Scientists have uncovered the mechanism of aging muscle recovery

With age, muscles gradually lose their strength and ability to recover from damage. Scientists have discovered a molecular mechanism that helps explain how physical activity counteracts these changes. The role of the DEAF1 gene in this process and why the discovery can help in the fight against age—related loss of muscle strength is described in the Izvestia article.

The mechanism of aging muscle recovery

Researchers from Duke University School of Medicine and the National University of Singapore, together with specialists from Singapore General Hospital and Cardiff University, have discovered a mechanism by which physical activity helps maintain the health of aging muscles. The results of the work are published in the journal Proceedings of the National Academy of Sciences (PNAS).

The DEAF1 gene plays a key role in this process. With age, its activity increases, which disrupts the balance between the production of new proteins and the removal of damaged ones. As a result, defective proteins accumulate in muscle cells, and the ability of tissues to maintain normal function and recover deteriorates.

Scientists have found that physical activity helps to reduce DEAF1 levels and restore the balance of cellular processes. This allows the muscles to get rid of damaged proteins more efficiently and maintain healthy tissue. At the same time, the study was conducted on fruit flies and mice, so the results cannot yet be directly transferred to humans.

Scientists talked about the role of the LMOD1 protein in muscle repair

Why muscles lose strength with age

For the normal functioning of muscle tissue, it is necessary to maintain a balance between the production of new proteins and the removal of old or damaged ones. Proteins form the structure of muscle cells and ensure their functioning, so timely updating of these components is necessary to maintain strength and repair tissues.

One of the main regulators of this process is the mTORC1 signaling pathway, which controls protein production and supports cell growth. If its activity becomes excessive, muscle cells begin to produce proteins more actively, but at the same time they do a worse job of removing damaged components. Over time, they accumulate and interfere with the normal functioning of cells.

The researchers found that with age, this imbalance is associated with an increase in DEAF1 levels. Normally, the activity of the gene is controlled by FOXO family proteins involved in gene regulation and maintenance of cellular processes. However, with age, FOXO activity decreases, weakening control over DEAF1. As a result, the activity of mTORC1 increases and the normal protein renewal in the muscles is disrupted.

Thus, scientists have identified a sequence of molecular changes that helps explain why it becomes more difficult for aging muscles to maintain healthy tissue and recover from damage.

Scientists have pointed out the benefits of strength training for muscle health

How exercise helps muscles get rid of damaged proteins

Researchers have found that exercise activates regulatory proteins that reduce DEAF1 levels. Due to this, mTORC1 activity returns to a more balanced state: muscle cells can continue to produce the necessary proteins and at the same time remove damaged ones more efficiently.

The results of experiments on fruit flies and elderly mice confirmed the role of DEAF1 in changing muscle strength. When the researchers increased the level of this gene, the muscles weakened faster. When its level was reduced, the balance between protein production and removal improved, and muscle strength was restored.

However, the mechanism has limitations. If the DEAF1 level becomes too high or the FOXO activity drops too much, exercise alone may not be enough to fully restore normal muscle processes. This may explain why older people react differently to physical activity.

We are not talking about the fact that exercise ceases to be useful, but the researchers point to the need to better understand the changes taking place in aging cells.

Scientists have changed their view on the benefits of high protein intake

Could the discovery help in the fight against age-related muscle loss

DEAF1 affects not only the functioning of mature muscle cells, but also muscle stem cells, which are involved in the repair and regeneration of tissue after damage. As we age, these cells become less efficient, making it more difficult for the body to repair muscles. Violations related to DEAF1 may further complicate this process.

Scientists suggest that exposure to DEAF1 in the future may become the basis for the development of methods for maintaining muscle strength and tissue repair. Such approaches could be useful for people who find it difficult to exercise, for example, for patients after major surgeries, serious illnesses, or with chronic conditions, including cancer.

One of the possible prospects is to learn how to reproduce some of the molecular effects of physical activity by influencing this gene. However, so far this is only a direction for future research: the effectiveness and safety of this approach in humans have not been established.

Thus, the work reveals one of the mechanisms by which exercise helps to maintain muscles. Now the researchers have to find out whether this knowledge can be used to develop additional methods for preventing age-related loss of muscle strength and maintaining mobility.