Vibration decreases the responsiveness of Ia afferents and spinal motoneurons in humans

After vibration, Hoffmann reflex (H reflex) amplitude is depressed; however, the mechanisms underlying these phenomena remain unknown. This study investigated the influence of frequency and duration of vibration on the H reflex amplitude, heteronymous facilitation of the tendon jerk (T wave) mediated by group Ia afferents, and cervicomedullary motor evoked potential (CMEP) amplitude in 18 healthy human subjects. The H reflex of the flexor carpi radialis (FCR) was induced by median nerve stimulation at the elbow, and the conditioning FCR stimulation enhanced the T wave of the biceps brachii (BB). After vibration was applied to the FCR muscle belly, the amplitudes of the H reflex and heteronymous facilitation of the T wave were depressed; these influences persisted after the removal of vibration in all subjects. For the H reflex, there was no difference in the amount of depression among the frequencies of vibration used (57, 77, and 100 Hz). Higher frequencies of vibration were associated with longer recovery times of postvibration depression, and a longer duration of vibration was associated with a longer recovery time of the depression. Similar results were observed for heteronymous facilitation of the T wave, suggesting that the depression is caused by a decrease in postsynaptic potentials evoked by Ia afferents in spinal motoneurons; it was probably due to reduction in the number of Ia afferents recruited by the median nerve stimulation. Moreover, because the FCR CMEP amplitude was depressed after vibration, vibration should affect the responsiveness of spinal motoneurons. These mechanisms are considered to contribute to the H reflex depression after vibration.NEW & NOTEWORTHY Vibration decreased the responsiveness of Ia afferents from the muscle exposed to vibration, and the duration of depressive effect was modulated by the duration and frequency of the vibration: a longer duration and a higher frequency of vibration led to a longer recovery time of the depression. In addition to this presynaptic effect, it also depressed the responsiveness of spinal motoneurons, indicating postsynaptic inhibition through specific circuits triggered by Ia impulses.