Alterations in Skeletal Muscle Strength and Mitochondrial Function Induced by Aging and Exercise

Abstract

<p><strong>Introduction:</strong> Mitochondria are important organelles for skeletal muscle function. Mitochondria are susceptible to many forms of stress that alters their morphology, energy generation and reactive oxygen species (ROS) production, which collectively promote degeneration and dysfunction in skeletal muscle. These processes are implicated in many health disorders, particularly in the aging process itself. Exercise is well established to increase muscle mitochondrial content and thus may attenuate several aspects of mitochondrial deterioration. <strong>Methods:</strong> Both human and animal models of mitochondrial stress (aging, ROS) were utilized in order to determine their effects on mitochondrial and muscle function. Additionally, exercise training was used in order to assess its therapeutic potential in ameliorating defects in oxidative capacity, muscle atrophy and metabolic adaptation in skeletal muscle. <strong>Results:</strong> Aging resulted in reduced strength, aerobic capacity, larger intramyocelluar lipid droplets and fewer mitochondria in skeletal muscle. These changes were related to suppressed lipid metabolism, mitochondrial dynamics and organelle turnover. Habitual aerobic exercise partially attenuated the age-related loss of muscle strength and aerobic capacity, presumably due in part to improved mitochondrial function. Persistent mitochondrial oxidative stress prevented mitochondrial adaptations to exercise training in mice, a phenomenon that may explain why exercise cannot fully counteract the effects of aging in skeletal muscle. <strong>Conclusions and significance:</strong> This work furthers our knowledge of the mitochondrial consequences of aging and the therapeutic potential of aerobic exercise within skeletal muscle. These results can be applied to other differentiated tissues that are severely affected by aging (brain, heart) and the effects described here are likely relevant to other conditions that result in muscle atrophy and energetic insufficiency.</p>