Abstract
The role of mitochondrial dysfunction and oxidative stress has been extensively characterized in the aetiology of sarcopenia (aging-associated loss of muscle mass) and muscle wasting as a result of muscle disuse. What remains less clear is whether the decline in skeletal muscle mitochondrial oxidative capacity is purely a function of the aging process or if the sedentary lifestyle of older adult subjects has confounded previous reports. The objective of the present study was to investigate if a recreationally active lifestyle in older adults can conserve skeletal muscle strength and functionality, chronic systemic inflammation, mitochondrial biogenesis and oxidative capacity, and cellular antioxidant capacity. To that end, muscle biopsies were taken from the vastus lateralis of young and age-matched recreationally active older and sedentary older men and women (N = 10/group; ♀ = ♂). We show that a physically active lifestyle is associated with the partial compensatory preservation of mitochondrial biogenesis, and cellular oxidative and antioxidant capacity in skeletal muscle of older adults. Conversely a sedentary lifestyle, associated with osteoarthritis-mediated physical inactivity, is associated with reduced mitochondrial function, dysregulation of cellular redox status and chronic systemic inflammation that renders the skeletal muscle intracellular environment prone to reactive oxygen species-mediated toxicity. We propose that an active lifestyle is an important determinant of quality of life and molecular progression of aging in skeletal muscle of the elderly, and is a viable therapy for attenuating and/or reversing skeletal muscle strength declines and mitochondrial abnormalities associated with aging.
Highlights
Individuals over the age of 69 y represent one of the fastest growing segments of the North American population [1]
We have shown that a sedentary lifestyle, associated with osteoarthritis mediated hypodynamia, promoted loss of muscle strength, weakness, and reductions in functional capacity, fat-free mass, and mitochondrial oxidative capacity concomitant with ‘‘low-grade’’ chronic inflammation in the skeletal muscle of older adults
In recreationally active older adults, mitochondrial biogenesis and electron transport chain (ETC) function are relatively preserved in skeletal muscle
Summary
Individuals over the age of 69 y represent one of the fastest growing segments of the North American population [1]. One of the most striking and debilitating age-associated alterations is the progressive loss of fat-free skeletal muscle mass, a phenomenon known as sarcopenia [4,5,6,7] This loss of muscle mass and strength, and the increase in body fat with aging are physiological phenomena that occur in part as a consequence of metabolic changes associated with a sedentary lifestyle in older adults [8,9]. Longitudinal studies have shown that regular physical activity may extend life expectancy, reduce morbidity (cancer, neurological disease, etc.), and reduce physical disability in later life [2,3,16,17,18,19] These findings suggest that preserving mobility and an active lifestyle is essential in maintaining a high quality of life in older adults
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