Exercise has long been recommended as one of the best ways for older adults to stay healthy and independent.
Regular physical activity helps people remain stronger, reduces the risk of falls, improves balance, and supports overall health.
Scientists have known these benefits for many years, but they have not fully understood exactly why exercise has such powerful effects inside aging muscles.
Now, researchers from Duke-NUS Medical School have uncovered an important part of the answer.
As people grow older, muscles naturally become smaller and weaker. This age-related muscle loss can make everyday tasks such as climbing stairs, carrying shopping bags, or getting out of a chair much harder.
Weaker muscles also increase the risk of falls, broken bones, hospital stays, and loss of independence. Keeping muscles healthy is therefore an important part of healthy aging.
The research team worked with scientists from Singapore General Hospital and Cardiff University to study what happens inside muscle cells as they age.
They discovered that aging changes the balance between building new proteins and removing damaged ones. Healthy muscles constantly replace worn-out proteins with new ones. This cleaning process keeps muscle cells working properly.
The researchers found that a growth system called mTORC1 becomes too active in older muscles. Instead of keeping a healthy balance, aging muscles spend too much energy making new proteins while becoming less effective at clearing away damaged ones. As damaged proteins build up, muscle cells become stressed and gradually lose strength.
The scientists then identified an important gene called DEAF1. They found that DEAF1 levels rise with age. Higher DEAF1 pushes the mTORC1 system even harder, making the imbalance worse. Normally, another group of proteins called FOXOs keeps DEAF1 under control. Unfortunately, FOXO activity naturally falls as people get older, allowing DEAF1 levels to rise.
The good news is that exercise can help restore this balance. Physical activity activates proteins that lower DEAF1 levels. This allows muscle cells to remove damaged proteins more efficiently, repair themselves, and remain stronger. The researchers describe this process as giving aging muscles the chance to clean themselves and recover.
The team also discovered that exercise may not work equally well for everyone. In some older muscles, DEAF1 becomes extremely high or FOXO activity becomes very low. In these situations, exercise alone may not completely restore the muscle’s natural repair system. This may explain why some older adults gain more strength from exercise than others.
To test their discovery, the researchers performed experiments in fruit flies and older mice. The results were remarkably similar in both species. Increasing DEAF1 caused muscles to weaken more quickly, while reducing DEAF1 improved muscle health and strength. This suggests the biological process is shared across different animals.
The findings could also help people recovering from surgery, cancer treatment, or serious illness. Scientists hope future medicines might reduce DEAF1 activity and reproduce some of the protective effects of exercise when regular physical activity is difficult.
The research was published in the Proceedings of the National Academy of Sciences (PNAS).
This study provides strong evidence because the researchers combined molecular biology with experiments in fruit flies and older mice, allowing them to test how the DEAF1 gene affects muscle aging. However, the work has not yet shown that treatments targeting DEAF1 will produce the same benefits in humans.
More clinical studies will be needed before new medicines become available. Even so, the findings help explain why exercise is so beneficial for aging muscles and may eventually lead to therapies that help people who are unable to exercise because of illness or disability.
If you care about muscle, please read studies about factors that can cause muscle weakness in older people, and scientists find a way to reverse high blood sugar and muscle loss.
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