A study led by Duke-NUS Medical School has identified a molecular pathway that helps explain how exercise protects aging muscle. In fruit flies and older mice, physical activity reduced the protein DEAF1, brought the growth pathway mTORC1 closer to a healthy level, improved the balance between making and removing proteins, and restored muscle strength. The work does not yet show that exercise reverses muscle aging in people.
What the study discovered
The research, led by Duke-NUS Medical School with Singapore General Hospital and Cardiff University, is reported in Sze Mun Choy and colleagues’ paper, “Exercise suppresses DEAF1 to normalize mTORC1 activity and reverse muscle aging,” published in Proceedings of the National Academy of Sciences in 2025 (volume 122, issue 48; DOI 10.1073/pnas.2508893122).
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Investigators identified DEAF1 as a central regulator of age-related muscle decline. DEAF1 levels increase in aging muscle. When its activity becomes too high, it pushes mechanistic target of rapamycin complex 1 (mTORC1), a pathway that controls cell growth and protein production, into an excessively active state.
That overactivity creates a damaging imbalance. Muscle cells continue emphasizing protein production, but become less effective at removing damaged or defective proteins. The resulting buildup undermines maintenance and repair, contributing to weaker muscle.
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How DEAF1, FOXO and mTORC1 interact
FOXO’s normal restraint
FOXO proteins normally help restrain DEAF1. Aging reduces FOXO activity, removing part of that control and allowing DEAF1 to rise. The study therefore describes an age-related chain: declining FOXO activity permits more DEAF1, elevated DEAF1 overactivates mTORC1, and excessive mTORC1 disrupts protein quality control.
Exercise resets the balance
Exercise activates regulatory proteins that lower DEAF1. With less DEAF1 present, mTORC1 moves toward a more appropriate level of activity rather than remaining chronically overactive. Muscle cells can then continue producing proteins needed for maintenance and repair while also improving clearance of damaged proteins.
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Lead author Assistant Professor Tang Hong-Wen summarized the proposed mechanism: “Exercise can reverse this process, correcting the imbalance.” In the study’s model, the effect is not simply more growth signaling; it is a better balance between rebuilding muscle components and cleaning out faulty ones.
What happened in the experiments
| Evidence | Manipulation or intervention | Observed outcome | What it means |
|---|---|---|---|
| Fruit flies | DEAF1 was raised or reduced | Higher DEAF1 weakened muscle; lower DEAF1 improved protein balance | Supports DEAF1 as a causal regulator in an animal model |
| Older mice | Exercise and DEAF1-related interventions | Lower DEAF1 was associated with improved muscle maintenance and restored strength | Shows the pathway operates in a mammal as well as in flies |
| Humans | No human intervention trial reported | No human effectiveness statistic or participant result is established | Clinical benefit remains unproven |
Seeing similar effects in flies and older mice suggests that DEAF1 has a conserved biological function. It does not establish that changing DEAF1, or following a particular exercise program, will produce the same result in people.
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Can exercise really make old muscles young again?
“Reverse muscle aging” in the paper refers to correcting measurable biological and functional features of aging in the tested animals. It does not mean that an older person’s muscles literally become identical to young adult muscle, nor that all age-related loss can be erased.
The report specifically says exercise may not fully restore repair capacity when DEAF1 is extremely elevated or FOXO activity has fallen substantially. That limitation offers one possible explanation for why older adults respond differently to the same physical activity: the underlying molecular state may determine how much of the pathway can still be reset.
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What the findings mean for people now
- The study supports exercise as a biologically plausible way to improve muscle maintenance, not merely as a method for building more muscle.
- It does not identify a proven exercise dose, intensity, duration or schedule for reversing aging in humans.
- It provides no human trial statistic, prevalence estimate, participant count or effect size that can be used to predict an individual’s response.
- People should not treat DEAF1 measurements or experimental pathway manipulation as established clinical care.
Professor Patrick Tan, Duke-NUS Senior Vice-Dean for Research, said the work helps explain why aging muscle loses repair capacity and why exercise can restore balance in some individuals. That is a mechanistic insight, not a clinical recommendation replacing individualized advice from a qualified health professional.
Could DEAF1-targeting drugs be developed?
The pathway points to possible future therapies that lower DEAF1 or mimic exercise-related signaling. Such approaches could be useful for people who cannot exercise sufficiently or whose FOXO-DEAF1 system responds poorly. At present, however, these are research possibilities. The study does not establish an approved DEAF1 treatment, a safe dose, or a consumer product.
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What remains to be tested
- Confirm whether exercise lowers DEAF1 in human skeletal muscle in controlled studies.
- Determine whether changes in DEAF1 and mTORC1 predict improvements in strength, mobility or recovery.
- Identify which exercise types and training loads produce the most reliable molecular response.
- Test safety and effectiveness of any DEAF1-directed drug or gene-based approach in clinical trials.
- Establish how age, disease, medication, nutrition and baseline FOXO activity alter the response.
The most accurate conclusion is therefore measured: exercise reversed aspects of muscle aging in flies and older mice by lowering DEAF1 and normalizing mTORC1-related protein handling. Whether the same mechanism can reliably restore human muscle remains an open clinical question.
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