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Differential changes in corticospinal and Ia input to tibialis anterior and soleus motor neurones during voluntary contraction in man

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Motor-evoked potentials (MEPs) were recorded in the tibialis anterior and soleus muscles following transcranial magnetic stimulation (TMS) of the motor cortex. In the soleus, the H-reflex amplitude increased with the contraction level to the same extent as that of MEPs, whereas in the tibialis anterior, the H-reflex amplitude increased significantly less than that of MEPs. The latency of the MEPs decreased with contraction, whereas this was not the case of the H-reflexes. In the tibialis anterior, the response probability of single-motor units (SMU) to TMS increased more substantially during voluntary contraction than following stimulation of the peroneal nerve. In the tibialis anterior, the response probability of SMU increased more substantially during voluntary contraction than following stimulation of the peroneal nerve. The short-latency facilitation, presumably monosynaptic of origin, of the soleus H-reflex evoked by subthreshold TMS increased as a function of the plantarflexion force. This was not the case for the heteronymous Ia facilitation of the soleus H-reflex following stimulation of the femoral nerve. It is concluded that the corticospinal input to lower limb motor neurones generated by TMS increases with the level of voluntary contraction, whereas this is true only to a limited extent for the synaptic input from Ia afferents. It is suggested that this reflects changes in the susceptibility of corticospinal cells to TMS during voluntary contraction.

Keywords: H-reflex; Ia afferents; corticospinal tract; motor cortex; motor neurones; spinal cord; transcranial magnetic stimulation; voluntary movement

Document Type: Research Article

Affiliations: 1: The Third Department of Internal Medicine, Division of Neurology, Clinicla Neurophysiology Lab., Shinshu University School of Medicine, Matsumoto, Japan 2: Laboratory of Neurophysiology, School of Medicine, University of Louvain, Brussels, Belgium 3: Physiologisches Institut, Christian-Albrechts-Universit├Ąt zu Kiel, Kiel, Germany 4: Division of Neurophysiology, Department of Medical Physiology, Panum Institute, University of Copenhagen, Copenhagen, Denmark

Publication date: September 1, 2000


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