Presynaptic inhibition mechanisms may subserve the spinal excitability modulation induced by neuromuscular electrical stimulation.

This study aimed at deciphering the origins of spinal excitability modulation that follows neuromuscular electrical stimulation (NMES). Ten participants (age: 24.6 ± 4.2 years) performed 2 randomized NMES sessions on plantar flexors with frequencies of stimulations of 20 or 100 Hz (pulse width: 1 ms) at 20% of maximal voluntary contraction (MVC). Before and after each session, the posterior tibial nerve was stimulated to record H-reflex of soleus (SOL), gastrocnemius medialis (GM) and gastrocnemius lateralis (GL). D1 presynaptic inhibition was assessed by conditioning H reflex with prior common peroneal nerve stimulation. Resting H-reflex of SOL decreased after both protocols, but in a greater extent following the 100 Hz session (100 Hz: -34.6 ± 7.3%, 20 Hz: -17.1 ± 3.8%; P = 0.002), accompanied by an increase of presynaptic inhibition (+22 ± 5.8% at 100 Hz vs. +8 ± 3.7% at 20 Hz, P < 0.001). GM and GL spinal excitability and presynaptic inhibition were also altered after NMES, but in a similarly extent after 20 Hz and 100 Hz protocols. Neuromuscular fatigue following a single session of NMES involves spinal presynaptic circuitry, even at low stimulation frequency. The spinal sensitivity to NMES seems also muscle dependent.