Dexamethasone (DEX) promotes proteolysis, which causes muscle atrophy. Muscle atrophy is connected to sarcopenia. We evaluated the effect of Curcuma longa L. water extract (CLW) on DEX-induced muscle atrophy. ICR mice were divided into three groups (eight mice per group) to investigate the capability of CLW in inhibiting muscle atrophy. The control group (Ex-CON) was administered distilled water (DW) by gavage and subjected to exercise; the muscle atrophy group (Ex-DEX) was administered DW by gavage, an injection of DEX (1 mg/kg body weight/day) intraperitoneally (IP), and subjected to exercise; and the treatment group (Ex-CLW) was administered CLW (1 g/kg body weight/day) by gavage, DEX IP injection, and subjected to exercise. Following the injection of DEX, the expression levels of myostatin, MuRF-1, and Atrogin-1 were increased. However, these expression levels were decreased in the Ex-CLW group, thereby leading to the conclusion that CLW inhibits muscle atrophy. ROS (that was overproduced by DEX) decreased antioxidant enzyme activity and increased malondialdehyde (MDA) levels, which led to muscle atrophy. When CLW was ingested, the antioxidant enzyme activities increased while the MDA levels decreased. These findings suggest that CLW could serve as a natural product for the prevention of muscle atrophy by modulating muscle atrophy-related genes and increasing antioxidant potential.

The aim of this study was to evaluate the effects of ethanol extracts of Vaccinium corymbosum (VCE) on exercise-induced fatigue in mice. Mice were randomly divided into three groups; nonexercise control group (CON), exercise control group (Ex-CON), and exercise and VCE supplementation group (Ex-VCE). Compared with Ex-CON, Ex-VCE showed increased endurance exercise capacity on day 21. In Ex-VCE mice, the accumulation of lactate was inhibited and the consumption of fatty acids was enhanced, indicating the delay of muscle fatigue. In addition, VCE supplementation elevated mRNA expression levels of mitochondrial biogenesis-associated genes such as peroxisome proliferator-activated receptor-1γ coactivator 1α (PGC-1α), nuclear respiratory factor (NRF), and mitochondrial transcription factor A (Tfam) and fatty acid β-oxidation-associated genes such as carnitine palmitoyltransferase-1 (CPT-1), β-hydroxyacyl coenzyme A dehydrogenase (β-HAD), and peroxisome proliferator-activated receptor-δ (PPAR-δ). These results suggest that VCE can potentially prevent muscle fatigue by enhancing mitochondrial biogenesis and fatty acid β-oxidation.