Elderly people could stay stronger for longer after key to muscle waste discovered


Muscles

Elderly people could stay stronger for longer after scientists discovered why muscles fail to repair themselves, and waste away with age.

A team at Nottingham Trent University analysed the genes inside muscle cells to find out how their performance differed between people in their 20s, compared to those in their 60s.

They discovered that young genes sent strong signals instructing the body to fully repair injuries, genes in older cells functioned less well, preventing complete regeneration.

The poor performance of genes led to thinner and less robust ‘myotubes’ – a type of cell that can fully develop into a muscle fibre.

Lead researcher Dr Livia Santos, an expert in musculoskeletal biology in Nottingham Trent University’s School of Science and Technology, said: “This goes some way towards explaining why muscle injuries may take longer to recover as we get older.”

She added: “We know that healthy muscle regenerates after we’ve had an injury but ageing impairs that regeneration potential and recovery gets harder the older we get.

“What we’ve observed, in terms of what happens inside the cells, helps us to better understand why we don’t heal as well or as quickly in older age.

“The pathways that control cell processes and development work differently in older cells and are downregulated, meaning regeneration is impacted the older we get.

“If we can understand these pathways, however, we could potentially identify new therapies and interventions to mitigate the problem.”

Muscle mass decreases approximately 3 to 8 per cent per decade after the age of 30 and this rate of decline speeds up after the age of 60.

Failing and injured muscles can lead to more injuries from falls and strains, setting up a vicious cycle that is hard to break.

The researchers studied muscle cells from healthy donors, chemically injuring cells, then assessing how they heal and regenerate back to their pre-injury baseline levels.

When they looked at cells from a 20-year-old and a 68-year-old donor, researchers found critical differences in repair mechanisms. Older genes no longer activated the same level of regeneration in the body.

Janelle Tarum, another researcher on the study, said: “There’s a very clear reduced regeneration capacity and weakened recovery of aged cells and we have been able to further understand the factors underlying this impairment.

“Our work enables us to examine muscle cell regeneration across the lifespan and this in turn could be key for future drug discovery for disease related to muscle ageing.”

The study, which also involved Manchester Metropolitan University and Liverpool John Moores University, is published in the Journal of Tissue Engineering and Regenerative Medicine.

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