Mechanisms modulating spinal excitability after nerve stimulation inducing extra torque.

The study included three experiments aiming to examine the mechanisms responsible for spinal excitability modulation, as assessed by the H-reflex, following stimulation trains delivered at two different frequencies (20 and 100 Hz) inducing extra torque (ET). A first experiment ( = 15) was conducted to evaluate changes in presynaptic inhibition acting on Ia afferents induced by these electrical stimulation trains, assessed by conditioning the soleus H-reflex (tibial nerve stimulation) with stimulation of the common peroneal nerve (D1 inhibition) and of the femoral nerve (heteronymous Ia facilitation, HF). A second experiment ( = 12) permitted to investigate homosynaptic postactivation depression (HPAD) changes after the stimulation trains. A third experiment ( = 14) analyzed changes in motoneuron intrinsic properties after the stimulation trains, by electrically stimulating the descending corticospinal tract at the thoracic level, evoking thoracic motor-evoked potentials (TMEP). Main results showed that in all experiments, spinal excitability decreased after the 20-Hz train ( < 0.05), whereas this parameter significantly increased after the 100-Hz stimulation ( < 0.05). D1 and HF were not significantly modified after either stimulation. HPAD was significantly decreased only after the 20-Hz train, whereas TMEP was significantly increased only after the 100-Hz train ( < 0.05). It is concluded that the decreased spinal excitability observed after the 20-Hz train cannot be attributed to D1 presynaptic inhibition but rather to increased HPAD of the Ia afferents terminals, whereas the increase of this parameter obtained after the 100-Hz train can be assigned to changes in intrinsic motoneuron properties allowing to maintain Ia-α-motoneurons transmission efficacy. Using different electrophysiological techniques, results show that the downregulation of spinal excitability observed after the 20-Hz train could be ascribed to homosynaptic postactivation depression of the Ia afferents terminals, whereas changes in intrinsic motoneuron properties could explain the increased spinal excitability observed after the 100-Hz train. A novel methodology for assessing soleus D1 presynaptic inhibition and heteronymous Ia facilitation, accounting for eventual modulations of test reflex amplitude throughout the session, was developed.