Motoneurone recruitment is altered with pain induced in non-muscular tissue.

Pain

NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, St. Lucia, Brisbane, Qld 4072, Australia.

Published: January 2009

Motoneurone discharge rate is reduced despite the maintenance of force when pain is induced via injection of hypertonic saline into muscle. Two aspects require consideration. First, hypertonic saline may have direct effects on axons other than small diameter pain fibres including the motoneurones that innervate the painful muscle. Second, it is unclear how force is maintained, when motoneurone discharge rate is decreased. We aimed to determine; (1) if motoneurone discharge rate is reduced during force-matched tasks when pain is induced in non-muscle tissue (to exclude direct effects on motoneurones) and (2) if the reduction of discharge rate is associated with additional changes in motoneurone recruitment over multiple muscle regions. Motoneurone discharge was recorded in the quadriceps with eight pairs of fine-wire electrodes. Seven subjects performed 30-s low-level, force-matched contractions before and during anterior knee pain, which was induced by a bolus (0.25ml) injection of 5% hypertonic saline into the infra-patellar fat pad. In total, 119 motor units were identified. Of these, 34 were identified both before and during pain. The discharge rate of these units decreased during pain from 8.9(1.5) to 7.2(1.4)Hz (P<0.0001). In addition, 31 units were recruited in the no-pain condition but not during pain, when 53 new units were recruited. These changes coincided with a large variability in gross muscle activity measures between muscle regions. These data confirm that motoneurone recruitment is altered when direct effects of saline on motoneurones are excluded. Recruitment of additional motor units may explain force maintenance despite reduced discharge rate of some units.

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http://dx.doi.org/10.1016/j.pain.2008.10.029DOI Listing

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