Human motor unit characteristics of the superior trapezius muscle with age-related comparisons

Current understanding of human motor unit (MU) control and aging is mostly derived from hand and limb muscles that have spinal motor neuron innervations. The aim here was to characterize and test whether a muscle with a shared innervation supply from brainstem and spinal MU populations would demonstrate similar age-related adaptations as those reported for other muscles. In humans, the superior trapezius (ST) muscle acts to elevate and stabilize the scapula and has primary efferent supply from the spinal accessory nerve (cranial nerve XI) located in the brainstem. We compared electrophysiological properties obtained from intramuscular and surface recordings between 10 young (22-33 yr) and 10 old (77-88 yr) men at a range of voluntary isometric contraction intensities (from 15 to 100% of maximal efforts). The old group was 41% weaker with 43% lower MU discharge frequencies compared with the young (47.2 ± 9.6 Hz young and 26.7 ± 5.8 Hz old, < 0.05) during maximal efforts. There was no difference in MU number estimation between age groups (228 ± 105 young and 209 ± 89 old, = 0.33). Furthermore, there were no differences in needle detected near fiber (NF) stability parameters of jitter or jiggle. The old group had lower amplitude and smaller area of the stimulated compound muscle action potential and smaller NF MU potential area with higher NF counts. Thus, despite age-related ST weakness and lower MU discharge rates, there was minimal evidence of MU loss or compensatory reinnervation. The human superior trapezius (ST) has shared spinal and brainstem motor neuron innervation providing a unique model to explore the impact of aging on motor unit (MU) properties. Although the ST showed higher MU discharge rates compared with most spinally innervated muscles, voluntary strength and mean MU rates were lower in old compared with young at all contraction intensities. There was no age-related difference in MU number estimates with minimal electrophysiological evidence of collateral reinnervation.