4.6 Article

Central and Peripheral Fatigue during Passive and Exercise-Induced Hyperthermia

期刊

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
卷 43, 期 9, 页码 1657-1665

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0b013e3182148a9a

关键词

CNS DRIVE; MAXIMAL VOLUNTARY CONTRACTION; CORE TEMPERATURE; CARDIOVASCULAR STRAIN

资金

  1. University of Sydney Faculty of Health Sciences

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PERIARD, J. D., C. CAILLAUD, and M. W. THOMPSON. Central and Peripheral Fatigue during Passive and Exercise-Induced Hyperthermia. Med. Sci. Sports Exerc., Vol. 43, No. 9, pp. 1657-1665, 2011. Purpose: Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined. Methods: On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (similar to 41 degrees C) until rectal temperature (T-re) increased to 39.5 degrees C. The ExH and PaH interventions were performed in ambient conditions of 38 degrees C and 60% relative humidity with T-re reaching 39.8 degrees C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC. Results: Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P G 0.01 vs control). However, the extent of decline in voluntary activation was maintained at similar to 90% during both PaH and ExHMVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (similar to 96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05). Conclusions: The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.

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