It is interesting to see the sizable degree to which sufficient physical activity can mitigate many of the effects of aging in muscle tissue. It is well known that exercise programs improve muscle function and reduce mortality in later life. In the study reported here, the intent was to distinguish (a) effects of aging from (b) effects of lack of exercise in later life on mitochondrial function in muscle tissue. Older people in wealthier parts of the world largely live a sedentary life. Few exercise to the degree that they should in order to maintain function and health. Researchers here find that reduced mitochondrial function in muscle in their study population is largely the result of insufficient exercise. They also note that an adequate level of exercise to maintain mitochondrial function in youth ceases to be adequate in later life, only reinforcing the importance of physical activity to health in old age.
One of the distinctive features of aging is the progressive loss of muscle mass and physical function, collectively known as sarcopenia. In parallel with the progressive loss of muscle function, mitochondrial respiratory activity in human skeletal muscle has been shown to decrease with advancing age in healthy men and women. Furthermore, protein levels of the mitochondrial master regulator peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α) were found to correlate with walking speed in healthy older adults. Some preclinical studies indeed suggest that the reduction in muscle mitochondrial function may underlie the decline in muscle health during aging. Therefore, it is tempting to speculate that augmenting mitochondrial function could be a potential strategy to counteract aging-associated decline in physical function.
Although some human studies have addressed age-related alterations in muscle mitochondrial function in relation to the decline in skeletal muscle function, the available data in humans is scarce and the few available studies often focus on either the decline in muscle function or concentrate primarily on the mitochondrial alterations. Additionally, the age-associated decline in mitochondrial function is not completely attributable to aging per se and may also be explained, in part, by an age-related decline in physical activity (PA). Decreased PA can adversely affect mitochondrial capacity.
To delineate these relationships, we conducted a cross-sectional study with detailed phenotyping in groups of young versus older human participants, with a range in oxidative capacity and physical function. The first aim of the study was to assess if mitochondrial function is reduced in older compared to young participants with a similar level of habitual PA, and to examine how mitochondrial function relates to muscle function.
Aging was associated with a decline in mitochondrial capacity, exercise capacity and efficiency, gait stability, muscle function, and insulin sensitivity, even when maintaining an adequate daily physical activity level. Our data also suggest that a further increase in physical activity level, achieved through regular exercise training, can largely negate the effects of aging. Finally, mitochondrial capacity correlated with exercise efficiency and insulin sensitivity. Together, our data support a link between mitochondrial function and age-associated deterioration of skeletal muscle.
Source: Fight Aging!