Why Exercise Keeps Aging Muscles Strong: Scientists…

Why Exercise Keeps Aging Muscles Strong: Scientists Discover a Key Molecular Switch Exercise has long been recognized as one of the most effective ways to stay healthy as we age. Regular physical activity helps preserve muscle strength, improves balance, supports metabolism, and reduces the risk of falls and frailty. But exactly how exercise protects aging muscles at the molecular level has remained a mystery. Now, a new study from Duke-NUS Medical School, published in the Proceedings of the National Academy of Sciences (PNAS), has identified a gene called DEAF1 that appears to act as a critical regulator of muscle aging. The research offers new insights into why exercise helps older muscles repair themselves and may eventually lead to new therapies for age-related muscle loss. Loss of muscle mass and strength is a natural part of aging. Beginning in middle age, muscles gradually become less efficient at repairing damage, leading to reduced strength, slower recovery from illness or injury, and an increased risk of falls and fractures. Healthy muscles do more than enable movement. They also play important roles in: Maintaining mobility and independence Regulating blood sugar Supporting metabolism Protecting bone health Improving recovery after illness As populations age, preserving muscle function has become an important public health priority. Researchers identified DEAF1 as a key regulator involved in muscle aging. The study found that DEAF1 levels increase as muscles age. Higher levels of this gene overstimulate a growth pathway known as mTORC1, which normally helps muscles produce proteins needed for growth and maintenance. However, when mTORC1 remains excessively active for prolonged periods, muscle cells begin prioritizing the production of new proteins while becoming less effective at clearing away damaged on