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.
Kitakaze et al. (Thu,) studied this question.