Protein Supplementation Enhances the Effects of Intermittent Loading on Skeletal Muscles by Activating the mTORC1 Signaling Pathway in a Rat Model of Disuse Atrophy.

Satoshi Fujita,Kazuo Hino,Sho Miyatake,Yuko Natsui,Goro Ebisu

doi:10.3390/nu12092729

Abstract

Inactivity leads to skeletal muscle atrophy, whereas intermittent loading (IL) during hind limb unloading (HU) attenuates muscle atrophy. However, the combined effects of IL and protein supplementation on disuse muscle atrophy are unclear. Therefore, we investigated the effects of IL and a high-protein oral nutritional supplement (HP) during HU on skeletal muscle mass and protein synthesis/breakdown. Male F344 rats were assigned to the control (CON), 14-day HU (HU), IL during HU (HU + IL), and IL during HU followed by HP administration (2.6 g protein/kg/day; HU + IL + HP) groups. Soleus and gastrocnemius muscles were sampled 30 min after the last IL and HP supplementation. HU decreased relative soleus and gastrocnemius muscle masses. Relative muscle masses and p70 ribosomal protein S6 kinase/ribosomal protein S6 phosphorylation in soleus and gastrocnemius muscles were higher in the HU + IL group than the HU group and further higher in the HU + IL + HP group than the HU + IL group in gastrocnemius muscle. Therefore, protein administration plus IL effectively prevented skeletal muscle atrophy induced by disuse, potentially via enhanced activation of targets downstream of mammalian target of rapamycin complex 1 (mTORC1) signaling pathway.

Highlights

Skeletal muscle mass is determined by the balance between protein synthesis and breakdown [1].Strategies that increase muscle protein synthesis and reduce protein breakdown are important for maintaining and increasing skeletal muscle mass
The mean caloric intake was significantly lower in the hind limb unloading (HU) group than in the CON group (p < 0.05), no significant differences were observed among the HU, HU + intermittent loading (IL), and HU + IL + high-protein oral nutritional supplement (HP) groups
We evaluated the effects of IL and oral administration of HP on skeletal muscle protein synthesis and breakdown in a rat model of HU-induced muscle atrophy

Summary

Introduction

Skeletal muscle mass is determined by the balance between protein synthesis and breakdown [1]. Strategies that increase muscle protein synthesis and reduce protein breakdown are important for maintaining and increasing skeletal muscle mass. Muscle protein synthesis is enhanced by resistance exercise and amino acids derived from dietary protein [2,3]. Essential amino acids (EAAs) stimulate muscle protein synthesis, and branched-chain amino acids (BCAAs), leucine, exhibit strong anabolic effects [4,5]. Skeletal muscle atrophy is induced by aging, starvation, inactivity, cancer cachexia, diabetes, chronic kidney disease, and many other pathologies [6,7,8,9]. Disuse-muscle atrophy is the loss of skeletal muscle under conditions such as cast immobilization, prolonged bed rest, and microgravity [10]

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