Effects of heat stress treatment and leucine supplementation on age‐related muscle loss in mice

Abstract

Acute heat stress treatment activates mammalian target of rapamycin (mTOR) signaling in skeletal muscle, leading to increase skeletal muscle protein synthesis and skeletal muscle mass. Leucine intake also activates mTOR signaling and stimulates protein synthesis. This study investigated the effects of heat stress treatment and leucine supplementation on sarcopenia (muscle loss with aging) in mice. C57BL/6J male mice (14 or 98 weeks old) were assigned randomly to young control (YC, N=6), old control (OC, n=9), heat stress (OH, n=7), leucine supplementation (OL, n=7), and heat stress and leucine supplementation (OLH) groups. Mice in OH and OLH groups were exposed to hot environment chamber (41ºC) for 40 min twice per week. Mice in OL and OLH groups were given ad libitum access to leucine‐supplemented water (114mM leucine). After 12‐week intervention, there were no differences in body weight and grip strength among groups. Body fat percentage in OLH group was significantly lower than that in OC group (29.0 ± 6.4 % vs. 39.1 ± 8.5 %, p < 0.05). The vastus lateralis muscle weight was significantly lower in OC, OH and OL groups compared with that of YC group, but the muscle weight in OLH group was significantly greater than that in OC group (191.9 ± 12.8 mg vs. 167.1 ± 10.1 mg, p < 0.05). Heat stress treatment induced the expression of heat shock protein 72 (HSP72) in muscle of OH and OLH groups (~5 fold, p < 0.05). There were no differences in the muscle mTOR signaling (the phosphorylation of mTOR, p70s6k, S6 and 4E‐BP1) between groups under overnight fasting condition. On the other hand, the expression of L‐type amino acid transporter 1 (LAT1) of muscle was significantly increased in OC, OH and OL groups compared with YC group (~3 fold, p < 0.05), but there were no difference between YC and OLH group. Our current observations show that the combination of heat stress treatment and leucine supplementation appears to be clinically beneficial for age‐related muscle loss. In addition, normal expression of LAT1 in muscle might contribute to suppression of muscle loss.Support or Funding InformationThis work was supported by JSPS KAKENHI Grant Number JP16K16565.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.