Myostatin Signaling in Skeletal Muscle: Implications for Athletic Performance.

Authors

Srishti Chandel, Deenathayalan Uvarajan, Mahalaxmi Iyer, Dibbanti HariKrishna Reddy, Zothan Siama, Bupesh Giridharan, Arul Narayanasamy, John M, Arvinder Wander, Balachandar Vellingiri

Published in

Comprehensive Physiology. Volume 16. Issue 3. Pages e70190.

Abstract

Myostatin, encoded by the MSTN gene, is a critical negative regulator of skeletal muscle growth and plays a central role in maintaining muscle homeostasis. It regulates satellite cell proliferation, differentiation, and protein synthesis through both Smad-dependent and non-Smad signaling pathways. Overexpression of myostatin promotes muscle atrophy and delays recovery, whereas reduced myostatin activity enhances protein synthesis and muscle regeneration, primarily by modulating the IGF-1/Akt/mTOR signaling pathway. Modulation of myostatin has been associated with improved metabolic function, increased insulin sensitivity, enhanced musculoskeletal adaptation, and improved performance sustainability. Genetic variations in MSTN and its receptors activin-type II receptor A (ACVR2A) and activin type II receptor B (ACVR2B) R2B contribute to inter-individual differences in muscle morphology, fiber-type distribution, and athletic performance. Specific polymorphisms, including rs1805086 and rs11333758, have been associated with variations in muscle strength, hypertrophy, and endurance capacity. Despite extensive research, a comprehensive evaluation of the relationship between MSTN signaling, skeletal muscle mass, and athletic performance remains limited. This review provides an integrated overview of myogenesis, MSTN-mediated signaling pathways, genetic polymorphisms, endocrine interactions, and therapeutic modulation strategies. We further discuss the implications of MSTN in muscle hypertrophy, inflammation, and sports performance, highlighting future research directions in precision sports genomics and translational muscle biology.

PMID:
42322019
Bibliographic data and abstract were imported from PubMed on 20 Jun 2026.

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