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Introduction

Trial Two. Trial Three. Trial One. Day One. Day One. Day One. Day Two. Day Two. Day Two. 1 Hour Flat Run. 1 Hour Downhill Run. 1 Hour Run with Carb Ingestion. 14 Days. 14 Days. 30 Minutes Rest. 30 Minutes Rest. 30 Minutes Rest. 40 Minutes Heat Stress 1. 40 Minutes

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Introduction

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Trial Two Trial Three Trial One Day One Day One Day One Day Two Day Two Day Two 1 Hour Flat Run 1 Hour Downhill Run 1 Hour Run with Carb Ingestion 14 Days 14 Days 30 Minutes Rest 30 Minutes Rest 30 Minutes Rest 40 Minutes Heat Stress 1 40 Minutes Heat Stress 1 40 Minutes Heat Stress 1 40 Minutes Heat Stress 2 40 Minutes Heat Stress 2 40 Minutes Heat Stress 2 The Effect of Exercise Induced Muscle Damage and Inflammation on Subsequent Thermoregulation During Exercise in the Heat Ryan Hillier-Smith, Cardiff University • Introduction • Athletes and military personnel who perform arduous physical activity in high ambient temperatures rely heavily on their thermoregulatory system to remove the heat which is produced by exercising muscles (1) • Any physiological or pathological process which can influence their ability to thermoregulate may place them in a compromised condition when they begin to exercise in the heat • This could predispose them to developing a potentially fatal exertional heat stroke (EHS) (2) • An increase in the concentration of cytokines in the blood has been implicated in the aetiology of EHS (3, 4) • Pyrogenic cytokines, such as inter leukin-6 (IL-6), can raise the thermoregulatory set point resulting in increased heat storage (5,6) • Eccentric exercise, such as downhill running, causes exercise induced muscle damage (EIMD) (7) • This, in turn, results in an inflammatory response which includes an increase in the level of circulating pyrogenic cytokines (8) • This study investigated how EIMD and the associated inflammatory response affects the ability of individuals to thermoregulate during subsequent bouts of exercise in high ambient temperatures Fig. 2; A participant performing the downhill exercise treatment • Methods • Repeated measures were performed on 3 male, recreationally active, sport science students who completed 3 trials in a randomised order((mean ± standard deviation) age 21 ± 1.2 yrs, BMI 21.8 ± 2.3 kg.m-2 and VO2max 63.3 ± 8.0 ml.kg-1.min-1) • The downhill trial involved 1 hour of 65% VO2max treadmill running at a 10% gradient declineand was designed to represent EIMD • The flat trial involved 1 hour of 65% VO2max treadmill running at a 1% gradient incline which was designed as the control trial for EIMD • The carbohydrate trial was the same as the flat trial but the participant was given a bolus of carbohydrate which aimed to control for inflammation (9) • In all trials the exercise treatment was followed by 2 exercise heat stresses • These consisted of 40 minutes of 65% VO2max treadmill running at a 1% gradient incline in an environmental chamber programmed to an ambient temperature of 33°C • Heat stress 1 occurred 30 minutes post exercise treatment • Heat stress 2 occurred 24.5 hours post exercise treatment (Fig. 1) • Muscle damage was inferred from participant ratings of delayed onset muscle soreness (DOMS) using Visual Analogue and 7 Point Likert Scales • Inflammation was measured using venous plasma IL-6 concentrations ([IL-6]) • Core temperature (Tc) was measured using a rectal thermistor and represented exercising thermoregulation • Results • DOMS was significantly higher (p < 0.05) post-treatment in the downhill trial when compared to the other trials • Plasma [IL-6] was significantly higher (p < 0.05) during the downhill trial after the first heat stress. • Tc was significantly higher (p < 0.05) in the downhill trial after 40 minutes of heat stress 1 (Fig. 3;A) • There was no significant difference in Tc between the trials during heat stress 2 (Fig. 3;B) Fig. 3; Tc during heat stress 1 (A) and heat stress 2 (B). *P < 0.05 indicates a significant difference between the downhill and carbohydrate trial. Values are means and standard deviation for 3 participants • Conclusion • This study suggests that EIMD and the accompanying inflammation causes an impairment in an individual’s ability to thermoregulate when they undergo exercise heat stress shortly after the muscle damaging event • However, the results also suggest that this impairment of thermoregulation is not present 24.5 hours post the muscle damaging event • Therefore, these findings have implications for athletes and military personnel who perform muscle damaging exercises shortly before performing arduous physical activity in high ambient temperatures Fig. 1; This schematic represents an example trial sequence for one participant References 1. Wendt, D., van Loon, L.J.C., and van Marken Lichtenbelt, W.D. (2007). Thermoregulation during exercise in the heat: strategies for maintaining health and performance. Sports Medicine, 37, 669–682. 2. Walsh, N.P., Gleeson M., Pyne, D.B., Nieman, D.C., Dhabhar, F.S., Shephard, R.J., Oliver, S.J., Bermon, S. and Kajeniene, A. (2011). Position statement part two: Maintaining immune health. Exercise Immunology. Review, 17, 64–103 3. Shephard, R.J. and Shek, P.N. (1999). Immune dysfunction as a factor in heat illness. Critical Reviews in Immunology, 19, 285-302 4. Lim, C.L. and Mackinnon, L.T. (2006). The roles of exercise-induced immune system disturbances in the pathology of heat stroke: the dual pathway model of heat stroke. Sports Medicine,36, 39-64 5. Bradford, C.D., Cotter, J.D., Thorburn, M.S., Walker, R.J. and Gerrard, D.F. (2007). Exercise can be pyrogenic in humans. The American Journal of Physiology - Regulatory Integrative and Comparative Physiology,292, R143-149 6. Shin, Y.-0., and Lee, J.-B. (2011). Effects of exercise training on plasma cytokine and chemokine levels, and thermoregulation. Journal of Thermal Biology, 36, 219-224 7. Fielding, R.A., Manfredi, T.J., Ding, W., Fiatarone, M.A., Evans, W.J. and Cannon, J.G. (1993). Acute phase response in exercise. III. Neutrophil and IL-1 beta accumulation in skeletal muscle. American Journal of Physiology - Regulatory Integrative and Comparative Physiology,265, R166-172 8. Cannon, J.G. and Kluger, M.J. (1983). Endogenous pyrogen activity in human plasma after exercise. Science,220, 617-619 9. Starkie, R.L., Arkinstall, M.J., Koukoulas, I., Hawley, J.A. and Febbraio, M.A. (2001). Carbohydrate Ingestion attenuates the increase in plasma interleukin-6, but not skeletal muscle interleukin-6 MRNA, during exercise in humans. The Journal of Physiology, 533, 585-591

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