Reduction in Ia afferent input via ischaemia alters motor unit discharge characteristics and estimates of persistent inward currents

Abstract

Persistent inward currents (PICs) govern motoneuron output and are influenced by diffuse neuromodulation and local inhibition. When large diameter afferent feedback is lost, as in some neurological conditions, PICs might additionally amplify and prolong synaptic inputs. Here, we examined whether reducing Ia afferent transmission via ischaemic nerve block alters PIC contribution to tibialis anterior (TA) motor unit (MU) discharge. Across two experiments 12 adults (5 female) performed triangular-shaped isometric dorsiflexion to 30% (Experiments 1 and 2) and 50% (Experiment 2) maximum voluntary force (MVF) at baseline, after a 20-minute rest (control), and during occlusion after inducing an ischaemic nerve block, confirmed by abolition of the soleus H-reflex. TA myoelectrical activity measured during contractions was decomposed into MU spike trains, and from smoothed MU discharges, discharge rate hysteresis ({Delta}F) and ascending non-linearity (brace height) were quantified. Results from Experiment 1 involving contractions matched to absolute force levels revealed increased peak discharge rate, {Delta}F, and brace height post-occlusion. However, {Delta}F normalised to maximal theoretical hysteresis did not change across time points. In Experiment 2, where MVF was reassessed at each timepoint and contractions were matched to relative force, peak discharge rate, normalised {Delta}F and brace height increased post-occlusion compared to pre-, across both contraction intensities. {Delta}F only increased post-occlusion at 50% MVF, with no changes at 30% MVF. These results show that ischaemic block of large-diameter axons, likely reducing reciprocal inhibition, increases PIC contribution to discharge rate modulation, highlighting the role of Ia afferent input in shaping motoneuron output in humans.