Adults who receive at least 150 minutes of moderate aerobic activity or 75 minutes of vigorous aerobic activity a week, reduce their risk for chronic disease by ensuring oxygen and nutrients are properly delivered to epithelial, connective and nervous body tissue.
Over time, these benefits become more pronounced. According to a new study conducted by researchers from Stanford University, habitual exercise influences molecular pathways important to the ageing process.
The older we get, the less efficiently our anatomy copes with our surroundings. This degeneration produces a number of different adverse scenarios and can be assessed via a declining function in stem cells.
With a crop of mouse models, the Stanford researchers determined that old mice were able to restore damaged tissue as well as damaged muscle stem cells after just three weeks of nightly aerobic exercise.
“Ageing impairs tissue repair. This defect is pronounced in skeletal muscle, whose regeneration by muscle stem cells (MuSCs) is robust in young-adult animals but inefficient in older organisms,” the authors wrote in the journal Nature Metabolism. “Here, we show that exercise in the form of voluntary wheel running accelerates muscle repair in old mice and improves old MuSC function. Through transcriptional profiling and genetic studies, we discovered that the restoration of old MuSC activation ability hinges on the restoration of Cyclin D1, whose expression declines with age in MuSCs.”
Exercise rejuvenates quiescent skeletal muscle stem cells in old mice
Recently, Ladders reported on the ways daily strenuous physical activity can yield adverse effects on overall health.
When done in excess, these kinds of routines put extreme demands on the cardiovascular system, which can lead to thickening of the muscle’s walls and tissue scarring over time.
Similarly, immoderate resistance training and intense endurance exercises have been studied to impair muscle stem cell function in their own ways.
The animals in the Stanford study were placed on mild exercise regimens that did not surpass their comfort levels.
Before analysing exercise’s effect on ageing, the team made sure that the muscle stem cells of the animals tasked with nightly aerobic exercises remained quiescent.
After comparing the sedentary control group with the active experiment group, the researchers found that the aged, sedentary mice were much less able to repair muscle damage compared to younger sedentary mice.
However, older mice that had exercised regularly were considerably better at repairing muscle damage. This outcome was evidenced in active mice of all ages.
The findings seem to suggest that regular exercise facilitates the healthy circulation of blood and alongside the rejuvenation of older stem cell function and the protein Cyclin D1.
These benefits support other factors that reduce one’s risk of developing cancer, heart disease and stroke.
“Through transcriptional profiling and genetic studies, we discovered that the restoration of old MuSC activation ability hinges on the restoration of Cyclin D1, whose expression declines with age in MuSCs. Pharmacologic studies revealed that Cyclin D1 maintains MuSC activation capacity by repressing TGF-β signalling. Taken together, these studies demonstrate that voluntary exercise is a practicable intervention for old MuSC rejuvenation. Furthermore, this work highlights the distinct role of Cyclin D1 in stem-cell quiescence,” the autos concluded.
Although the Department of Health’s exercise guidelines should do the trick, experts are currently working on developing supplements to clinically mimic this process.