Abstract

Glucocorticoid excess is a critical factor contributing to muscle atrophy. Both endogenous and exogenous glucocorticoids negatively affect the preservation of muscle mass and function. To date, the most effective intervention to prevent muscle atrophy is to apply a mechanical load in the form of resistance exercise. However, glucocorticoid-induced skeletal muscle atrophy easily causes fatigue in daily physical activities, such as climbing stairs and walking at a brisk pace, and reduces body movements to cause a decreased ability to perform physical activity. Therefore, providing adequate nutrients in these circumstances is a key factor in limiting muscle wasting and improving muscle mass recovery. The present review will provide an up-to-date review of the effects of various nutrients, including amino acids such as branched-chain amino acids (BCAAs) and β–hydroxy β–methylbutyrate (HMB), fatty acids such as omega-3, and vitamins and their derivates on the prevention and improvement of glucocorticoid-induced muscle atrophy.

Highlights

  • Skeletal muscle is the largest metabolic organ (40~50% of the body mass) and protein reservoir (50~75% of all body proteins) in the human body [1]

  • When clinical studies were performed in younger [58] and older [59] human adults to investigate the effects of omega-3 fatty acid administration (8 weeks supplementation of 1.86 g/d of eicosapentaenoic acid (EPA) and 1.50 g/d docosahexaenoic acid (DHA)) on the rates of mixed skeletal muscle protein synthesis in the fasted state and in response to a hyper-aminoacidemic-hyperinsulinemic infusion [58,59], DHA and EPA administration followed by subsequent incorporation into membrane phospholipids showed no effects on fasted rates of mixed muscle protein synthesis in response to the hyper-aminoacidemic-hyperinsulinemic infusion, whereas there was an enhancement of mixed muscle protein synthesis compared to before administration [58,59]

  • Accumulated evidence supports that nutrients may help improve glucocorticoid-induced muscle atrophy through various mechanisms regulating the balance between protein synthesis and protein degradation, i.e., protein turnover

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Summary

Introduction

Skeletal muscle is the largest metabolic organ (40~50% of the body mass) and protein reservoir (50~75% of all body proteins) in the human body [1]. Glucocorticoid-induced skeletal muscle atrophy has little or no effect on slowtwitch type I muscle fibers but is known to induce selective loss of fast-twitch type II muscle fibers [14] This glucocorticoid-induced muscle proteolysis is mainly mediated by the activation of catabolic pathways, including the ubiquitin-proteasome and autophagylysosomal system [23]. Myostatin, a potent inhibitor of muscle growth, is released by glucocorticoids to stimulate phosphorylation of Smad2/3 and dephosphorylate Akt to increase ubiquitin-proteasome activity, leading to muscle atrophy [29]. These pathways are generally known to be regulated by specific transcription factors, such as forkhead box O (FoxO), which are phosphorylated and inactivated by Akt in the cytoplasm [29] (Figure 1).

The Role of Nutrients
Amino Acids
Clinical Relevance of Amino Acids in Muscle Atrophy
Fatty Acids
Clinical Relevance of Fatty Acids in Muscle Atrophy
Vitamins
Clinical Relevance of Vitamins in Muscle Atrophy
Minerals
Clinical Relevance of Minerals in Muscle Atrophy
Findings
Conclusions
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