The researchers from King’s College London, Harvard University and Massachusetts General Hospital also discovered how to halt the ageing process in mice by administering a common a protein inhibiting drug.
The study looked at stem cells found inside muscle and responsible for repairing injury to find out why the ability of muscles to regenerate declines with age.
A dormant reservoir of stem cells is present inside every muscle, ready to be activated by exercise and injury to repair any damage. When needed, these cells divide into hundreds of new muscle fibres that repair the muscle.
At the end of the repairing process some of these cells also replenish the pool of dormant stem cells so that the muscle retains the ability to repair over and over again.
The researchers carried out a study on old mice and found the number of dormant stem cells present in the pool reduces with age, which could explain the decline in the muscle’s ability to repair and regenerate as it gets older.
When these old muscles were scrutinised, high levels of FGF2, a protein that has the ability to stimulate cells to divide.
While encouraging stem cells to divide and repair muscle is a normal and crucial process, they found that FGF2 could also awaken the dormant pool of stem cells even when they were not needed which over time meant the pool was depleted.
This meant that when the muscle really needed stem cells to repair itself there were insufficient to allow the muscle to respond properly.
Following this finding, the researchers were successful in inhibiting FGF2 in old muscles in order to prevent the stem cell pool from being kick-started into action unnecessarily by administering a common FGF2 inhibitor drug.
Dr Albert Basson, Senior Lecturer 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.
Kieran Jones, co-author of the study from King’s, added: ‘We do not yet know how or why levels of the protein FGF2 increase with age, triggering stem cells to be activated when they are not needed. This is something that needs to be explored.
‘The next step is to analyse old muscle in humans to see if the same mechanism could be responsible for stem cell depletion in human muscle fibres, leading to loss of mass and wastage.’