Tonic muscle pain does not increase fusimotor drive to human leg muscles: implications for chronic muscle pain

Abstract

Experimental pain induced in animals has shown that noxious stimulation of group III and IV afferents increases the firing of muscle spindles via a reflex excitation of fusimotor (γ) motoneurones. Chronic muscle pain has been hypothesized to develop as a result of a vicious cycle involving this mechanism. In order to explore the effects of long-lasting muscle pain on the fusimotor system, single unit muscle spindle afferents were recorded from 15 subjects. Afferent activity was recorded from foot and ankle extensor muscles whilst infusing hypertonic saline into the tibialis anterior muscle of the ipsilateral leg, producing moderate-strong pain lasting for ∼60 min. A change in fusimotor drive was inferred by observing changes in the mean discharge rate of spontaneously active muscle spindle afferents. Homonymous and heteronymous muscles remained relaxed and showed no increase in activity, arguing against any fusimotor-driven increase in motor activity, and there was no net change in the firing of muscle spindle afferents. We conclude that long-lasting stimulation of group III and IV afferents fails to excite fusimotor neurones and increase muscle spindle discharge. Accordingly, the vicious cycle theory has no functional basis for the development of myalgia in human subjects.