Muscle blood flow and mitochondrial function: influence of aging.

Skeletal muscle mitochondrial capacity (mito), tissue blood flow (BF) capacity, and oxygen exchange capacity (e.g., DO2) appear to be well matched. The different skeletal muscle fiber types and muscle remodeled, due to inactivity (e.g., related to aging or disease) or exercise training, exhibit widely differing aerobic capacities (VO2max). Yet, there are remarkably coordinated alterations in these 3 parameters in each of these conditions. With such a balance, there is likely shared control among these parameters in limiting VO2max of muscle, although this is a matter of considerable debate. The reduction in aerobic capacity in elderly can be improved by submaximal aerobic exercise training; this is related to increases in muscle mitochondria concentration and capillarity, but probably not BF capacity, as this is limited by central cardiovascular function. Thus, exercise-induced biochemical adaptations and angiogenesis occur in the elderly. The increase in muscle capillarity likely contributes to the increased oxygen exchange capacity, typical of endurance type training. The increase in [mito] appears essential to realize the increased in muscle VO2max with training and amplifies the rate-limiting influence of the muscles oxygen exchange capacity. Further, vascular remodeling induced by exercise in the elderly could be effective at improving flow capacity, if limited by peripheral obstruction. Thus, the limits to aerobic function specific to aged muscle appear most influenced by inactivity, whereas central cardiovascular changes impact whole body performance. Some may consider the aged myocyte as a small, inactive, normal myocyte in need of activity!