Scientists discover how exercise reverses muscle aging
Scientists have uncovered a hidden biological mechanism that helps explain how exercise can reverse some of the damage caused by muscle aging. The key is a gene called DEAF1, which becomes overactive with age and interferes with the muscles’ ability to clear damaged proteins and repair themselves. Exercise can help restore this balance, allowing older muscles to rebuild and regain strength, although the benefits may…
Key points
- Duke-NUS-led study identifies DEAF1 gene as a driver of muscle aging.
- Exercise lowers DEAF1, restoring protein cleanup and muscle repair balance.
- Experiments in fruit flies and mice showed reducing DEAF1 restored muscle strength.
Scientists have identified a biological mechanism that helps explain how exercise protects aging muscles and restores their ability to repair themselves. The research, led by Duke-NUS Medical School with Singapore General Hospital and Cardiff University, was published in the Proceedings of the National Academy of Sciences (PNAS).
The team traced the problem to a gene called DEAF1, which rises with age and drives excessive activity in a signaling pathway called mTORC1. This disrupts the balance between producing new proteins and clearing damaged ones, weakening muscle maintenance.
How exercise restores balance
The researchers found that exercise activates regulatory proteins that reduce DEAF1 levels, returning mTORC1 activity to a healthier balance. This allows aging muscle cells to remove damaged proteins while continuing to produce new ones.
Assistant Professor Tang Hong-Wen, the study's lead author from Duke-NUS, said exercise can reverse the process and help aging muscles stay stronger and more resilient. However, when DEAF1 levels become extremely elevated or FOXO activity falls too low, exercise may no longer fully restore normal muscle repair.
Exercise can reverse this process, correcting the imbalance. Physical activity activates certain proteins which lower DEAF1 levels, bringing the growth pathway back into balance.
— Assistant Professor Tang Hong-Wen
Experiments and future treatments
In experiments using fruit flies and older mice, increasing DEAF1 weakened muscles rapidly, while reducing it improved protein balance and restored muscle strength. The similar effects across species suggest DEAF1 is part of an evolutionarily conserved system.
The findings point to DEAF1 as a potential target for therapies that could help people who have difficulty exercising, such as those recovering from surgery, serious illness or cancer. Whether manipulating DEAF1 is safe and effective in humans remains to be established.
