An easy and simple way to maintain muscle health

Researchers discovered that regular exercise helps reset signaling pathways in muscle tissue, thus combating age-related muscle weakness. They also found that the regulatory compound mTORC1, responsible for protein growth and regeneration, becomes overactive in the muscles of older adults, leading to the accumulation of damaged molecules and accelerating the development of muscle wasting disease. The transcription factor DEAF1 plays a pivotal role in this process: when overactive, it amplifies mTORC1 signaling and disrupts the natural process of muscle cell regeneration.

Research has shown that physical exercise reduces DEAF1 activity by activating protective proteins of the FOXO family. As a result, mTORC1 function returns to a more youthful state, and cells get rid of defective proteins more effectively. When scientists inhibited the FOXO gene or artificially raised DEAF1 gene levels, the benefits of exercise almost disappeared.

Experiments on model organisms confirmed the generality of this mechanism: reducing the activity of the DEAF1 gene alone improved molecular condition and muscle strength with age.

Researchers believe that the identified FOXO–DEAF1–mTORC1 pathway may form the basis for developing new approaches to maintaining muscle health in aging, including pharmacological methods to mimic some of the benefits of exercise.