Regulatory Role of MicroRNAs in Muscle Atrophy during Exercise Intervention

Abstract

Skeletal muscle comprising approximately 40% of body weight is highly important for locomotion and metabolic homeostasis. The growth and regeneration of skeletal muscle are highly organized processes; thus, it is not surprising to reveal certain complexity during these regulatory processes. Recently, a large number of evidence indicate that microRNAs can result in obvious impacts on growth, regeneration and metabolism of skeletal muscle. In this review, recent research achievements of microRNAs in regulating myogenesis, atrophy and aging during exercise intervention are discussed, which will provide the guidance for developing potential applications of microRNAs in health promotion and rehabilitation of sports injuries.

Keywords: exercise; microRNA; muscle atrophy; myogenesis; sport injury.

Figure 1

Effect of exercise on miRNAs. (A) A single bout of resistance exercise in men reduces miR-1 expression and does not affect the expression of miR-133a and -206. The miR-1 can promote protein synthesis through the IGF-1/Akt signal pathway. The change in the expression of miR-378 is positively correlated with the improved quality of skeletal muscle due to resistance exercise. Similarly, miR-378 inhibits PGC-1β-mediated mitochondrial metabolic effects by MED13 and CRAT; (B) a single bout of endurance exercise in mice reduces the expression of miR-23a and increases the expression of miR-1, -181 and -107. Endurance training increases the expression of miR-21 and decreases the expression of miR-696, -709 and -720 in mice. ↑ increased; ↓ decreased; → unchanged; ⊥ inhibited. IGF: insulin-like growth factor; Akt: protein kinase B; PGC-1: peroxisome proliferation-activated receptor-γ coactivator-1; MED13: mediator complex subunit 13; CRAT: carnitine acetyltransferase; VEGF: vascular endothelial growth factor.