Exercise in the heat blunts improvements in aerobic power

PGC-1a has been termed the master regulator of mitochondrial biogenesis. The exercise-induced rise in PGC-1a transcription is blunted when acute exercise takes place in the heat. However, it is unknown if this alteration has functional implications after heat acclimation and exercise training.

To determine the impact of 3 weeks of aerobic exercise training in the heat (33 °C) compared to training in room temperature (20 °C) on thermoregulation, PGC-1a mRNA response, and aerobic power.

Twenty-one untrained college aged males (age, 24 ± 4 years; height, 178 ± 6 cm) were randomly assigned to 3 weeks of aerobic exercise training in either 33 °C (n = 12) or 20 °C (n = 11) environmental temperatures.

The 20 °C training group increased 20 °C [Formula: see text]̇O_2peak from 3.21 ± 0.77 to 3.66 ± 0.78 L·min^-1 (p < 0.001) while the 33 °C training group did not improve (pre, 3.16 ± 0.48 L·min^-1; post, 3.28 ± 0.63 L·min^-1; p = 0.283). PGC-1a increased in response to acute aerobic exercise more in 20 °C (6.6 ± 0.7 fold) than 33 °C (4.6 ± 0.7 fold, p = 0.031) before training, but was no different after training in 20 °C (2.4 ± 0.3 fold) or 33 °C (2.4 ± 0.5 fold, p = 0.999). No quantitative alterations in mitochondrial DNA were detected with training or between temperatures (p > 0.05).

This research indicates that exercise in the heat may limit the effectiveness of aerobic exercise at increasing aerobic power. Furthermore, this study demonstrates that heat induced blunting of the normal exercise induced PGC-1a response is eliminated after 3 weeks of heat acclimation.