Perspectives on Epigenetic Markers in Adaptation to Physical Exercise

International audience

English. Physical exercise regulates several signaling pathways to generate skeletal muscle adaptations, such as improvement of cell metabolism and myofibrillar remodeling. Thus, exercise modulates the number, functioning, and turnover of cellular organelles (e.g., mitochondria and ribosomes), contributing to lower perturbations of cellular homeostasis and preserving muscle efficiency [1-3]. While unaccustomed subjects generate global cellular responses and adaptations, specific adjustments are promoted in well-trained athletes [1-3]. Importantly, these adaptations depend on training modalities. For instance, resistance exercise elicits increases in muscle mass and strength related to increased myofiber size, raised myosin ATPase activity, and myofibrillar adjustments, such as the transition of myosin heavy chains isoforms [4, 5]. Moreover, training adaptations are impacted by a plethora of variables, including dietary factors, exercise intensity and volume, recovery processes, several environmental (e.g., hypoxia and temperature), and genetic/epigenetic factors [2, 3]. Thus, exercise modulates the constituents of the epigenetic toolbox to promote skeletal muscle adaptation. Among these mechanisms, DNA methylation (i.e., the addition of methyl groups to the fifth carbon of the cytosine ring of DNA) and the involvement of microRNAs (miRNAs) are of growing interest, and recent studies have highlighted their critical roles in both acute response and long-term adaptations [3, 6]. Epigenetics mechanisms are relevant for cells to adapt when encountering physiological or environmental stimuli. miRNAs are small (~22 nucleotides), non-coding RNAs that inhibit or impair translation by binding to the 3' UTR (untranslated region) of their target mRNA. However, binding can occur on other complementarity sites. In the case.