A study reveals the “key to youthful muscles”.. How does exercise reverse the effects of aging?

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A new study, published in the journal PNAS and whose details were reported on the Science Daily website, revealed that exercise not only contributes to strengthening muscles, but can also reverse some of the biological changes associated with aging, by restoring the muscles’ ability to repair themselves and get rid of damaged proteins. The study was led by researchers from Duke-NUS School of Medicine in collaboration with Singapore General Hospital and Cardiff University.

As people age, they suffer from a gradual decline in muscle mass and strength, which makes it more difficult to perform daily activities and raises the risk of falls and fractures. Muscle weakness also affects the speed of recovery from injuries and diseases, in addition to its role in disrupting the regulation of sugar levels and metabolism.

The researchers explained that maintaining muscle health depends on a delicate balance between producing new proteins and getting rid of old or damaged proteins. This process is regulated by a cellular pathway known as mTORC1, which is responsible for controlling cell growth and protein production.

But as we age, this pathway may become overactive, with cells putting greater effort into producing proteins rather than getting rid of damaged ones. This leads to the accumulation of defective proteins within muscle tissue, impairing its performance and ability to regenerate.

Scientists were able to identify a gene called DEAF1 as one of the main drivers of this defect. The study revealed that the levels of this gene rise with age, leading to excessive activation of the mTORC1 pathway and weakening the natural maintenance processes within the muscles.

Under normal conditions, DEAF1 levels are controlled by a group of proteins known as FOXO, which help maintain cell health and regulate gene activity. However, the effectiveness of these proteins decreases with age, allowing DEAF1 levels to rise and muscle imbalance to occur.

The results showed that exercise is able to break this cycle. It activates regulatory proteins that reduce DEAF1 levels and restore mTORC1 activity to a more balanced state. As a result, muscle cells regain their ability to get rid of damaged proteins and produce new ones more efficiently.

The study's lead researcher, Tang Hong-wen, said that physical activity "restores the cellular growth pathway to balance, allowing aging muscles to get rid of damaged proteins and rebuild themselves properly, becoming stronger and more flexible."

The researchers also pointed out that the importance of the discovery is not limited to combating the natural aging of muscles, but rather extends to muscle stem cells responsible for repairing tissues after injuries. Disruption of DEAF1 may limit the ability of these cells to regenerate as they age.

The scientific team believes that the discovered gene may represent a promising target for future treatments that mimic some of the molecular benefits of exercise, especially for people who are unable to engage in physical activity due to chronic diseases or recovering from surgical operations.

However, the researchers stressed that these results are still in their early stages, as the experiments were conducted on fruit flies and mice, and need further studies to confirm the safety and effectiveness of targeting DEAF1 in humans.