Does Heat Acclimation Upregulate Skeletal Muscle Markers Of Oxidative Metabolism And Mitochondrial Biogenesis?

Heat acclimation (HA) increases tolerance to exercise performed in the heat and may improve aerobic fitness and performance in highly trained individuals. However, it is unknown if HA effects the expression of proteins related to mitochondrial biogenesis and oxidative capacity in skeletal muscle in active young individuals. PURPOSE: To investigate the effect of HA on the expression of oxidative and mitochondrial proteins in the skeletal muscle of healthy, active young-adult males and females. METHODS: In a quasi-experimental design, thirteen (7 males, 6 females) aerobically fit (VO2max > 75th percentile) individuals underwent 10-days of HA over 14-days. Participants performed two 45-minute bouts of exercise (walking at 30-40% maximal velocity) with 10 minutes rest per session in a hot environment (dry temperature ~42°C, relative humidity 30-50%). Pre- and post-HA VO2max (room temperature), second ventilatory threshold (VT), protein expression of PGC-1α, TFAM, CaMK, Cytochromes I-IV, and HSP72 were measured pre-HA and post-HA. Heat acclimation was determined comparing heart rate (HR), core temperature (CT), sweat rate, and ratings of perceived exertion (RPE) on days 1 and 10. RESULTS: Participants were acclimated as indicated by pre- and post-HA resting-CT (37.3 ± 0.38 vs. 37.1 ± 0.28°C; p = 0.04), maximal-CT (38.8 ± 0.35 vs. 38.2 ± 0.38°C; p<0.0001), mean-HR (138.5 ± 17.7 vs. 125.9 ± 14.0 bpm; p=0.03), maximal-HR (170.2 ± 26.4 vs. 149.4 ± 24.5 bpm; p=0.003), mean-RPE (12.4 ± 1.2 vs. 9.8 ± 1.1; p< 0.0001), and maximal-RPE (15.0 ± 1.6 vs. 12.2 ± 1.9; p=0.002). Pre- to Post-HA VO2max (50.2 ± 8.6 vs. 51.7 ± 11.2 mL/kg/min; p=0.08) and VT (31.2 ± 7.0 vs. 33.9 ± 8.7; p=0.19) were unchanged. Protein expression was unchanged pre- to post-HA; (PGC-1α p=0.21, TFAM p=0.34, CaMK 0-0.19, Cytochromes I p=0.73; II p=0.85, III p=0.62, IV p=0.70, Hsp72 p=0.27). CONCLUSIONS: 10-days of low intensity exercise in the heat resulted in HA, but did not increase aerobic fitness or markers of mitochondrial biogenesis and oxidative metabolism in physically active individuals. Supported by a research grant from the College of Education, University of New Mexico.