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Longevity Briefs: Declining Strength With Age Isn’t Just About Muscle

Posted on 18 August 2021

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Muscle strength and mass declines with age, a process known as sarcopenia. This not only leads to a reduction in strength, but also to other forms of frailty as muscle tissue plays an important role in the body’s metabolism – for example, reduced muscle tissue is associated with higher levels of inflammation. Many researchers suspect that sarcopenia is not just a muscular problem, but a neuromuscular problem. It is possible that damage to the neuromuscular junctions (the synapses that connect the motor neurons from the brain to the muscle fibres) is primarily responsible for sarcopenia, with reduced signalling to the muscle leading to a reduction in muscle maintenance. If this is the case, the neuromuscular junction may be a promising target for preventing or reversing sarcopenia.

At the neuromuscular junction, release of the neurotransmitter acetylcholine (ACh) in response to electrical signals from the brain triggers muscle contraction.
Source (Left)
Source (Right)

What did the researchers do: In this article, researchers review our current knowledge of the role of the neuromuscular junction in muscle ageing.

Key takeaway(s) from this research: The authors argue that there is evidence suggesting that changes in the neuromuscular junction are at least partially implicated in declining muscle strength. They point to the decline in muscle quality as well as quantity (aged muscles generate less force per unit of mass), a decline in delivery of important molecules to the synapse, structural deterioration and a reduction in the number of acetylcholine (ACh) receptors on the muscle fibre.

The authors suggest that targeting the neuromuscular junction may be a viable approach to treating sarcopenia, as evidence has shown that some gene therapies (such as those that reduce structural changes and increase the expression of ACh receptors) can improve muscle function in mice. They admit, however, that it is difficult to isolate the effects of the neuromuscular junction in these experiments. Unless we find a way to restore the neuromuscular junction to a more youthful state without affecting other aspects of ageing, a conclusion concerning its importance in sarcopenia may be difficult to reach.

In terms of currently practicable lifestyle interventions, caloric restriction has been shown to preserve neuromuscular function in mice, though whether this is effective in humans is unknown. It is however well established that in humans, exercise (both endurance and resistance exercise) reduces age-related changes in the neuromuscular junction and in the muscle itself.

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