New Findings 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 exercise conditions. What is the main finding and its importance?We showed that heat acclimation did not affect maximal cardiac output or maximal aerobic power in thermoneutral normoxic or 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 (V̇O2 peak ) 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 cardiorespiratory and thermoregulatory responses to exercise in normoxic, hypoxic and hot conditions. Twelve men [V̇O2 peak 54.7(standard deviation 5.7) ml kg−1 min−1] participated in a HA protocol consisting of 10 daily 90‐min controlled‐hyperthermia (target rectal temperature, Tre = 38.5°C) exercise sessions. Before and after HA, we determined V̇O2 peak in thermoneutral normoxic (NOR), thermoneutral hypoxic (fractional inspired O2 = 13.5%; HYP) and hot (35°C, 50% relative humidity; HE) conditions in a randomized and counterbalanced order. Preceding each maximal cycling test, a 30‐min steady‐state exercise bout at 40% of the NOR peak power output was used to evaluate thermoregulatory responses. Heat acclimation induced the expected adaptations in HE: reduced Tre and submaximal heart rate, enhanced sweating response and expanded plasma volume. However, HA did not affect V̇O2 peak or maximal cardiac output (P = 0.61). The peak power output 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 Tre 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 V̇O2 peak in normoxic or hypoxic conditions.

We examined the effects of acclimatization to normobaric hypoxia on aerobic performance and exercise thermoregulatory responses under normoxic, hypoxic and hot conditions. Twelve males performed tests of maximal oxygen uptake (V̇O) in normoxic (NOR), hypoxic (13.5% FO; HYP) and hot (35℃, 50% RH; HE) conditions in a randomized manner before and after a 10-day continuous normobaric hypoxic exposure (FO = 13.65(0.35)%, PO = 87(3) mmHg). The acclimatization protocol included daily exercise (60min @ 50% hypoxia-specific peak power output, W). All maximal tests were preceded by a steady-state exercise (30 min at 40% W) to assess the sweating response. Hematological data were assessed from venous blood samples obtained before and after acclimatization. V̇O increased by 10.7% (P = 0.002) and 7.9% (P = 0.03) from pre- to post-acclimatization in NOR and HE, respectively, whereas no differences were found in HYP (pre: 39.9(3.8) vs post: 39.4(5.1) mL.kg.min, P = 1.0). However, the increase in V̇O did not translate into increased W in either NOR or HE. Maximal heart rate and ventilation remained unchanged following acclimatization. Νo differences were noted in the sweating gain and thresholds independent of the acclimatization or environmental conditions. Hypoxic acclimatization markedly increased hemoglobin (P < 0.001), hematocrit (P < 0.001) and extracellular HSP72 (P = 0.01). These data suggest that 10 days of normobaric hypoxic acclimatization combined with moderate-intensity exercise training improves V̇O in NOR and HE, but does not seem to affect exercise performance or thermoregulatory responses in any of the tested environmental conditions.

Moderate‐intensity exercise sessions are incorporated into heat‐acclimation and hypoxic‐training protocols to improve performance in hot and hypoxic environments, respectively. Consequently, a training effect might contribute to aerobic performance gains, at least in less fit participants. To explore the interaction between fitness level and a training stimulus commonly applied during acclimation protocols, we recruited 10 young males of a higher (more fit‐MF, peak aerobic power [VO2peak]: 57.9 [6.2] ml·kg−1·min−1) and 10 of a lower (less fit‐LF, VO2peak: 41.7 [5.0] ml·kg−1·min−1) fitness level. They underwent 10 daily exercise sessions (60 min@50% peak power output [Wpeak]) in thermoneutral conditions. The participants performed exercise testing on a cycle ergometer before and after the training period in normoxic (NOR), hypoxic (13.5% FiO2; HYP), and hot (35°C, 50% RH; HE) conditions in a randomized and counterbalanced order. Each test consisted of two stages; a steady‐state exercise (30 min@40% NOR Wpeak to evaluate thermoregulatory function) followed by incremental exercise to exhaustion. VO2peak increased by 9.2 (8.5)% (p = .024) and 10.2 (15.4)% (p = .037) only in the LF group in NOR and HE, respectively. Wpeak increases were correlated with baseline values in NOR (r = −.58, p = .010) and HYP (r = −.52, p = .018). MF individuals improved gross mechanical efficiency in HYP. Peak sweat rate increased in both groups in HE, whereas MF participants activated the forehead sweating response at lower rectal temperatures post‐training. In conclusion, an increase in VO2peak but not mechanical efficiency seems probable in LF males after a 10‐day moderate‐exercise training protocol.