
Scientists from Duke-NUS Medical School have discovered how exercise helps aging muscles heal and stay strong. Their research explains why staying active is one of the best ways to keep your strength and mobility as you get older.
The research team worked with partners from Singapore General Hospital and Cardiff University. They found that exercise helps fix a chemical imbalance in muscle cells that happens as we age. This imbalance makes it harder for muscles to repair themselves and stay healthy.
Muscles are important for moving, staying fit, and controlling blood sugar. As we get older, our muscles slowly weaken. This makes falls more likely, slows recovery from sickness or injury, and can make daily tasks harder. In aging countries like Singapore, strong muscles are key for helping older people stay independent.
At the heart of muscle health is a growth pathway called mTORC1. This pathway helps muscles build new proteins. But as muscles age, mTORC1 becomes too active. It keeps making new proteins but doesn’t clean out the old, damaged ones. These damaged proteins build up and hurt the muscle’s ability to work.
The researchers discovered that a gene called DEAF1 is the reason mTORC1 becomes overactive. DEAF1 levels rise in aging muscles, and this pushes mTORC1 into overdrive. Normally, a group of proteins called FOXOs keeps DEAF1 under control. But as we age, FOXO activity drops, and DEAF1 levels climb too high.
The good news is that exercise can lower DEAF1 levels—at least when the FOXO proteins are still working. Dr. Tang Hong-Wen, the lead researcher, explained that physical activity activates proteins that reduce DEAF1 and bring the muscle system back into balance.
This allows old muscles to clean out damaged parts and rebuild themselves properly, making them stronger and more flexible again.
However, when DEAF1 is too high or FOXO levels are too low—as in very old muscles—exercise might not work as well. This could be why some older adults don’t benefit from exercise as much as others. It shows that knowing how muscles age is just as important as encouraging physical activity.
To test their ideas, the scientists studied both fruit flies and older mice. In both animals, increasing DEAF1 caused muscles to weaken quickly. Lowering DEAF1 helped muscles recover, showing that this gene plays a major role in muscle strength in different species.
The study also shows that DEAF1 affects muscle stem cells. These are special cells that help muscles repair themselves. As people age, these stem cells don’t work as well. If DEAF1 is not balanced, recovery is even slower.
This discovery could help more than just older people. People recovering from illness, surgery, or diseases like cancer might also benefit. If scientists can adjust DEAF1, they might copy the good effects of exercise even for those who can’t move much.
Priscillia Choy Sze Mun, the first author of the study, said, “Exercise tells muscles to clean up and reset. Lowering DEAF1 helps old muscles become stronger, like pressing a rewind button.”
Professor Patrick Tan, Senior Vice-Dean at Duke-NUS, said the research gives us a deeper understanding of why older muscles lose their repair abilities and how exercise helps fix that. The discovery of DEAF1 could lead to new treatments that keep muscles healthy in aging populations.
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.
For more health information, please see recent studies about an easy, cheap way to maintain muscles, and results showing these vegetables essential for your muscle strength.
This study brings hope for better muscle care in the future. It was published in PNAS.
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