Effect of short-term exercise-heat acclimation on ventilatory and cerebral blood flow responses to passive heating at rest in humans

• Published in: Journal of applied physiology (1985) Vol. 119; no. 5; pp. 435 - 444
• Main Authors: Fujii, Naoto, Tsuji, Bun, Honda, Yasushi, Kondo, Narihiko, Nishiyasu, Takeshi
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.09.2015
• Subjects: Acclimatization; Acclimatization - physiology; Adult; Arterial Pressure - physiology; Blood; Body Temperature Regulation - physiology; Cerebrovascular Circulation - physiology; Cold Temperature; Esophagus; Exercise; Exercise - physiology; Fever; Fever - physiopathology; Heating; Heating - methods; Homeostasis - physiology; Hot Temperature; Humans; Hyperventilation - physiopathology; Male; Oxygen; Oxygen uptake; Physical training; Plasma Volume - physiology; Rest - physiology; Sweating - physiology; Ventilation; cerebral perfusion; orthostatic tolerance; respiratory alkalosis; exercise training; control of breathing
• ISSN: 8750-7587; 1522-1601; 1522-1601
• DOI: 10.1152/japplphysiol.01049.2014

Hyperthermia induces hyperventilation and cerebral hypoperfusion in resting humans. We tested the hypothesis that short-term exercise-heat acclimation would alleviate those effects. Twenty healthy male subjects were divided into two groups that performed exercise training in the heat (TR-HEAT, n = 10) or cold (TR-COLD, n = 10). Before and after the training, the subjects in both groups participated in passive-heat tests at rest. Training was performed at 37°C (TR-HEAT) or 10°C (TR-COLD) and entailed four 20-min bouts of cycling at 50% peak oxygen uptake separated by 10-min recoveries daily for 6 consecutive days. After TR-HEAT, esophageal temperature was lowered when measured before and during passive heating, as was the esophageal temperature threshold for cutaneous active vasodilation, whereas plasma volume was increased (all P < 0.05). These traditional indices of successful heat acclimation were not all induced by TR-COLD (all P > 0.05). TR-HEAT had no significant effect on passive heating-induced increases in minute ventilation, even when evaluated as the esophageal temperature threshold for increases in minute ventilation and the slope relating minute ventilation to esophageal temperature (all P > 0.05). By contrast, TR-HEAT attenuated the passive heating-induced reduction in the cerebral vascular conductance index (middle cerebral artery mean blood velocity/mean arterial pressure) (all P < 0.05). TR-COLD did not attenuate the increase in minute ventilation or the decrease in the cerebral vascular conductance index observed during passive heating (all P > 0.05). These data suggest that in resting heated humans, short-term heat acclimation achieved through moderate-intensity exercise training (i.e., 50% peak oxygen uptake) in the heat does not influence hyperthermia-induced hyperventilation, but it does potentially attenuate cerebral hypoperfusion.