Firing behavior of triceps brachii motor units after spinal cord injury Christine K. Thomas Mary Tucker, Galina Kozhina, Blair Calancie The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami MILLER School of Medicine, Miami, FL 33136 Triceps brachii muscles are often paralyzed partially after cervical spinal cord injury in humans. Motor units become paralyzed because inputs from higher center are disrupted, the trauma induces motoneuron death or both processes occur. Thus, only a few triceps brachii motor units remain under voluntary control. At the whole muscle level, forces are weak compared to those generated in the muscles of uninjured people. Our aims were to examine: 1) whether chronic cervical spinal cord injury changes triceps brachii motor unit firing rates during voluntary contractions; 2) the prevalence of motor unit firing rate saturation; 3) whether baclofen changes triceps brachii motor unit firing rates during voluntary contractions. Baclofen is a medication usually taken to dampen involuntary contractions (spasms) of paralyzed muscles. Baclofen, a GABAB agonist, largely acts presynatically to block signal conduction at primary afferent terminals (Price et al. Nature 307: 71-74, 1984). Much higher doses are needed for postsynaptic effects, which include increases in the amplitude of persistent inward currents in motoneurons because reductions in calcium currents are less that the increases in sodium currents (Li et al. J Neurophysiol 92:2694-703, 2004). Subjects with chronic (> 1 year) spinal cord injury at C5, C6 or C7 from a motor vehicle or diving accident, a gunshot or a fall participated in this study. Each person performed a series of isometric submaximal and maximal voluntary contractions (5 s) of triceps brachii. Records were made of triceps brachii intramuscular electromyographic activity (EMG) to identify the firing behavior of different motor units, triceps and biceps brachii surface EMG, and force. Data were included provided that: 1) there were increases in the triceps surface EMG up to maximal force. Otherwise force may have been produced by contractions of muscles other than triceps brachii; 2) the firing behavior of a motor unit could be followed from recruitment to maximal force. Data were obtained from 40 motor units, 1-6 units per muscle. Motor units were recruited up to near maximal force. At recruitment, motor units fired at low rates (< 20 Hz). Firing rates increased with force. Most motor units (69 %) continued to increase their firing rate up to maximal force. Only 31 % of units showed a saturation in motor unit firing rate, and typically at high forces (≥ 80 % maximal force). There was a broad range of motor units firing rates during maximal voluntary contractions (12-70 Hz). Within a muscle, the firing behavior of different motor units varied, both in terms of absolute firing rates and the relative change in firing rate with force. Approximately half the data came from individuals who take baclofen chronically. Maximal voluntary motor unit firing rates were higher in individuals using baclofen (mean ± SE: 42 ± 3 Hz) versus not (25 ± 2 Hz), the latter comparable to data from uninjured control subjects. Higher motor unit firing rates during strong and maximal voluntary contractions with baclofen were not attributable to differences in coactivation of triceps and biceps brachii, firing rate saturation, injury level, or sex. Even though baclofen dampens spasms of paralyzed muscles, more effort may be required to recruit motoneurons voluntarily. However, once motoneurons are activated, the postsynaptic effects of baclofen may emerge and be reflected in higher motor unit firing rates. While these higher firing rates will facilitate voluntary contractions, they will also strengthen muscle spasms. These data suggest that presynaptic control of muscle spasms is warranted if voluntary strength is to be maintained. Funded by USPHS grant NS30226 and The Miami Project to Cure Paralysis.
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