MOLECULAR MECHANISMS OF SKELETAL MUSCLE ADAPTATION DURING PHYSICAL TRAINING AND AGING

Abstract

This article provides an in-depth analysis of the molecular processes that regulate skeletal muscle adaptation under two contrasting physiological conditions: physical training and aging. It explores how cellular signaling pathways, gene expression, mitochondrial biogenesis, and protein turnover contribute to muscle plasticity, hypertrophy, and maintenance. The study highlights the roles of key molecular regulators such as AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and myostatin in controlling muscle mass and performance. The interaction between exercise-induced signaling and age-related molecular decline is examined to understand how training mitigates sarcopenia and functional deterioration. These insights form a scientific foundation for developing strategies to preserve muscle health across the lifespan. This article investigates the intricate molecular mechanisms underlying skeletal muscle adaptation in response to physical training and the degenerative effects of aging. The research emphasizes how distinct cellular signaling pathways, transcriptional regulators, and mitochondrial processes influence the dynamic remodeling of muscle fibers. Physical activity activates molecular cascades that enhance energy metabolism, improve protein synthesis, and stimulate mitochondrial renewal, while aging triggers a progressive decline in these same pathways. The study aims to elucidate how exercise reprograms molecular responses to counteract sarcopenia, oxidative damage, and metabolic inefficiency. By integrating recent advances in molecular biology and physiology, this work provides a detailed perspective on how targeted interventions can preserve muscle performance and metabolic resilience throughout the human lifespan.