Published on: Dec 04, 2025
A recent study from Duke-NUS Medical School sheds light on why muscles weaken with age and why exercise remains one of the most effective defenses.
Researchers discovered that a gene regulator called DEAF1 drives a key muscle-maintenance system, mTORC1, into overdrive as we age. While mTORC1 supports muscle growth and repair in youth, chronic overactivation later in life can damage muscle cells instead.
mTORC1 is essential for muscle growth but becomes chronically overactive with aging—a paradox that has been difficult to untangle, said Hong-Wen Tang, PhD, senior author and assistant professor at Duke-NUS and Singapore General Hospital. The study, published in the Proceedings of the National Academy of Sciences, identifies DEAF1 as a key culprit behind this dysregulation.
Exercise reverses the process
The researchers found that DEAF1 pushes mTORC1 to produce excess proteins and fail to clear damaged ones, gradually weakening muscles. Strikingly, exercise lowers DEAF1 levels, effectively resetting the pathway. “Exercise doesn’t just repair damage—it targets the switch causing muscle aging.
Experiments with aging mice revealed that endurance workouts reduced mTORC1 activity and strengthened muscles, while sedentary mice showed continued decline. The effect is mediated by FOXO genes, which suppress DEAF1 during exercise, restoring balance to mTORC1.
Implications for new therapies
The study highlights the FOXO-DEAF1-mTORC1 axis as a central mechanism of age-related muscle loss and points to potential treatments. Drugs that inhibit DEAF1 or activate FOXO could mimic some benefits of exercise, offering a new strategy against sarcopenia.
This discovery provides a clearer roadmap for studying mTORC1 dysregulation and developing therapies to preserve muscle health with age.
Source: https://medschool.duke.edu/news/why-muscles-weaken-age-and-how-exercise-fights-back
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