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Updated: Jun 19, 2026

Non-invasive Assessment of Changes in Corticomotoneuronal Transmission in Humans
Published on: May 24, 2017
Short-latency crossed inhibitory responses in the human soleus muscle
Peter W Stubbs1, Natalie Mrachacz-Kersting
1Centre for Sensory-Motor Interaction, Department of Health Science and Technology, The University of Aalborg, Aalborg, Denmark.
Abstract:
Even though interlimb coordination is critical in bipedal locomotion, the role of muscle afferent mediated feedback is unknown. The aim of this study was to establish if ipsilateral muscle generated afferent feedback can influence contralateral muscle activation patterns in the human lower limb and to elucidate the mechanisms involved. The effect of ipsilateral tibial nerve stimulation on contralateral soleus (cSOL) responses were quantified. Three interventions were investigated, 1) electrical stimulation applied to the tibial nerve at stimulation intensities from 0 to 100% of maximal M-wave (M-max) with the cSOL contracted from 5 to 15% of maximal voluntary contraction (MVC) and 15 to 30% MVC, 2) ispsilateral tibial nerve stimulation at 75% M-max prior to, during, and following the application of ischemia to the ipsilateral thigh. 3) Electrical stimulation applied to the ipsilateral sural (SuN) and medial plantar nerves at stimulation intensities from 1 to 3 times perceptual threshold. A short-latency depression in the cSOL electromyogram (EMG; onset: 37-41 ms) was observed following ipsilateral tibial nerve stimulation. The magnitude of this depression increased (P = 0.0005 and P = 0.000001) with increasing stimulus intensities. Ischemia delayed the time of the minimum of the cSOL depression (P = 0.04). SuN and medial plantar nerve stimulation evoked a longer latency depression [average; 91.2 ms (SuN); 142 ms (medial plantar nerve)] and therefore do not contribute to the response. This is the first study to demonstrate a short-latency depression in the cSOL following ipsilateral tibial nerve stimulation. Due to its short latency, the response is spinally mediated. The involvement of crossed spinal interneurons receiving input from low-threshold muscle afferents is discussed.
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