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Researchers from Duke-NUS Medical School and partner institutions identified a pathway linking the gene DEAF1, the mTORC1 growth signal and declining muscle maintenance with age. In fruit flies and mice, exercise helped rebalance the pathway and support removal of damaged proteins; whether the mechanism works the same way in people remains unknown.
Researchers led by Duke-NUS Medical School report a molecular pathway that may help explain how exercise supports repair in aging muscle. In experiments with fruit flies and mice, physical activity reduced activity of the gene DEAF1 and helped rebalance the mTORC1 signaling system. The findings, published in PNAS, offer a possible explanation for age-related differences in exercise response, but do not establish that the mechanism works in humans.
The team, working with researchers from Singapore General Hospital and Cardiff University, traced part of the age-related maintenance problem to increasing DEAF1 activity. The study describes DEAF1 as a driver of excessive activity in mTORC1, a pathway that helps regulate cell growth and protein production. When the signal is too active, cells may make proteins while becoming less effective at clearing damaged ones.
In the researchers’ account, a family of regulatory proteins called FOXOs normally helps keep DEAF1 in check. FOXO activity declines with age, weakening that restraint. The resulting rise in DEAF1 can push mTORC1 out of balance and interfere with the cycle of producing and removing proteins that supports muscle-cell function.
In the animal experiments, exercise activated regulatory proteins that lowered DEAF1 levels. The researchers report that this helped bring mTORC1 activity toward a healthier balance and supported removal of damaged proteins while allowing new proteins to be made. Their experiments also found that changing DEAF1 levels affected muscle strength in these models. The report says the team found a limit: when DEAF1 was very high or FOXO activity very low, exercise might not fully restore normal repair. The study does not show that exercise reverses all aspects of muscle aging.
The researchers also report that DEAF1 influences muscle stem cells, which help repair and regenerate muscle tissue. They identify DEAF1 as a possible target for future research into muscle maintenance and recovery. Any potential therapies, and their effects in people, remain unestablished.
A Possible Path to Better Muscle Maintenance
Age-related muscle weakness can affect mobility and independence, as well as recovery from injury or illness. Muscle tissue also contributes to blood-sugar regulation, so declining muscle function can have effects beyond strength. The study offers a biological explanation for how exercise may support the upkeep of muscle cells, rather than only prompting them to grow.
The findings could help researchers investigate why older adults do not all respond to exercise in the same way. If the DEAF1–FOXO–mTORC1 pathway is relevant in people, it may point to targets for future research into preserving muscle function. That is a possibility, not a treatment established by these experiments: the reported work used fruit flies and mice, and the source provides no human trial results or clinical recommendations based on the pathway.
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The Protein-Cleanup Process Behind the Finding
Muscle cells continually make proteins and dispose of proteins that are damaged or no longer useful. The balance matters because proteins help form the structure and working machinery of cells. The study focuses on mTORC1, a growth-regulating signal involved in protein production, and how its activity may become poorly controlled as muscle ages.
Earlier understanding had linked excessive mTORC1 activity and the buildup of damaged proteins to muscle deterioration, but the source report says the mechanism driving the imbalance was unclear. The new research places DEAF1 and FOXO regulation in that chain of events and reports that exercise can influence it in animal experiments. The work was led by Duke-NUS Medical School with Singapore General Hospital and Cardiff University, and was published in the Proceedings of the National Academy of Sciences.
“Exercise can reverse this process, correcting the imbalance.”
— Assistant Professor Tang Hong-Wen, the study’s lead author at Duke-NUS Medical School
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Human Effects Have Not Been Established
The experiments described were conducted in fruit flies and mice. It remains unclear whether exercise changes DEAF1, FOXO and mTORC1 in the same way in human muscle, how large any effect might be, or whether it leads to measurable improvements in strength, mobility or recovery. The source report does not provide details of a human study.
The researchers also report that exercise may be less able to restore repair when DEAF1 is extremely elevated or FOXO activity is very low. The degree to which this limitation applies across aging people, and whether those biological conditions can be measured or altered safely, is not established. The findings do not mean exercise is ineffective for older adults; they describe a possible mechanism and a potential limit in the models studied.
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Human Research Must Test the Pathway
The next step is to test whether the same pathway operates in human muscle and whether changes in its activity correspond with functional outcomes. Studies would need to clarify how exercise affects DEAF1 and related signals in people of different ages and health backgrounds, and whether the reported cellular changes are linked to meaningful changes in muscle function.
Until such evidence is available, the report supports further research rather than a new clinical treatment or a specific exercise prescription. The source material does not announce a human trial, a timetable for one, or a planned therapy targeting DEAF1. Those details remain unreported.
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Key Questions
What did the researchers find?
They reported that rising DEAF1 activity can push mTORC1 out of balance as muscle ages, disrupting protein maintenance. In fruit flies and mice, exercise lowered DEAF1 activity and supported the removal of damaged proteins.
Does this prove exercise reverses muscle aging in people?
No. The experiments described were conducted in fruit flies and mice. Human effects, including any impact on strength or mobility, have not been established by the reported findings.
Why might older people respond differently to exercise?
The study suggests that very high DEAF1 levels or very low FOXO activity may limit how fully exercise restores muscle-cell repair. Whether this explains differences in exercise response among people remains to be tested.
Does the study recommend a particular exercise routine?
No specific routine is provided in the source report. The findings explain a possible biological mechanism in animal models and do not establish a new exercise prescription or treatment.
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