahi, J., and Verbitsky, O. 2001. Enhancement of Tibialis Anterior Recovery by 1

Intermittent Sequential Pneumatic Compression of the Legs. Basic Appl Myol 11(2): 87–2

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FIGURE LEGENDS 1

Figure 1. Panels A-D: parameters of anaerobic cycling performance and heart rate (HR) during 2

Wingate tests (WAnT). Following 30 minutes of treatment with external pneumatic compression 3

(EPC), WAnTs were performed consecutively with 3 minutes of active rest between bouts. A) 4

Peak anaerobic power (highest 1 second running average during 30-second WAnT) in Watts, B) 5

average power (mean power for the entire 30-second WAnT) in Watts, C) the fatigue index 6

(percent drop in power from first 5 seconds of the test to the last 5 seconds of the test), and D) 7

HR immediately before or after performance of respective WAnTs. Panels E-F: HR and blood 8

lactate concentrations (BLa) during passive recovery following WAnT3. When a significant 9

main effect of time was observed, post hoc analysis for between time points comparisons was 10

performed using Student’s paired t-tests with Bonferroni correction for multiple comparisons. 11

Time points with different letter superscripts denotes significant between time point difference 12

(P<0.05). Values are presented as mean ± SD. 13

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Panels A-D: parameters of anaerobic cycling performance and heart rate (HR) during Wingate tests (WAnT). Following 30 minutes of treatment with external pneumatic compression (EPC), WAnTs were

performed consecutively with 3 minutes of active rest between bouts. A) Peak anaerobic power (highest 1 second running average during 30-second WAnT) in Watts, B) average power (mean power for the entire 30-second WAnT) in Watts, C) the fatigue index (percent drop in power from first 5 seconds of the test to

the last 5 seconds of the test), and D) HR immediately before or after performance of respective WAnTs. Panels E-F: HR and blood lactate concentrations (BLa) during passive recovery following

WAnT3. When a significant main effect of time was observed, post hoc analysis for between time points

comparisons was performed using Student’s paired t-tests with Bonferroni correction for multiple comparisons. Time points with different letter superscripts denotes significant between time point difference

(P<0.05). Values are presented as mean ± SD. 210x205mm (300 x 300 DPI)

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