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A comparison of human thermoregulatory response following dynamic exercise and warm-water immersion
G P Kenny1, G G Giesbrecht, J S Thoden
1Faculty of Medicine, Department of Physiology, University of Ottawa, Canada.
Abstract:
We tested the hypothesis that the prolonged elevated plateau of esophageal temperature (Tes) following moderate exercise is a function of some exercise-related factors and not the increase in heat content and Tes during exercise, by comparing the response to increase Tes during exercise (endogenous heating) and warm-water immersion (exogenous heating). Nine healthy, young [24.0 (1.9) years] subjects performed two separate experiments: (1) 15 min of treadmill exercise at 70% (VO2max) and 15 min rest in a climatic chamber at 29 degrees C, followed by 15 min of immersion in a 42 degrees C water bath and a further 60 min of recovery in the climatic chamber [exercise-water (EW)]; and (2) 15 min of immersion in a 42 degrees C water bath followed by 60 min of recovery in the climatic chamber [water-only (WO)]. Esophageal (Tes) and skin (Tsk) temperatures were recorded at 5-s intervals throughout. The Tes at which the forearm to finger temperature gradient (Tfa-Tfi) abruptly decreases was used to identify the threshold for forearm cutaneous vessel dilation (Thdil) during exercise. Pre-exercise Tes values were 36.64 degrees C and 36.74 degrees C for EW and WO respectively. The EW post-exercise Tes value fell to a stable level of 37.12 degrees C and this value differed by 0.48 degree C (P < 0.05) from baseline, but was similar to Thdil (37.09 degrees C). Despite a 1.2 degrees C increase in Tes during the subsequent warm-water immersion, Tes returned to the post-exercise value (37.11 degrees C). The WO post-immersion Tes fell to a stable plateau of 36.9 degrees C, which was not statistically different from the pre-immersion Tes. The data for both warm-water treatments support the hypothesis that increases in Tes and heat content alone are not the primary mechanisms for the post-exercise elevation in Tes and Thdil. These data also support our previous observation that the exercise-induced elevation in Thdil persists into recovery.
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