New research distinguishes for the first time a key reason for declining muscle repair during aging and a way to stop this process in mice using a certain drug.

This groundbreaking study, published in Nature, explains why muscle mass decreases with age, an important factor in weakness, causing lack of mobility and falls in elders.

Previous research has told us that stem cells can play a crucial role in stimulating muscle regeneration. This particular study looked at stem cells found in muscles that are responsible for repairing injuries and why the muscles’ capacity of regeneration deteriorates with age.

An inactive supply of stem cells is present inside every muscle, ready to be put into action by exercise or injury to fix any damage. When these stem cells are needed, they can divide into hundreds of new muscle threads and repair the injured muscle. At the end of the repairing process, a few of these cells refill the supply of dormant stem cells, enabling the muscle to carry on repairing itself continuously.

Researchers used elderly mice to conduct this study and found the number of inactive stem cells in the extra pool decreases with age, explaining the decline in the muscle’s ability to regenerate and repair as the body gets older. When these muscles were examined, the scientists found high levels of FGF2, a protein that has the capacity to trigger the division of cells. While stimulating inactive cells to split and repair muscle is a normal and vital process, they found FGF2 could awaken the dormant stem cells even when they were not needed. Continuous activation of the dormant stem cells meant depletion of the surplus, leaving the muscles without necessary stem cells when repair was really needed.

After this finding, the team attempted to obstruct FGF2 in old muscles in order to prevent the stem cell surplus from being activated unnecessarily. By giving the mice a common FGF2 inhibitor drug, they were able to slow down the decline in the number of muscle stem cells.

Dr Albert Basson, Senior Lecturer from the Department of Craniofacial Development and Stem Cell Biology at the King’s College London Dental Institute, said:

“Preventing or reversing muscle wasting in old age in humans is still a way off, but this study has for the first time revealed a process which could be responsible for age-related muscle wasting, which is extremely exciting. The finding opens up the possibility that one day we could develop treatments to make old muscles young again. If we could do this, we may be able to enable people to live more mobile, independent lives as they age.”

Preventing stem cell recovery can lead to their eventual termination, meaning it is crucial for adult stem cells to rest between episodes of intense activity. The reason why FGF2 levels increase with age and cause unneeded stem cells to be activated is still unknown. The next step is to analyze why unneeded stem cells are activated, and see if the same mechanism is responsible for the loss of muscle mass by stem cell depletion in human muscle fibers.

Written by Kelly Fitzgerald