It’s a humbling fact of life that our muscles decline as we age which is why you didn’t see any 50-year-olds competing for Olympic Gold in figure skating at the 2018 Winter Games.
You can blame your muscle stem cells for this. Also called satellite cells, these adult stem cells lie mostly dormant in muscle tissue until, in response to exercise or injury, they begin to divide, specialize and replenish damaged muscle cells. But, this restorative function declines over time diminishing the ability of aging muscle stem cells to grow new muscle, and in turn, leading to a gradual deterioration in strength and agility.
While this connection between aging muscle and stem cells has been well-known, the underlying reasons are less well understood. However, a recent Nature Communications study by researchers at the Karolinska Institute in Sweden makes an important inroad: muscle stem cells from healthy, older individuals have a surprising number of genetic mutations compared to their younger counterparts.
To carry out the comparison, the researchers isolated muscle stem cells from muscle biopsies taken from groups of young (21-24 yrs) and more senior (68-75 yrs) healthy adults. Single cell DNA sequencing (which creates a genetic blueprint for individual cells) showed that the older stem cells had accumulated 2 to 3 times more mutations in genes that are active in the muscle stem cells. This higher “burden” of mutations also appeared to impair cell function: in the older group, those stem cells with higher numbers of mutations had a lower capacity to divide and specialize into certain types of muscle cells. The younger stem cells did not show this behavior suggesting they are better protected from these mutations, as team lead, Professor Maria Eriksson, explained in a press release:
“We can demonstrate that this protection diminishes the older you become, indicating an impairment in the cell’s capacity to repair their DNA. And this is something we should be able to influence with new drugs.”
In addition to possible drug interventions, Dr. Eriksson is also interested in evaluating the role of exercise to counteract the effects of these mutations:
“We aim to discover whether it is possible to individually influence the burden of mutations. Our results may be beneficial for the development of exercise programs, particularly those designed for an aging population.”