Heat stress treatment completely rescues denervation‐induced reduction of mitochondrial enzyme activity in skeletal muscle (1162.10)

Abstract

Contrary to exercise training, physical inactivity decreases mitochondrial content and oxidative capacity in skeletal muscle, which contributes to muscle atrophy and dysfunction. In this study, we examined whether heat stress treatment effectively counters disuse‐induced negative adaptations of mitochondria in skeletal muscle. As a result, maximal citrate synthase (CS) activity, a biomarker of mitochondrial content, and 3‐hydroxyacyl CoA dehydrogenase (3‐HAD), a biomarker of maximal capacity for beta oxidation, in gastrocnemius muscle of ICR mice were significantly decreased following 10 days of experimental physical inactivity, produced by unilateral sciatic nerve transection (CS: ‐33.8% P<0.01, 3‐HAD: ‐38.3% P<0.001, vs sham‐operated limb without heat stress). However, daily heat stress treatment, produced by exposure of mice to a hot environment (40 °C, 30 min/day), completely rescued denervation‐induced reduction of CS and 3‐HAD activities (CS: ‐ 5.1% P=0.90, 3‐HAD: +2.9% P=0.96, vs sham‐operated limb without heat stress). Our current observations show that heat stress treatment appears to be clinically beneficial for people who have difficulty participating in sufficient exercise training such as the elderly, injured athletes, and patients with nerve damage.