Skeletal muscle aging, often accompanied by sarcopenia and metabolic dysfunction, is closely associated with an imbalance in epigenetic regulation involving histone acetylation (HATs) and deacetylation (HDACs). HATs activate muscle metabolic genes (such as PGC-1α and GLUT4) by enhancing chromatin accessibility, thereby promoting mitochondrial biogenesis and glucose metabolism. Conversely, HDACs contribute to muscle atrophy by inhibiting transcription. Studies have revealed that endurance exercise activates HATs through the AMPK/CaMK signaling pathway, while resistance training enhances transcriptional activity by reducing HDAC4/5 levels. Both types of exercise can delay age-related muscle function decline. During the aging process, a decrease in histone acetylation levels coupled with an increase in HDACs activity suppresses the expression of muscle repair genes, exacerbating mitochondrial dysfunction. Targeted interventions, such as the use of HDAC inhibitors, have been shown to reverse pathological gene networks and promote regeneration in animal models. Future research should integrate single-cell epigenomics and multi-omics approaches to elucidate the mechanisms underlying exercise-induced chromatin remodeling, aiming to develop precision treatment strategies. This article systematically elucidates the central role of the HATs/HDACs balance in muscle health and aging, providing a theoretical basis for delaying muscle decline through exercise and epigenetic interventions.