Postexercise muscle cooling enhances gene expression of PGC-1α.

PURPOSE: This study aimed to investigate the influence of localized muscle cooling on postexercise vascular, metabolic, and mitochondrial-related gene expression.

METHODS: Nine physically active males performed 30 min of continuous running at 70% of their maximal aerobic velocity, followed by intermittent running to exhaustion at 100% maximal aerobic velocity. After exercise, subjects immersed one leg in a cold water bath (10°C, COLD) to the level of their gluteal fold for 15 min. The contralateral leg remained outside the water bath and served as control (CON). Core body temperature was monitored throughout the experiment, whereas muscle biopsies and muscle temperature (Tm) measurements were obtained from the vastus lateralis before exercise (PRE), immediately postexercise (POST-EX, Tm only), immediately after cooling, and 3 h postexercise (POST-3H).

RESULTS: Exercise significantly increased core body temperature (PRE, 37.1°C ± 0.4°C vs POST-EX, 39.3°C ± 0.5°C, P < 0.001) and Tm in both CON (PRE, 33.9°C ± 0.7°C vs POST-EX, 39.1°C ± 0.5°C) and COLD legs (PRE, 34.2°C ± 0.9°C vs POST-EX, 39.4°C ± 0.3°C), respectively (P < 0.001). After cooling, Tm was significantly lower in COLD (28.9°C ± 2.3°C vs 37.0°C ± 0.8°C, P < 0.001) whereas PGC-1α messenger RNA expression was significantly higher in COLD at POST-3H (P = 0.014). Significant time effects were evident for changes in vascular endothelial growth factor (P = 0.038) and neuronal nitric oxide synthase (P = 0.019) expression. However, no significant condition effects between COLD and CON were evident for changes in both vascular endothelial growth factor and neuronal nitric oxide synthase expressions.

CONCLUSIONS: These data indicate that an acute postexercise cooling intervention enhances the gene expression of PGC-1α and may therefore provide a valuable strategy to enhance exercise-induced mitochondrial biogenesis.