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- Alex Hutchinson (@sweatscience)
Scientists don’t know exactly why or how we get old, but they have a few theories. One of them is that mutations in mitochondrial DNA gradually accumulate until body systems stop working properly — a theory supported by the premature aging observed in mice genetically engineered to rapidly accumulate mutations in mitochondrial DNA. Yesterday, McMaster University researcher Mark Tarnopolsky‘s group published a paper in the Proceedings of the National Academy of Sciences in which these fast-aging mice ran on a treadmill — with extremely encouraging results:
[T]hose who had endurance exercise training three times a week looked as young as healthy mice while their sedentary siblings were balding, greying, physically inactive, socially isolated and less fertile. [press release here]
Sounds pretty good… and the changes weren’t just on the outside. In the exercising mice, their brains didn’t shrink, their muscles didn’t waste, their hearts didn’t weaken, they didn’t die prematurely, and so on and so on. Of course, mutations in mitochondrial DNA were still accumulating — but the basic cellular response to endurance training is that you increase the amount of mitochondria in your cells, so the researchers suspect that having lots of healthy mitochondria made the mice less susceptible to problems stemming from the mutations.
This isn’t the only theory about aging. Telomere length is another idea that has received a lot of attention recently, for example — but that too seems to respond dramatically to endurance exercise. Of course, conflicts of interest should be reported in studies like this: Tarnopolsky is a highly accomplished ultra-runner! 🙂