The research, led by Duke-NUS Medical School in Singapore in collaboration with Singapore General Hospital and Cardiff University, identified a gene called DEAF1 that becomes increasingly active as muscles age, disrupting the processes needed to maintain healthy muscle tissue.
Published in the Proceedings of the National Academy of Sciences (PNAS), the study found that exercise can help restore the balance between producing proteins and removing damaged ones inside muscle cells.
Muscles gradually lose strength and function with age, making everyday activities more difficult and increasing the risk of falls and fractures.
Researchers say maintaining muscle health is essential for preserving mobility and independence in older adults.
At the cellular level, muscles must continuously produce new proteins while clearing away damaged ones.
This process is partly controlled by a signalling pathway called mTORC1, which regulates protein production and cell growth.
The researchers found that DEAF1 levels can rise with age, causing excessive activity in this pathway.
As a result, muscle cells produce proteins without efficiently removing damaged ones, gradually affecting their ability to function and repair themselves.
Normally, proteins known as FOXOs help regulate DEAF1. However, FOXO activity tends to decline with age, allowing DEAF1 levels to increase and further disrupting muscle maintenance.
Exercise appeared to interrupt this process by activating regulatory proteins that reduce DEAF1 levels.
This helped restore mTORC1 activity to a healthier balance, allowing muscle cells to clear damaged proteins and maintain healthy tissue.
To investigate the mechanism, researchers conducted experiments in fruit flies and older mice.
Increasing DEAF1 levels caused muscles to weaken more rapidly, while reducing the gene’s activity improved protein maintenance and restored muscle strength.
However, the researchers found that exercise might not fully restore normal muscle repair when DEAF1 levels become extremely high or FOXO activity falls too low.
The findings may also help explain why older adults respond differently to exercise.
Researchers suggested that targeting DEAF1 could eventually lead to treatments that help preserve muscle strength, particularly among people who struggle to exercise because of illness, surgery or other health conditions.
Nevertheless, the research was conducted in animals, and further studies are needed to establish whether targeting the same mechanism can safely improve muscle health in humans.
For now, the study provides new insight into how exercise supports muscle maintenance and could guide future efforts to prevent age-related muscle loss.
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