Persistent inward currents (PICs) provide gain control of motoneuron output and are influenced by both neuromodulation and inhibitory inputs. However, if feedback from large-diameter axons is altered through neurological or musculoskeletal impairment, amplification and prolongation of synaptic inputs by PICs may be facilitated, potentially altering neuromuscular performance. Over two experiments, we tested the hypothesis that reduced Ia afferent input from lower limb muscles increases tibialis anterior (TA) motor unit (MU) discharge rate hysteresis.

In Experiment 1, 10 neurologically intact adults (4 female) performed triangular-shaped isometric dorsiflexion to 30% maximum voluntary force (MVF) at the beginning of the experiment (PRE1), and after 20 minutes of rest (PRE2; control condition). A sphygmomanometer cuff was then inflated to 200 mmHg above the knee to induce ischaemic nerve block, verified by soleus H-reflex abolition, before repeating the contractions (POST). Experiment 2 involved 8 neurologically intact adults (3 female) with triangular contractions performed to the same relative contraction intensity (30% and 50% MVF) at PRE1, PRE2 and POST, based on the condition-specific MVF.

Myoelectrical activity of the TA was measured using a 64-electrode array and the signals were decomposed into individual MU spike trains. Discharge rate hysteresis (ΔF) in both absolute and relative terms (normalised to the maximal theoretical hysteresis) were quantified.

In Experiment 1, peak discharge rate increased at POST (28.3 [24.8, 31.7] pps) compared to PRE1 (19.8 [16.3, 23.3] pps, p<0.001) and PRE2 (20.9 [17.4, 24.4] pps, p<0.001). ΔF at POST (5.14 [4.11, 6.18] pps) was greater than at PRE1 (4.65 [3.61, 5.68] pps, p=0.038) and PRE2 (4.55 [3.52, 5.58] pps, p=0.007). Normalised ΔF was similar at POST (47.7 [31.7, 63.0]%), PRE1 (39.0 [23.0, 54.9]%, p=0.685) and PRE2 (43.0 [28.1, 57.9]% p=0.895).

In Experiment 2, at 30% MVF peak discharge rate was similar at POST (18.9 [15.7, 22.1] pps), PRE1 (18.7 [15.5, 21.9] pps, p=0.867) and PRE2 (18.4 [15.2, 21.6] pps, p=0.385). At 50% MVF peak discharge rate increased at POST (27.1 [23.9, 30.3] pps) compared to PRE1 (25.3 [22.1, 28.5] pps, p<0.001) and PRE2 (25.2 [22.0, 28.4] pps, p<0.001). At 30% MVF, ΔF remained unchanged at POST (4.62 [3.35, 5.89] pps) compared to PRE1 (4.75 [3.48, 6.02] pps, p=0.830) and PRE2 (4.39 [3.12, 5.66] pps, p=0.551). However, at 50% MVF, ΔF increased at POST (5.71 [4.43, 6.99] pps) compared to PRE1 (4.71 [3.44, 5.98] pps, p<0.001) and PRE2 (4.80 [3.52, 6.07] pps, p<0.001). At 30% MVF, normalised ΔF increased at POST (57.0 [51.5, 62.4]%) compared to PRE1 (50.0 [44.7, 55.4]%, p=0.015) and PRE2 (49.9 [44.6, 55.3]%, p=0.013). At 50% MVF a difference in normalised ΔF was maintained at POST (56.6 [50.8, 62.5]%) compared to PRE1 (41.7 [36.3, 47.2]%, p<0.001) and PRE2 (42.6 [36.9, 48.3]%, p<0.001). No differences were observed for any variables between PRE1 and PRE2 for both experiments (p≥0.199).

Ischaemic block of large-diameter axons led to increased ΔF and normalised ΔF, suggesting increased PIC contribution to discharge rate modulation in conditions of reduced inhibitory input, providing insight into the role of Ia afferent input on MU discharge patterns and neuromuscular performance.