The hundreds of mitochondria present in every cell are responsible for generating the chemical energy store molecule adenosine triphosphate to power cell processes. Dysfunction in the mitochondrial population is characteristic of aging and thought to be a meaningful contribution to loss of tissue function. This dysfunction arises in part because the quality control mechanisms that cull damaged mitochondria become less effective. When functioning correctly, the processes of mitophagy identify and flag damaged mitochondria, which are then conducted to a lysosome, engulfed, and broken down. The remaining mitochondria replicate to make up their numbers. Many interventions known to modestly slow aging or aspects of aging, exercise included, improve the operation of mitophagy and consequently improve mitochondrial function. How much of the overall benefit arises from improved mitophagy versus other mechanisms is a hard question to answer, however.
Sarcopenia is a syndrome associated with aging, characterized by a progressive decline in skeletal muscle mass and function. Its onset compromises the health and longevity of older adults by increasing susceptibility to falls, fractures, and various comorbid conditions, thereby diminishing quality of life and capacity for independent living. Accumulating evidence indicates that moderate-intensity aerobic exercise is an effective strategy for promoting overall health in older adults and exerts a beneficial effect that mitigates age-related sarcopenia. However, the underlying molecular mechanisms through which exercise confers these protective effects remain incompletely understood.
In this study, we established a naturally aging mouse model to investigate the effects of a 16-week treadmill-based aerobic exercise regimen on skeletal muscle physiology. Results showed that aerobic exercise mitigated age-related declines in muscle mass and function, enhanced markers associated with protein synthesis, reduced oxidative stress, and modulated the expression of genes and proteins implicated in mitochondrial quality control. Notably, a single session of aerobic exercise acutely elevated circulating levels of β-hydroxybutyrate (β-HB) and upregulated the expression of BDH1, HCAR2, and PPARG in the skeletal muscle, suggesting a possible role of β-HB-related signaling in exercise-induced muscle adaptations. However, although these findings support the beneficial effects of aerobic exercise on skeletal muscle aging, further investigation is warranted to elucidate the causal relationships and to characterize the chronic signaling mechanisms involved.
Link: https://doi.org/10.3390/metabo15070472
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