Here are the results of an analysis of the effects of exercise on aging and longevity in mice: it is expected to slow the onset of age-related frailty, but unlike the practice of calorie restriction it fails to extend either average or maximum life span.
Exercise has been unequivocally associated with a slowing of age-specific mortality increases in rats and with an increased median lifespan. However, the results in mice [to date] are not that clear.
Male C57Bl/6J mice, individually caged, were randomly assigned to one of two groups: sedentary (n = 72) or spontaneous wheel-runners (n = 72). We evaluated longevity and several health parameters including grip strength, motor coordination, exercise capacity (VO2max) and skeletal muscle mitochondrial biogenesis. We also measured the cortical levels of the brain-derived neurotrophic factor (BDNF), a neurotrophin associated with brain plasticity. In addition, we measured systemic oxidative stress and the expression and activity of two genes involved in antioxidant defense in the liver (that is, glutathione peroxidase (GPx) and manganese superoxide dismutase (Mn-SOD)). Genes that encode antioxidant enzymes are considered longevity genes because their over-expression may modulate lifespan.
Exercise does not cause an increase in either average lifespan or maximal lifespan. Maximal lifespan was defined as the age at which the longer-lived animal died. In our mice it was 950 days. Average lifespan was defined as the age at which 50% of the animals died. It was 750 days for sedentary mice and 770 for wheel-runners. Aging was associated with an increase in oxidative stress biomarkers and in the activity of the antioxidant enzymes, GPx and Mn-SOD, in the liver in mice. Life-long spontaneous exercise did not prolong longevity but prevented several signs of frailty (that is, decrease in strength, endurance and motor coordination). This improvement was accompanied by a significant increase in the mitochondrial biogenesis in skeletal muscle and in the cortical BDNF levels.