Mechanical Overload-Induced Retinoid Metabolism Is Involved in Protein Synthesis in Skeletal Muscle of Female Mice

抄録

Although exercise is the most effective strategy for increasing the skeletal muscle mass, the underlying molecular mechanisms remain poorly understood. We previously demonstrated that β-carotene, a provitamin A compound, enhances muscle mass through a retinoic acid receptor γ (RARγ)-dependent pathway. However, the involvement of vitamin A in exercise-induced muscle hypertrophy remains unclear. In this study, we used a mouse model of functional overload to mimic resistance exercise and investigated the role of vitamin A in overload-induced muscle growth. Overload increased the expression of Rdh10, Dhrs9 and Aldh1a2, an enzyme required for active vitamin A synthesis in the skeletal muscle. In contrast, the expression of Aldh1a1, Dhrs3, and Rarb was decreased by the overload. Vitamin A deficiency significantly suppressed overload-induced muscle hypertrophy and protein synthesis. Moreover, local administration of an RAR antagonist to the skeletal muscle reduced overload-induced protein synthesis. These findings suggest that vitamin A contributes to skeletal muscle hypertrophy during muscle overload by promoting protein synthesis via RAR-mediated signaling.