Exercise in the heat blunts improvements in aerobic power

Introduction 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. Purpose To determine the impact of 3 weeks of aerobic exercise training in the heat (33 degrees C) compared to training in room temperature (20 degrees C) on thermoregulation, PGC-1a mRNA response, and aerobic power. Methods 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 degrees C (n = 12) or 20 degrees C (n = 11) environmental temperatures. Results The 20 degrees C training group increased 20 degrees C (V) over dotO(2peak) from 3.21 +/- 0.77 to 3.66 +/- 0.78 L center dot min(-1) (p < 0.001) while the 33 degrees C training group did not improve (pre, 3.16 +/- 0.48 L center dot min(-1); post, 3.28 +/- 0.63 L center dot min(-1); p = 0.283). PGC-1a increased in response to acute aerobic exercise more in 20 degrees C (6.6 +/- 0.7 fold) than 33 degrees C (4.6 +/- 0.7 fold, p = 0.031) before training, but was no different after training in 20 degrees C (2.4 +/- 0.3 fold) or 33 degrees 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). Conclusions 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.