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J Physiol Vol 408 pp 185-198
Copyright © 1989 by The Physiological Society
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Unloading of tendon organ discharges by in-series motor units in cat peroneal muscles.

G Horcholle-Bossavit, L Jami, J Petit, R Vejsada and D Zytnicki

Laboratoire de Neurophysiologie, Collège de France, Paris.

1. The discharges from individual Golgi tendon organs of peroneus tertius and brevis muscles were recorded in anaesthetized cats during the isometric contractions of single motor units. Upon combined contractions of several motor units, two sorts of unloading effects were observed. 2. First, the contraction of a motor unit which, by itself, was without action on a tendon organ could produce a reduction in the response of the receptor to one of its activating motor units. Unloading effects exerted by such in-parallel motor units could effectively interfere with the actions of in-series motor units on the receptor. 3. Second, the contraction of a motor unit activating a tendon organ could reduce the response of this tendon organ to the contraction of another of its activating units. This new type of unloading effect, exerted by in-series motor units, was demonstrated by the fact that the simultaneous contraction of both units elicited less discharge from the receptor than the contraction of a single unit. 4. Unfused contractions of a fast-type motor unit eliciting a response in which the tendon organ discharge was driven 1:1 at the frequency of stimulation of the motor unit, could exert unloading actions on the response of the receptor to another motor unit eliciting a higher discharge frequency. 5. In-series unloading actions were exerted not only by fast-type motor units developing large forces, but also by relatively small slow-type motor units. 6. The high incidence of in-parallel and in-series unloading effects suggests that their consequences may be functionally significant. When large numbers of motor units are being recruited in a muscle, unloading effects might result in a limitation of the Ib afferent discharges from this muscle, preventing an excessive increase of autogenetic inhibition.







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