Research conducted by scientists from Duke-NUS Medical School, Singapore General Hospital, and Cardiff University has revealed that exercise can effectively reverse muscle aging by enhancing the body’s cellular mechanisms responsible for tissue repair. This discovery highlights the significant role physical activity plays in maintaining strength and mobility as individuals age.
As people reach midlife, muscle function typically begins to decline. This deterioration increases the risk of falls, slows recovery from injuries, and can lead to complications such as poor blood sugar regulation. The recent study, published in the journal PNAS, identifies a critical growth pathway known as mTORC1 that regulates protein production and tissue health. Research indicates that aging disrupts the balance of this pathway, resulting in an accumulation of damaged proteins that contribute to muscle weakness.
The research team pinpointed the transcription factor DEAF1 as a key player in this dysregulation. As people age, DEAF1 becomes overactive, which disrupts normal protein turnover in muscles. In younger tissues, this process operates smoothly, but the aging process hampers its efficiency. Regulatory proteins known as FOXOs are responsible for managing DEAF1 activity, but their effectiveness diminishes with age, leading to accelerated muscle loss.
Exercise Reverses Age-Related Muscle Decline
The findings suggest that exercise can counteract this negative trend by restoring the balance of the mTORC1 pathway. “Exercise can reverse this process, correcting the imbalance,” stated Tang Hong-Wen, an associate professor at Duke-NUS. He explained that physical activity activates proteins that reduce DEAF1 levels, allowing aging muscles to clear out damaged proteins and rebuild themselves effectively.
The study indicates that when DEAF1 levels are excessively high, or FOXO proteins lose their function, exercise alone may not suffice to restore muscle power. This could explain why some older adults experience greater benefits from physical activity than others. Lead author Priscillia Choy Sze Mun commented, “Exercise tells muscles to ‘clean up and reset.’ Lowering DEAF1 helps older muscles regain strength and balance, almost like hitting the rewind button.”
Implications for Aging Populations
The research involved experiments on older mice and fruit flies, where increasing DEAF1 levels led to greater muscle weakness, while reducing its activity promoted muscle repair and strength. Despite the simpler biological models, the consistency of results across species suggests that humans may also be subject to similar age-related pathways.
DEAF1 is already recognized for its influence on muscle stem cells, which are vital for tissue repair and growth. As these stem cells decline with age, manipulating DEAF1 levels could present a new avenue for preserving the cellular advantages of exercise, even in individuals who may not engage in extensive physical activity.
“This study helps explain, at a molecular level, why aging muscles lose their ability to repair themselves and why exercise can restore that balance in some individuals,” noted Patrick Tan, a professor at Duke-NUS. The identification of DEAF1 as a critical regulator in this process opens the door to potential new strategies aimed at enhancing muscle health and quality of life in aging populations.
As societies face rapidly aging demographics, understanding the mechanisms behind muscle aging and repair could lead to innovative interventions that promote healthier, more active lifestyles for older adults.
