Adaptation of exercise ventilation during an actively-induced hyperthermia following passive heat acclimation

Author:

Beaudin Andrew E.,Clegg Miriam E.,Walsh Michael L.,White Matthew D.

Abstract

Hyperthermia-induced hyperventilation has been proposed to be a human thermolytic thermoregulatory response and to contribute to the disproportionate increase in exercise ventilation (V̇e) relative to metabolic needs during high-intensity exercise. In this study it was hypothesized that V̇e would adapt similar to human eccrine sweating (ĖSW) following a passive heat acclimation (HA). All participants performed an incremental exercise test on a cycle ergometer from rest to exhaustion before and after a 10-day passive exposure for 2 h/day to either 50°C and 20% relative humidity (RH) ( n = 8, Acclimation group) or 24°C and 32% RH ( n = 4, Control group). Attainment of HA was confirmed by a significant decrease ( P = 0.025) of the esophageal temperature (Tes) threshold for the onset of ĖSW and a significantly elevated ĖSW ( P ≤ 0.040) during the post-HA exercise tests. HA also gave a significant decrease in resting Tes ( P = 0.006) and a significant increase in plasma volume ( P = 0.005). Ventilatory adaptations during exercise tests following HA included significantly decreased Tes thresholds ( P ≤ 0.005) for the onset of increases in the ventilatory equivalents for O2 (V̇e/V̇o2) and CO2 (V̇e/V̇co2) and a significantly increased V̇e ( P ≤ 0.017) at all levels of Tes. Elevated V̇e was a function of a significantly greater tidal volume ( P = 0.003) at lower Tes and of breathing frequency ( P ≤ 0.005) at higher Tes. Following HA, the ventilatory threshold was uninfluenced and the relationships between V̇o2 and either V̇e/V̇o2 or V̇e/V̇co2 did not explain the resulting hyperventilation. In conclusion, the results support that exercise V̇e following passive HA responds similarly to ĖSW, and the mechanism accounting for this adaptation is independent of changes of the ventilatory threshold or relationships between V̇o2 with each of V̇e/V̇o2 and V̇e/V̇co2.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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