Thermoregulatory responses to exercise at a fixed rate of heat production are not altered by acute hypoxia

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg^–1·min^–1] completed 45 min of cycling, once in normoxia (NORM; FIO2 = 0.21) and twice in hypoxia (HYP1/HYP2; FIO2= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1) two distinctly different %Vo_2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (H_prod) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2) the same %Vo_2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different H_prod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %Vo_2peak, changes in rectal temperature (T_re) and changes in esophageal temperature (T_es) were greater at end-exercise in NORM [T_re: 0.76 (0.19)°C; T_es: 0.64 (0.22)°C] compared with HYP2 [T_re: 0.56 (0.22)°C, P < 0.01; T_es: 0.42 (0.21)°C, P < 0.01]. As a result of a greater H_prod (P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %Vo_2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm^–2·min^–1] compared with HYP2 [0.71 (0.19) mg·cm^–2·min^–1]. However, at a fixed H_prod, T_re [0.75 (0.24)°C; P = 0.77] and T_es [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm^–2·min^–1] was not different (P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %Vo_2peak, determines changes in core temperature and sweating during exercise.

NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %Vo_2max) does not influence changes in thermoregulatory responses.

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