The Role of DNA Methylation in Regulating Skeletal Muscle Adaptation to Exercise: A Literature Review

Abstract

Introduction: The skeletal muscle tissue has a remarkable degree of plasticity. In the case of exercise training, the skeletal muscle adapts to match the specific stress imposed by the training modality. Aerobic exercise training promotes oxidative metabolism, angiogenesis, and fiber type switching from type IIb to IIa. Conversely, resistance exercise training promotes muscle protein synthesis and a hypertrophic response of the skeletal muscle. Regardless of training modality, the tissular adaptation of the skeletal muscle is a consequence of underlying changes in gene expression. Changes in promoter DNA methylation regulate genes' activation, or silencing, by influencing euchromatin and heterochromatin organization, respectively, ultimately determining chromatin accessibility to transcriptional machinery. It surmises that dynamic DNA methylation mechanisms would regulate acute exercise-responsive genes in skeletal muscle. In the context of exercise training, alterations in DNA methylation of gene promoters could support long-term changes in gene expression or restrict the responsiveness of acute exercise genes.

Methods: This literature review will involve a comprehensive search of peer-reviewed articles published after the year 2000 in databases including UBC Library, PubMed, Google Scholar, and Web of Science. Articles selected for inclusion were screened based on relevance to the topic and quality of evidence. Data extraction was focused on identifying key findings related to DNA methylation changes in skeletal muscle following exercise interventions.

Results: Resistance training alters DNA methylation in skeletal muscle, enhancing genes for muscle growth and strength. Aerobic training reduces DNA methylation, boosting genes for mitochondrial biogenesis, glucose metabolism, and muscle endurance.

Discussion: The discussion highlights that both aerobic and resistance training induce long-term epigenetic modifications in skeletal muscle, creating a "memory" that enhances muscle adaptability and performance in future exercises. These findings suggest potential therapeutic applications for muscle-wasting diseases and metabolic disorders, emphasizing the need for personalized exercise regimens to maximize health benefits.

Conclusion: This literature review emphasizes the pivotal role of DNA methylation in skeletal muscle adaptation to exercise, highlighting the distinct epigenetic modifications induced by aerobic and resistance training that enhance muscle function and metabolic health.