The transcriptional coactivator PGC-1α is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling

Abstract

Significance Skeletal muscle hypertrophy is mainly induced by growth hormones and mechanical overload and exerts health beneficial effects. The mammalian target of rapamycin complex 1 (mTORC1) and the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) are key regulators of skeletal muscle mass and energy metabolism, respectively. Thus, acting in concert, mTORC1 and PGC-1α interplay is thought to regulate skeletal muscle function. Our results indicate that PGC-1α is not required for skeletal muscle hypertrophy and a slow-contractile phenotype induced by chronic overload of the plantaris muscle. In fact, PGC-1α gene expression and global energy metabolism were repressed in this experimental context of muscle hypertrophy. Hence, these results exclude PGC-1α as the main regulator of skeletal muscle remodeling after chronic overload.