Divergent response of low- versus high-threshold motor units to experimental muscle pain

The neural strategies behind the control of force during muscle pain are not well understood as previous research has been limited in assessing pain responses only during low-force contractions. Here we compared, for the first time, the behaviour of motor units recruited at low and high forces in response to pain. The results showed that motor units activated at low forces were inhibited while those recruited at higher forces increased their activity in response to pain. When analysing lower- and higher-threshold motor unit behaviour at high forces we observed differential changes in discharge rate and recruitment threshold across the motor unit pool. These adjustments allow the exertion of high forces in acutely painful conditions but could eventually lead to greater fatigue and stress of the muscle tissue.

During low-force contractions, motor unit discharge rates decrease when muscle pain is induced by injecting nociceptive substances into the muscle. Despite this consistent observation, it is currently unknown how the central nervous system regulates motor unit behaviour in the presence of muscle pain at high forces. For this reason, we analysed the tibialis anterior motor unit behaviour at low and high forces. Surface EMG signals were recorded from 15 healthy participants (mean age (SD) 26 (3) years, six females) using a 64-electrode grid while performing isometric ankle dorsiflexion contractions at 20% and 70% of the maximum voluntary force (MVC). Signals were decomposed and the same motor units were tracked across painful (intramuscular hypertonic saline injection) and non-painful (baseline, isotonic saline, post-pain) contractions. At 20% MVC, discharge rates decreased significantly in the painful condition (baseline vs. pain: 12.7 (1.1) Hz to 11.5 (0.9) Hz, P < 0.001). Conversely, at 70% MVC, discharge rates increased significantly during pain (baseline vs. pain: 19.7 (2.8) Hz to 21.3 (3.5) Hz, p = 0.029) and recruitment thresholds decreased (baseline vs. pain: 59.0 (3.9) %MVC to 55.9 (3.2) %MVC, p = 0.02). These results show that there is a differential adjustment between low- and high-threshold motor units during painful conditions. An increase in excitatory drive to high-threshold motor units is likely required to compensate for the inhibitory influence of nociceptive afferent inputs on low-threshold motor units. These differential mechanisms allow the force output to be maintained during acute pain but this strategy could lead to increased muscle fatigue and symptom aggravation in the long term.