Muscle tends to weaken with age, and researchers are still working out why. A new study in fruit flies, mouse muscle cells and aged mice may help explain why. It involved no human participants, so it can’t tell us yet what exercise does for people.
The gene linked to muscle aging in animals
Researchers at Duke-NUS Medical School found, in fruit flies, mouse muscle cells and aged mice, that a gene called DEAF1 builds up in aging muscle and pushes a growth pathway called mTORC1 out of balance[1]. mTORC1 normally tells muscle cells when to grow and when to clean out damaged proteins. When DEAF1 piles up, mTORC1 becomes overactive: the muscle makes too much protein and does too little clean-up, so damaged material accumulates.
In these animal models it’s more than a correlation: when the researchers raised or lowered DEAF1 in flies and mice, mTORC1 activity and muscle health changed with it. That is evidence of cause within those models, not in people.
In aged mice, exercise turned the gene down
Here’s the part that makes the study interesting: in aged mice, exercise (treadmill running and a resistance wheel) lowered DEAF1, reduced mTORC1 activity and improved markers of muscle health. The effect ran through a signaling protein called FOXO. This was not tested in people, so the study does not show that exercise has the same effect in human muscle. This gives researchers a specific pathway to study, rather than a vague “exercise is good for you.” The authors say targeting this pathway “may offer therapeutic potential.” That is speculation at this stage: no human work exists, and in the mice, blocking FOXO blocked the benefit of exercise, so the pathway may not be simple to target.
What this means for your training (and what it doesn’t)
This study doesn’t change how anyone should train, because it wasn’t a training study. It adds one possible piece of the “why” from animal research: a specific pathway in aging muscle that exercise appeared to influence in mice. Whether the same thing happens in people is still an open question.
Muscle strength matters for everyday independence later in life – strength, balance, the ability to get up off the floor without thinking about it. Knowing a possible mechanism doesn’t change the workout, and one animal study can’t settle the question for people. If you have a heart or joint condition, talk to your clinician before starting resistance training.
↑︎ Choy SM, Goh KY, Lee WX, et al. Exercise suppresses DEAF1 to normalize mTORC1 activity and reverse muscle aging. Proceedings of the National Academy of Sciences, 2025;122(48):e2508893122. DOI: https://doi.org/10.1073/pnas.2508893122
Kurt Greiner
Kurt is a digital strategist and IT professional blending emerging technology with practical application to help businesses and individuals streamline their digital presence. His current work focuses on the intersection of intentional living and technological resilience, exploring how individuals can leverage modern tools to navigate the second half of life with purpose.
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