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McMaster University: Exercise compensates for mitochondrial DNA damage in mice

The mitochondrial theory of aging postulates that the lifelong accumulation of somatic mitochondrial DNA (mtDNA) mutations leads to progressive decline in tissue function. To what extent can exercise slow that decline?

Using mice that were genetically engineered for elevated mtDNA mutations, researchers at McMaster University found that 45 minutes of treadmill exercise three times a week stopped the expected rapid aging. The genetically modified mice that exercised on a treadmill three times a week, were comparable to healthy mice, while sedentary mice aged rapidly, becoming bald, gray-haired, weak, socially isolated an less fertile.

The abstract of the article reporting on the research is here, but the article is behind a pay-wall. You can, however, see the detailed supporting material without paying. The supporting material includes four movies that show the effect of exercise. Check this one out:

Click to play the movie

Mice on a treadmill -- which one works out?

This study is great news if you are a genetically engineered mouse, and it may offer a partial explanation of aging and the benefits of exercise in some humans.