Heat acclimation does not affect maximal aerobic power in thermoneutral normoxic or hypoxic conditions.
Alexandros SotiridisTadej DebevecUrša CiuhaOla EikenIgor B MekjavićPublished in: Experimental physiology (2019)
Heat acclimation (HA) mitigates heat-induced decrements in maximal aerobic power ( <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"> <mml:msub><mml:mover><mml:mi>V</mml:mi> <mml:mo>̇</mml:mo></mml:mover> <mml:mrow><mml:msub><mml:mi>O</mml:mi> <mml:mn>2</mml:mn></mml:msub> <mml:mi>peak</mml:mi> </mml:mrow> </mml:msub> </mml:math> ) 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 [ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"> <mml:msub><mml:mover><mml:mi>V</mml:mi> <mml:mo>̇</mml:mo></mml:mover> <mml:mrow><mml:msub><mml:mi>O</mml:mi> <mml:mn>2</mml:mn></mml:msub> <mml:mi>peak</mml:mi> </mml:mrow> </mml:msub> </mml:math> 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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"> <mml:msub><mml:mover><mml:mi>V</mml:mi> <mml:mo>̇</mml:mo></mml:mover> <mml:mrow><mml:msub><mml:mi>O</mml:mi> <mml:mn>2</mml:mn></mml:msub> <mml:mi>peak</mml:mi> </mml:mrow> </mml:msub> </mml:math> 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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"> <mml:msub><mml:mover><mml:mi>V</mml:mi> <mml:mo>̇</mml:mo></mml:mover> <mml:mrow><mml:msub><mml:mi>O</mml:mi> <mml:mn>2</mml:mn></mml:msub> <mml:mi>peak</mml:mi> </mml:mrow> </mml:msub> </mml:math> 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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"> <mml:msub><mml:mover><mml:mi>V</mml:mi> <mml:mo>̇</mml:mo></mml:mover> <mml:mrow><mml:msub><mml:mi>O</mml:mi> <mml:mn>2</mml:mn></mml:msub> <mml:mi>peak</mml:mi> </mml:mrow> </mml:msub> </mml:math> in normoxic or hypoxic conditions.