# Skeletal Muscle Atrophy Induced by Dexamethasone Is Attenuated by Amino Acid Complex Supplementation in Rats

## TL;DR

This study shows that amino acid complex supplementation can reduce muscle atrophy caused by dexamethasone in rats, improving muscle strength and recovery.

## Contribution

The study demonstrates that high-dose amino acid complex supplementation effectively prevents and treats dexamethasone-induced muscle atrophy in a rat model.

## Key findings

- High-dose amino acid complex supplementation significantly improved exercise capacity and preserved muscle protein in dexamethasone-treated rats.
- Electron microscopy showed better muscle fiber preservation in the high-dose amino acid complex group compared to the dexamethasone-only group.
- Amino acid complex supplementation reduced muscle damage markers and improved muscle tissue structure in the rat model.

## Abstract

Muscle atrophy, a physiological decline in muscle mass and strength due in ageing, occurs through an imbalance between protein breakdown and synthesis. The purpose of this study was to verify whether amino acid complex supplementation (ACS) can prevent and treat muscle loss in a dexamethasone (Dexa, 800 μg/kg)-induced rat model of sarcopenia. Sprague Dawley rats (6 weeks old) were assigned to seven groups: (i) normal control, (ii) positive control (high-dose ACS, 500 mg), (iii) Dexa only, (iv) Dexa + high-dose ACS (500 mg), (v) Dexa + medium-dose ACS (300 mg), (vi) Dexa + low-dose ACS (100 mg), or (vii) Dexa + liquid amino acid complex formulation (LF, 2 mL), administered orally for 4 weeks. Exercise capacity tests were performed five times using a treadmill test (TT) and forced swimming test (FST). The body weight increase in each group was less than that of the normal group. The blood biochemical indices, AST levels, and AST/ALT ratio significantly increased in the Dexa-treated medium-dose ACS group. The total muscle protein also significantly increased in all ACS groups. In the Dexa-treated LF group, CK decreased below the normal level. Exercise capacity, assessed by TT and FST, increased the most in the positive control and Dexa-treated high-dose ACS groups. In the TT, the Dexa-only group increased by about 18%, but the Dexa-treated high-dose ACS group increased by about 110%. Additionally, in the FST, Dexa-treated rats receiving a high dose of ACS demonstrated significantly increased exercise time and capacity. Electron microscopic (EM) and hematoxylin and eosin (H&E) observations of muscle tissue revealed muscle fiber atrophy in the gastrocnemius muscles of the Dexa-only group. In the EM findings of the Dexa-treated high-dose ACS group, the M-line and Z-line were clearer than in the Dexa-only group, and the mitochondria were partially preserved. In conclusion, the ACS-treated rats showed a clear recovery from muscle damage based on serum indices, total muscle protein mass, and the microscopic findings on muscle tissue. Notably, a high dose of ACS demonstrated the most effective protection and recovery of muscle tissue in the Dexa-induced sarcopenia rat model.