Research from Duke-NUS Medical School, in collaboration with Singapore General Hospital and Cardiff University, reveals that exercise can counteract muscle aging by restoring the cellular ability to repair and grow muscle tissue. This breakthrough highlights the significance of physical activity in maintaining strength and mobility in older adults.
As individuals age, muscle function typically declines, leading to increased risks of falls, slower recovery from injuries, and poor blood sugar regulation. The study identifies a critical growth pathway known as mTORC1, which plays a pivotal role in protein production and tissue health. The researchers found that aging disrupts the balance of this pathway, resulting in the accumulation of damaged proteins that contribute to muscle weakness.
The study identifies a transcription factor called DEAF1, which becomes overactive in older muscles and disrupts the usual protein exchange that occurs in younger tissues. As people age, the regulatory proteins known as FOXOs lose their effectiveness in managing DEAF1, leading to accelerated muscle loss.
Exercise as a Restorative Force
Physical activity emerges as a crucial element in reversing the effects of aging on muscle tissue. According to Tang Hong-Wen, an associate professor at Duke-NUS, “Exercise can reverse this process, correcting the imbalance.” By activating certain proteins that lower DEAF1 levels, exercise allows aging muscles to clear out damaged proteins and rebuild effectively.
This study indicates that when DEAF1 levels are elevated or FOXO activity is diminished, exercise alone may not be sufficient to restore muscle power. The findings suggest that the benefits of physical activity can vary among older adults, depending on individual physiological responses.
Lead author Priscillia Choy Sze Mun emphasizes the importance of this research, stating, “Exercise tells muscles to ‘clean up and reset.'” Lowering DEAF1 levels enables older muscles to regain strength and balance, akin to hitting a rewind button on muscle health.
Implications for Aging Populations
The research team conducted experiments using older mice and fruit flies, observing a consistent pattern: increased DEAF1 levels led to muscle weakness, while reducing its activity restored balance and promoted muscle repair. Although these models are simpler than human physiology, the underlying mechanisms appear to be similar, suggesting that age-related dysregulation of muscle tissue affects multiple species.
DEAF1 is already recognized for its influence on muscle stem cells, which are crucial for tissue repair and regrowth. As these stem cells decline with age, the ability to manipulate DEAF1 levels could enhance the cellular benefits of exercise, potentially extending muscle health into later years, even for those with limited physical activity.
Professor Patrick Tan from Duke-NUS notes, “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.” By identifying DEAF1 as a key regulator in muscle repair processes, these findings could pave the way for innovative strategies to enhance the quality of life for aging populations.
The research was published in the journal PNAS in March 2024, underscoring its relevance in addressing the challenges posed by an aging society. As millions of older adults face the risks associated with muscle decline, understanding the mechanisms behind muscle repair and the role of exercise becomes increasingly significant.