Sarcopenia: Neurological Point of View

Abstract

Sarcopenia is an age-related geriatric syndrome which is characterized by the gradual loss of muscle mass, muscle strength, and muscle quality. There are a lot of neurologic insults on sarcopenia at various levels from the brain to the neuromuscular junctions (NMJs) to generate a volitional task. Dopaminergic downregulation, inadequate motor programming and motor coordination impairment lead to decline of supraspinal drive. Motor unit reorganization and inflammatory changes in motor neuron decrease conduction velocity and amplitude of compound muscle action potential. Furthermore, NMJ remodeling and age related neurophysiological alterations may contribute to neuromuscular impairment. Sarcopenia is an age-associated, lifelong process which links to multiple etiological factors. Although not all the causes are completely understood, we suggest that compromised nervous system function may be one of the important contributors to the sarcopenia.

Keywords: Aging; Motor neurons; Nervous system; Neuromuscular junction; Sarcopenia.

Fig. 1. Potential sites and physiological mechanisms that regulate strength. The neuromuscular system contains several potential sites that can affect voluntary force or power production, such as 1) excitatory drive from supraspinal centers, 2) α-motoneuron excitability, 3) antagonistic muscle activity, 4) motor unit recruitment and rate coding, 5) neuromuscular transmission, 6) muscle mass, 7) excitation-contraction coupling processes, and 8) muscle morphology and architecture. [Reprinted from “Sarcopenia =/= dynapenia”, by Clark BC and Manini TM, 2008, J Gerontol A Biol Sci Med Sci, 63, pp.829-34.

Fig. 2. Summary of neurological mechanisms of sarcopenia. EPSP, excitatory postsynaptic potentials; NCV, nerve conduction velocity; CMAP, compound muscle action potentials; NMJ, neuromuscular junction.

Fig. 3. Effect of age on the motor unit, depicting, young and aged motor units. This drawing depicts the pronounced denervation of type II fibers and the recruitment of type I fibers into surviving motor units in older subjects.

Fig. 4. Anatomical remodeling at neuromuscular junction; 1) Widening of synaptic clefts, 2) degeneration of junctional folds at the post synaptic region, and 3) the number of perijunctional acetylcholine receptors is increased.