H-reflex modulation during passive lengthening and shortening of the human triceps surae
Corresponding author A. G. Cresswell: Department of Neuroscience, Karolinska Institute, Box 5626, SE-11486 Stockholm, Sweden. Email: firstname.lastname@example.org
- 1The present study investigated the effects of lengthening and shortening actions on H-reflex amplitude. H-reflexes were evoked in the soleus (SOL) and medial gastrocnemius (MG) of human subjects during passive isometric, lengthening and shortening actions performed at angular velocities of 0, ±2, ±5 and ±15 deg s−1.
- 2H-reflex amplitudes in both SOL and MG were significantly depressed during passive lengthening actions and facilitated during passive shortening actions, when compared with the isometric H-reflex amplitude.
- 3Four experiments were performed in which the latencies from the onset of movement to delivery of the stimulus were altered. Passive H-reflex modulation during lengthening actions was found to begin at latencies of less than 60 ms suggesting that this inhibition was due to peripheral and/or spinal mechanisms.
- 4It is postulated that the H-reflex modulation seen in the present study is related to the tonic discharge of muscle spindle afferents and the consequent effects of transmission within the Ia pathway. Inhibition of the H-reflex at less than 60 ms after the onset of muscle lengthening may be attributed to several mechanisms, which cannot be distinguished using the current protocol. These may include the inability to evoke volleys in Ia fibres that are refractory following muscle spindle discharge during rapid muscle lengthening, a reduced probability of transmitter release from the presynaptic terminal (homosynaptic post-activation depression) and presynaptic inhibition of Ia afferents from plantar flexor agonists. Short latency facilitation of the H-reflex may be attributed to temporal summation of excitatory postsynaptic potentials arising from muscle spindle afferents during rapid muscle lengthening. At longer latencies, presynaptic inhibition of Ia afferents cannot be excluded as a potential inhibitory mechanism.