JULIEN D. PE ́RIARD, CORINNE CAILLAUD, and MARTIN W. THOMPSON
Aspetar, Research and Education Centre, Qatar Orthopaedic and Sports Medicine Hospital, Doha, QATAR; and Discipline of Exercise and Sport Science, Faculty of Health Sciences, University of Sydney, Lidcombe, AUSTRALIA.
PE ́RIARD, 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 (È41-C) until rectal temperature (Tre) increased to 39.5-C. The ExH and PaH interventions were performed in ambient conditions of 38-C and 60% relative humidity with Tre reaching 39.8-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 G 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 È90% during both PaH and ExH MVC. 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 (È96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P G 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.
Endurance exercise performance is markedly reduced in hot compared with temperate environments. The mechanism underlying this response may involve hyperthermia as the independent cause of fatigue (21,32). During exercise in hot conditions, fatigue in trained humans has been associated with the attainment of a ‘‘critical’’ core temperature (È40-C) (32,34) despite different initial temperatures and rates of heat storage (21). This decrement in performance is proposed to originate from a hyperthermia-induced inability of the central nervous system (CNS) to activate sufficient skeletal muscle to produce or maintain a required force (i.e., central fatigue) (33,34).