A hypothesis for neural control of the speed of muscle contraction in the mammal.
A hypothesis for neural control of the contractile properties of muscle is presented. The hypothesis is based on two assumptions: i) the motoneurons innervating both the fast- and slow-twitch muscles in the mammal possess an identical neurotrophic substance which accelerates the speed of muscle contraction, and ii) slow contractions of the slow-twitch muscle are induced by the low frequency discharges of the innervating motoneurons. The presence of such a trophic substance in the motoneurons is supported by the prolongation of contraction time in both the fast- and slow-twitch muscles following denervation. Furthermore, a given slow-twitch muscle dually reinnervated by the fast and slow muscle nerves contracts at the same speed regardless of which nerve is stimulated, if identical neural activity patterns are chronically imposed upon the two nerves. The presence of effective neural activity patterns in the motoneurons innervating the slow-twitch muscle is supported by an increase in the contraction speed of the slow-twitch muscle following virtual elimination of motoneuron activity by transection of the spinal cord. Under such conditions, contraction time of the fast-twitch muscle remains unchanged. Also, cord transection of newborn animals does not affect the postnatal acceleration in contraction time of the fast-twitch muscle, while the postnatal changes of contraction of the slow-twitch muscle mimic those of the fast-twitch muscle. The contraction time of slow-twitch muscle fibers is correlated with the duration of after-hyperpolarization (AHP) in the motoneurons, which regulates the discharge frequency. The duration of AHP increases with age in the motoneurons innervating the slow-twitch muscle but not in those innervating the fast-twitch muscle. It is proposed that the maintenance of slow contractions in the slow-twitch muscle during muscle differentiation is due to the appearance of low frequency discharges in the innervating motoneurons as a result of the postnatal prolongation of the AHP. The implications and limitations of the proposed hypothesis are discussed.
D000375:Aging; D000818:Animals; D002454:Cell Differentiation; D004553:Electric Conductivity; D008959:Models, Neurological; D009043:Motor Activity; D009046:Motor Neurons / Q000502:physiology*; D009119:Muscle Contraction; D009121:Muscle Denervation; D024510:Muscle Development; D009132:Muscles / Q000294:innervation*