Age-dependent motor unit remodelling in human limb muscles

Abstract

Voluntary control of skeletal muscle enables humans to interact with and manipulate the environment. Lower muscle mass, weakness and poor coordination are common complaints in older age and reduce physical capabilities. Attention has focused on ways of maintaining muscle size and strength by exercise, diet or hormone replacement. Without appropriate neural innervation, however, muscle cannot function. Emerging evidence points to a neural basis of muscle loss. Motor unit number estimates indicate that by age around 71 years, healthy older people have around 40 % fewer motor units. The surviving low- and moderate-threshold motor units recruited for moderate intensity contractions are enlarged by around 50 % and show increased fibre density, presumably due to collateral reinnervation of denervated fibres. Motor unit potentials show increased complexity and the stability of neuromuscular junction transmissions is decreased. The available evidence is limited by a lack of longitudinal studies, relatively small sample sizes, a tendency to examine the small peripheral muscles and relatively few investigations into the consequences of motor unit remodelling for muscle size and control of movements in older age. Loss of motor neurons and remodelling of surviving motor units constitutes the major change in ageing muscles and probably contributes to muscle loss and functional impairments. The deterioration and remodelling of motor units likely imposes constraints on the way in which the central nervous system controls movements.

Keywords: Ageing; Motor neuron; Motor unit; Muscle; Sarcopenia.

Figures

Fig. 1

Motor unit recordings. a Schematic showing surface and indwelling needle electrodes at the muscle motor point. A typical concentric needle electrode may capture MUPs from up to around 2000 muscle fibres. b Raw data recorded from the vastus lateralis of a healthy older man showing force, intramuscular and surface EMG traces. c A single motor unit potential showing amplitude, duration and complexity in terms of phases (P) and turns (T)

Fig. 2

MUNE values, CMAP, sMUP and MUP values in old compared with young. The dashed horizontal line indicates the median MUNE in old and the dotted horizontal line indicates the median MUP or sMUP in old expressed as % of young from the various studies. Where multiple older age groups or contraction intensities were reported in a single study, the age range 60–80 years and closest intensity to 25 % MVC were used in this figure. TA Tibialis anterior, BB biceps brachii, BB&Br biceps brachii and brachialis, EDB extensor digitorum brevis. Data are from: VL (Piasecki et al. 2015) TA1 (Power et al. 2010); TA2 (Hourigan et al. 2015); TA3 (Dalton et al. 2008); BB1 (Galea 1996); BB2 (Power et al. 2012); BB&Br (Brown et al. 1988); Soleus (Dalton et al. 2008); Thenar (Galea 1996); EDB1 (Galea 1996) and EDB2 (Campbell et al. 1973)

Fig. 3

MRI image from a young man showing connective tissue accumulations around the vastus lateralis motor point (arrow). The surface-recorded CMAP was 66 % smaller, the sMUP was 60 % smaller and the MUPs were 46 % larger than average for young men

Fig. 4

Atrophic muscles in older age. Compared with young, a typical healthy 75 year old man has around 15 % lower appendicular lean mass (McPhee et al. 2013); 30 % smaller knee extensor muscles (Maden-Wilkinson et al. 2014); 35 % lower knee extension strength (McPhee et al. 2013) and 35 % lower leg power (Stenroth et al. 2015); 20–40 % fewer muscle fibres in the VL, fibre-type grouping and small, angular fibres (Lexell et al. ; Lexell and Downham 1991)