PNAS: Physical exercise slows muscle aging in elderly people.
Scientists have discovered that regular physical exercise can reprogram the signaling pathways in muscle tissue, thereby counteracting age-related decline. The study, published in the Proceedings of the National Academy of Sciences (PNAS), reveals how exercise interferes with key processes of protein metabolism in muscles.
The authors showed that in elderly muscles, the regulatory complex mTORC1 is excessively activated, which is responsible for protein growth and renewal. Instead of maintaining balance, this leads to the accumulation of damaged molecules and accelerated development of sarcopenia. A central role in this process is played by the transcription factor DEAF1: when its activity is elevated, it amplifies mTORC1 signals and disrupts the normal renewal of muscle cells.
Physical exercise, as experiments showed, reduces DEAF1 activity by activating protective proteins from the FOXO family. As a result, the functioning of mTORC1 returns to a more "youthful" mode, and cells become more efficient at eliminating defective proteins. When the scientists artificially suppressed FOXO or increased DEAF1 levels, the positive effects of training virtually disappeared.
Experiments on model organisms confirmed the universality of the mechanism: reducing DEAF1 activity alone improved the molecular state and strength of aging muscles. The researchers believe that the identified chain of FOXO–DEAF1–mTORC1 may serve as the basis for new approaches to maintaining muscle health in older age, including pharmacological methods to replicate some of the benefits of physical exercise.
