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Published on: April 12, 2016
Increase in group II excitation from ankle muscles to thigh motoneurones during human standing
Véronique Marchand-Pauvert1, Guillaume Nicolas, Philippe Marque
1Unité mixte de recherche Inserm U731, UPMC, Physiologie et Physiopathologie de la Motricité chez l'Homme, Médecine Physique et Réadaptation, GHU Pitié-Salpêtrière, 47 bd de l'Hôpital, 75651 Paris cedex 13, France. veronique.marchand@chups.jussieu.fr
Abstract:
In standing subjects, we investigated the excitation of quadriceps (Q) motoneurones by muscle afferents from tibialis anterior (TA) and the excitation of semitendinosus (ST) motoneurones by muscle afferents from gastrocnemius medialis (GM). Standing with a backward lean stretches the anterior muscle pair (TA and Q) and they must be co-contracted to maintain balance. Equally, forward lean stretches the posterior muscle pair (GM and ST) and they must be co-contracted. We used these conditions of enhanced lean to increase the influence of gamma static motoneurones on muscle spindle afferents, which enhances the background input from these afferents to extrafusal motoneurones. The effects of the conditioning volleys on motoneurone excitability was estimated using the modulation of the on-going rectified EMG and of the H reflex. Stimulation of afferents from TA in the deep peroneal nerve at 1.5-2 x MT (motor threshold) evoked early group I and late group II excitation of Q motoneurones. Stimulation of afferents in the GM nerve at 1.3-1.8 MT evoked only late group II excitation of ST motoneurones. The late excitation produced by the group II afferents was significantly greater when subjects were standing and leaning than when they voluntarily co-contracted the same muscle pairs at the same levels of activation. The early effect produced by the group I afferents was unchanged. We propose that this increase in excitation by group II afferents reflects a posture-related withdrawal of a tonic inhibition that is exerted by descending noradrenergic control and is specific to the synaptic actions of group II afferents.
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