Heat stress treatment rescues denervation-induced loss of mitochondrial enzymes, but not substrate transporters in gastrocnemius muscle

ACSM Conference on Integrative Physiology of Exercise

PURPOSE: To examine whether heat stress treatment rescues experimental physical inactivity-induced metabolic dysfunction in skeletal muscle.

METHODS: Male ICR mice were involved in this study. We employed 10 days of sciatic nerve transection as an experimental physical inactivity. Daily heat stress treatment was produced by exposure of mice to hot environment (40 ºC, 30 min/day). Twenty-four hours after final treatment, gastrocnemius muscle was dissected out and prepared for western blotting. To evaluate metabolic adaptations, we measured protein contents of 1) mitochondrial enzymes, 2) a master regulator of mitochondrial biogenesis (PGC-1-alpha), and 3) substrate transporters.

RESULTS: Sciatic nerve transection significantly decreased protein contents of UQCRC2, COX I, ATP5A, PGC-1-alpha, GLUT4 and MCT4. Heat stress treatment countered sciatic nerve transection-induced loss of UQCRC2, COX I, and ATP5A, but not PGC-1-alpha, GLUT4 and MCT4.

CONCLUSIONS: Heat stress treatment selectively rescues sciatic nerve transection-induced loss of mitochondrial enzymes, but not concomitant loss of transcriptional regulators for mitochondrial enzymes and substrate transporters in mouse gastrocnemius muscle.

Yuki Tamura, Yutaka Matsunaga, Yu Kitaoka, Daisuke Hoshino, and Hideo Hatta