Physical Training Counteracts Mitochondrial Alterations in Myoblasts and Myotubes Derived From Muscle Satellite Cells of Old Mice: An In Vitro Ultrastructural Study

Skeletal muscle is a complex organ that undergoes aging through a multifactorial process leading to muscle atrophy and strength reduction. Mitochondrial dysfunctions prove to be a critical contributor to skeletal muscle aging, affecting the regenerative functions and differentiation of muscle satellite cells (MuSCs). Physical exercise is a nonpharmacological approach that positively affects mitochondrial functions, promoting increased mitochondrial biogenesis, enzyme activities, and respiration in the aging skeletal muscle. By means of morphological and morphometrical analyses at transmission electron microscopy, this in vitro study identified the fine structural modifications induced in mitochondria of MuSC-derived myoblasts by a long-term adapted physical exercise applied to old mice, and verified the persistence of the exercise-driven changes in the myoblast-derived myotubes. In myoblasts, physical exercise decreased mitochondrial volume while increasing mitochondrial elongation and cristae extension in comparison to the sedentary condition, a mitochondrial remodeling suggestive of higher functionality. In myotubes, physical exercise increased mitochondrial volume and decreased cristae extension, partially reverting the age-associated alterations. These findings demonstrate that physical exercise administered in elderly exerts positive effects on mitochondria of the progeny of resident MuSCs.