Heat acclimation does not affect maximal aerobic power in thermoneutral normoxic or hypoxic conditions

What is the central question of this study? Controlled‐hyperthermia heat acclimation protocols induce an array of thermoregulatory and cardiovascular adaptations that facilitate exercise in hot conditions. We investigated whether this ergogenic potential can be transferred to thermoneutral normoxic or hypoxic exercising conditions. What is the main finding and its importance? We show that heat acclimation did not affect maximal cardiac output or maximal aerobic power in thermoneutral normoxic/hypoxic conditions. Heat acclimation augmented the sweating response in thermoneutral normoxic conditions. The cross‐adaptation theory according to which heat acclimation could facilitate hypoxic exercise capacity is not supported by our data.

Abstract

Heat acclimation (HA) mitigates heat‐induced decrements in maximal aerobic power (V̇O_2peak) and augments exercise thermoregulatory responses in the heat. Whether this beneficial effect of HA is observed in hypoxic or thermoneutral conditions remains unresolved. We explored the effects of HA on exercise cardiorespiratory and thermoregulatory responses in normoxic, hypoxic, and hot conditions. Twelve males (V̇O _2peak 54.7(5.7) mL·kg⁻¹·min⁻¹) participated in a HA protocol comprising 10 daily 90‐min controlled‐hyperthermia (target rectal temperature, T_re = 38.5 °C) exercise sessions. Before and after HA, we determined V̇O_2peak in thermoneutral normoxic (NOR), thermoneutral hypoxic (13.5% F_iO₂; HYP) and hot (35 °C, 50% RH; HE) conditions in a randomized and counterbalanced order. Preceding each maximal cycling test, a 30‐min steady‐state exercise at 40% of the NOR peak power output (W_peak) was employed to evaluate thermoregulatory responses. HA induced the expected adaptations in HE: reduced T_re and submaximal heart rate (HR), enhanced sweating response and expanded plasma volume. However, HA did not affect V̇O_2peak or maximal cardiac output (CO_max) (P = 0.61). W_peak was increased post‐HA in NOR (P < 0.001) and HE (P < 0.001) by 41 ± 21 and 26 ± 22 W, respectively but not in HYP (P = 0.14). Gross mechanical efficiency was higher (P = 0.004) whereas resting T_re and sweating thresholds were lower (P < 0.01) post‐HA across environments. Nevertheless, the gain of the sweating response decreased (P = 0.05) in HYP. In conclusion, our data do not support a beneficial cross‐over effect of HA on V̇O_2peak in normoxic or hypoxic conditions.

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