Moderate regular exercise has been shown to slow many of the degenerations of aging. Like calorie restriction, exercise exerts hormetic effects on the biochemistry of mammals, wherein low levels of stress boost repair and maintenance mechanisms, which in turn leads to improved health over time. Interestingly, exercise appears to slow down the accumulation of mitochondrial damage in at least some tissues, and regular readers will know that mitochondria play a pivotal role in age-related degeneration:
Aging is associated with a reduction in muscle mass and strength, which compromises functional independence. Skeletal muscle also shows an increase in mitochondrial dysfunction and oxidative stress in older adults. ... It has been shown that resistance-exercise training increases muscle strength and function in older adults, in association with a reduction in markers of oxidative stress and an improvement in mitochondrial function.
If you look back a few years, you'll find tentative evidence that the benefits of exercise extend to slowing the advance of Parkinson's disease. This is probably a mitochondrial connection, as progressive mitochondrial dysfunction is implicated in some fraction of Parkinson's cases. Some unfortunate folk have genes that make this sort of dysfunction - and the resulting loss of vital neurons that leads to the visible symptoms of Parkinson's disease - more likely to occur earlier in life. They are less resistant to this form of biochemical wear and tear, in other words.
Here's a short article on recent research adding more weight to the exercise-mitochondria-Parkinson's connection:
"Clinical reports have implicated exercise training in improving the physical performance and mobility of people with Parkinson's disease, but no one has demonstrated, either clinically or in laboratory models, whether exercise can delay the progression of neuronal degeneration," says senior author Yuen-Sum Lau at the Univ. of Houston. "This study was aimed at investigating this possibility and at examining how exercise protects neural mitochondria."
At the end of the study, the exercise-trained Parkinson's mice had significantly higher brain dopamine content and exhibited greater brain mitochondrial activity than the sedentary mice. They also performed better in a test that assessed their balancing abilities.
"This research provides scientific evidence that long-term endurance exercise protects brain mitochondria and dopamine-producing neurons from undergoing progressive degeneration as demonstrated in the chronic mice model of Parkinson's disease," says Lau.
A thought to finish with: investors are presently pouring billions into research intended to capture some fraction of the benefits of exercise or calorie restriction in a pill. You'd probably pay good money for the results of that research, given that the benefits over time are far greater than any presently existing therapy targeted at common age-related diseases. So why aren't you out there getting these benefits for free, the old-fashioned way?