Fight Aging!

Sarcopenia is the name given to the characteristic loss of muscle mass and strength with age. It is one of the better conditions to use in order to illustrate the point that the research community often approaches complex aspects of aging in the manner of the blind men and the elephant. Every group is specialized, and focused on one specific aspect of the overall situation. So one can look at a recent paper on stem cell decline as the dominant cause of sarcopenia and come away quite convinced, and then read the paper I'll point out today, that paints issues with the interface between nerves and muscles - the motor unit - as an important cause of sarcopenia, and start to think that perhaps it isn't all stem cells.

The same is true of many other possible causes of sarcopenia. Some researchers have run studies of strength training and suggest that substantial fractions of the loss of muscle with age are due to lack of exercise. Others have investigated age-related defects in the processing of amino acids such as leucine necessary for the construction of proteins in muscle tissue, or the falling dietary intake of protein that seems common in older individuals, or the contribution of cellular senescence. At some point, these and other views of the problem must be synthesized into a complete understanding, and the contradictory evidence reconciled.

Given the pace of progress in applied biotechnology, it seems that the best approach to determining the important causes of sarcopenia is to work towards a fix for each potential cause, one by one, and in isolation from one another. The degree to which any particular fix improves or reverses sarcopenia is the metric by which the related potential cause can be judged primary or secondary, an actual cause or a secondary consequence of some other, more important mechanism. As implementing therapies becomes easier in comparison to reverse engineering all of the details of any specific slice of cellular biochemistry, this approach will only become more attractive. Efforts to restore muscle stem cell activity are far enough advanced to make this an area worth keeping an eye on.

Can we turn back time? Muscles' own protective systems could help reduce frailty

As people grow older, their leg muscles become progressively smaller and weaker, leading to frailty and disability. While this process inevitably affects everyone living long enough, until now the process has not been understood. New research suggests that muscle wasting follows on from changes in the nervous system. By the age of 75, individuals typically have around 30-50% fewer nerves controlling their legs. This leaves parts of their muscles disconnected from the nervous system, making them functionally useless and so they waste away.

However, healthy muscles have a form of protection, in that surviving nerves can send out new branches to rescue some, but not all, of the detached muscle fibres. This protective mechanism is most successful in older adults with large, healthy muscles. When the internal protective mechanism is not successful and nerves are unable to send out new branches, it can result in extensive muscle loss. This can result in a condition called sarcopenia, which affects an estimated 10-20% of people aged over 65 years.

The researchers are currently looking at whether regular exercise in middle- and older-age slows the process of muscles becoming disconnected from the nervous system, or improves the success of nerve branching to rescue detached muscle fibres. The goal is to identify the best type of exercise - strength training or endurance - and to understand the physiology of why the nerve-muscle changes occur as we get older.

Failure to expand the motor unit size to compensate for declining motor unit numbers distinguishes sarcopenic from non-sarcopenic older men

Sarcopenia results from the progressive loss of skeletal muscle mass and reduced function in older age. It is likely to be associated with the well-documented reduction of motor unit numbers innervating limb muscles and the increase in size of surviving motor units via reinnervation of denervated fibres. However no evidence currently exists to confirm the extent of motor unit remodelling in sarcopenic individuals. The aim of the present study was to compare motor unit size and number between young (n = 48), non-sarcopenic old (n = 13), pre-sarcopenic (n = 53) and sarcopenic (n = 29) men.

Motor unit potentials (MUPs) were isolated from intramuscular and surface electromyographic recordings. The motor unit numbers were reduced in all groups of old compared with young. Motor unit potentials were enlarged in non-sarcopenic and pre-sarcopenic men compared with young, but not in the vastus lateralis of sarcopenic old. The results suggest that extensive motor unit remodelling occurs relatively early during ageing, exceeds the loss of muscle mass, and precedes sarcopenia. Reinnervation of denervated muscle fibres likely expands the motor unit size in non-sarcopenic and pre-sarcopenic old, but not in the sarcopenic old. These findings suggest that a failure to expand the motor unit size distinguishes sarcopenic from pre-sarcopenic muscles.