Studies in recent years have continued to illuminate the beneficial ways that exercise can influence the aging process, helping to address Sight loss, heart damage Y promote muscle repair, to cite a few examples. New research has added to this body of knowledge through experiments on old mice, which after undergoing an increasingly demanding physical conditioning regimen exhibited characteristics of mice eight weeks younger, compared to a control group of sedentary rodents.
The research focuses on a biological process known as DNA methylation, in which groups of atoms called methyl groups interact with the DNA molecule and alter the expression of our genes. This process is affected by a variety of environmental factors, such as diet and stress, throughout our lives and is therefore considered an epigenetic mechanism. associated with aging. DNA methylation tends to increase as we age.
“Changes in DNA methylation throughout life tend to occur in a somewhat systematic way,” explained study author Kevin Murach of the University of Arkansas. “To the point where you can look at someone’s DNA from a given tissue sample and pretty accurately predict their chronological age.”
The study involved mice near the end of their lives at 22 months of age, who were put through a progressive exercise regimen involving a weighted running wheel over the course of two months. This program resembles a human soldier carrying a heavy backpack for many miles, and was designed to ensure that the mice build muscle at all times.
Study of mice at the end of the program showed that exercise in old age had blunted epigenetic aging in their skeletal muscle. So much so that the epigenetic age of the tissue was found to be around eight weeks younger than a sedentary group of age-matched mice. While the results are promising and reinforce the idea that exercise is good for health, more work is needed to uncover the connection between methylation and muscle function.
The scientists plan to conduct further studies exploring this connection and to investigate whether altered methylation, through exercise or otherwise, can lead to changes in muscle health and function.
“If so, what are the consequences of this?” Murach said. “Do changes at these very specific methylation sites have an actual phenotype that stems from that? Is it what is causing the aging or is it just associated with it? Is it just something that happens along with a variety of other things that happen during the aging process? So that’s what we don’t know.”
The research was published in the journal aging cell.
Fountain: University of Arkansas
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