Researchers have uncovered a molecular "switch" that helps explain why exercise keeps ageing muscles healthy. By reducing levels of a gene called DEAF1, physical activity allows older muscles to clear out damage, repair themselves, and maintain strength.

A new study from Duke-NUS Medical School shows that physical activity can restore the natural repair systems that weaken with age, helping muscles recover and maintain function later in life. 

The research team, working with collaborators from Singapore General Hospital and Cardiff University, found that exercise helps correct an important imbalance that develops inside ageing muscle cells.

The findings, published in the Proceedings of the National Academy of Sciences (PNAS), provide new insight into the biological mechanisms behind muscle ageing and could eventually lead to new approaches for preventing age-related muscle loss.Healthy muscles do much more than enable movement. 

They are essential for maintaining metabolism, regulating blood sugar levels, and supporting overall health. From middle age onward, muscle strength and function gradually decline, raising the risk of falls, fractures, and delayed recovery from illness or injury.

The consequences extend beyond individual health. As populations age, muscle loss can increase demands on caregivers and healthcare systems. Preserving muscle function is therefore an important part of maintaining independence and quality of life.

One of the key regulators of muscle health is a growth pathway called mTORC1, which helps control protein production and muscle maintenance.

In ageing muscles, this pathway can become excssively active. When that happens, muscles focus more on building new proteins while becoming less efficient at removing damaged ones.

Over time, these damaged proteins accumulate inside muscle cells, placing them under stress and contributing to the gradual loss of strength associated with ageing.The researchers identified a gene called DEAF1 as an important factor behind this process.

According to the study, DEAF1 levels rise in ageing muscles. As DEAF1 increases, it drives mTORC1 activity higher, disrupting the normal balance between protein production and protein removal. This imbalance accelerates muscle deterioration.

Under normal conditions, DEAF1 is regulated by a group of proteins known as FOXOs. However, FOXO activity naturally declines with age. As a result, DEAF1 is no longer kept under tight control, allowing its levels to increase and pushing muscles further away from repair and maintenance.