Specific modulation of presynaptic and recurrent inhibition of the soleus muscle during lengthening and shortening submaximal and maximal contractions.

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The study analyzed neural mechanisms mediating spinal excitability modulation during eccentric (ECC) movement (passive muscle lengthening, submaximal, and maximal ECC contractions) as compared with concentric (CON) conditions. Twenty-two healthy subjects participated in three experiments. Experiment A (n = 13) examined D1 presynaptic inhibition (D1 PI) and recurrent inhibition (RI) modulation during passive muscle lengthening and shortening, by conditioning the soleus (SOL) H-reflex with common peroneal nerve submaximal and tibial nerve maximal stimulation, respectively. Experiment B (n = 13) analyzed the effect of passive muscle lengthening on D1 PI and heteronymous Ia facilitation (HF, conditioning the SOL H-reflex by femoral stimulation). Experiment C (n = 13) focused on the effect of muscle contraction level (20%, 50%, and 100% of maximal voluntary contraction) on D1 PI and RI. Results showed a significantly higher level of D1 PI during passive muscle lengthening than shortening (P < 0.01), whereas RI and HF were not affected by passive muscle movement. D1 PI and RI were both higher during ECC as compared with CON contractions (P < 0.001). However, the amount of D1 PI was independent of the torque level, whereas RI was reduced as the torque level increased (P < 0.05). The decreased spinal excitability induced by muscle lengthening during both passive and active conditions is mainly attributed to D1 PI, whereas RI also plays a role in the control of the specific motoneuron output during ECC contractions. Both inhibitory mechanisms are centrally controlled, but the fact that they evolve differently with torque increases, suggests a distinct supraspinal control.NEW & NOTEWORTHY Presynaptic (PI) and recurrent inhibitions (RI) were studied during passive muscle lengthening and eccentric contractions. Results indicate that the increased PI during passive muscle lengthening accounts for the decreased spinal excitability at rest. During eccentric contraction both mechanisms contribute to spinal excitability modulation. The same amount of PI was observed during eccentric contractions, while RI decreased as developed torque increased. This distinct modulation according to torque level suggests a distinct supraspinal control of these mechanisms.