As you probably know by now, the well-supported mitochondrial free radical theory of aging tells us that damage to the DNA in mitochondria, the power plants of our cells, is an important root cause of aging. You can look back in the archives for an explanation as to exactly why that is the case.
There's every reason to expect that methods to repair or otherwise negate mitochondrial DNA (mtDNA) damage will produce great benefits, and a reversal of one contribution to the aging process. A number of different approaches are presently in various stages in the laboratory, including the SENS Foundation's MitoSENS strategy:
rather than fixing mitochondrial mutations, we can make them harmless to us. By putting "backup copies" of these few remaining genes into the nucleus, we can prevent the harm caused by any mutations that may occur of the original versions. Even without the mitochondrial DNA, the proteins that it encodes will still be produced and incorporated into the mitochondrial machinery, allowing the cellular power plants to continue humming along normally.
For today, however, I'll point your attention to an open access paper on how exercise interacts with damaged mitochondrial DNA. It puts forward a mechanism (and offers evidence in support) by which exercise acts to slow this one contribution to aging:
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. Patients with sporadic mitochondrial cytopathies show an accumulation of mitochondrial DNA mutations and deletions in mature muscle, but not in satellite cells. Such patients have shown an activation of the satellite cells following myotoxic trauma and resistance, likely due to a fusion of the relatively quiescent satellite cells with mature muscle, which dilutes the mutational burden, a process called mitochondrial DNA shifting. Preliminary data strongly suggest that mitochondrial DNA shifting occurs in skeletal muscle from older adults following resistance-exercise training.
Which raises some interesting questions, such as how the satellite progenitor cells are evading mitochondrial damage. Not to mention:
Although the actual number of deletions is lower after training, how are the dysfunctional mitochondria removed (autophagy)? What intensity of training is required to activate the satellite cells to induce shifting? Can we enhance satellite cell activation in older adults to maximize shifting? Are we actually inducing shifting from satellite cells or are we simply removing the mutant mtDNA by autophagy?
Then again, the whole thing might just be another health benefit of enhanced autophagy and the satellite cells a good red herring. We shall no doubt learn more in the years ahead.
However it turns out, we can't exercise our way to agelessness, however. Studies suggest that an extra decade, give or take, is the plausible difference in life expectancy between regular exercise and a sedentary life style. While exercise and calorie restriction both appear to slow most (even near all) of the effects of aging, far better technologies aimed at repairing the damage rather than slowing its accumulation are both possible and needed.
Tarnopolsky, M. (2009). Mitochondrial DNA shifting in older adults following resistance exercise training Applied Physiology, Nutrition, and Metabolism, 34 (3), 348-354 DOI: 10.1139/H09-022