Ago-antagonist muscle spindle inputs contribute together to joint movement coding in man
- PMID: 9593876
- DOI: 10.1016/s0006-8993(98)00092-4
Ago-antagonist muscle spindle inputs contribute together to joint movement coding in man
Abstract
The proprioceptive feedback associated with the performance of even quite simple movements is always generated by the whole set of muscles subjected to mechanical deformation (lengthening, shortening, contraction, etc.) during that particular movement. The question was addressed here as to how muscle spindle feedbacks arising from agonist and antagonist muscles may contribute to the coding of movement parameters such as the direction and velocity. For this purpose, the activity of single muscle spindle afferents located in the lateral peroneal nerve was analysed using the microneurographic technique, in human subjects performing repetitive voluntary movements, i.e., plantar/dorsal flexions of the ankle, at three different velocities (3, 4.5 and 6 degrees/s). The data obtained suggest that in humans, the direction of a slow movement may be specified on the basis of the spindle discharge rate, which is greater in the stretched than in the shortened muscle, and that the velocity of this movement might be correlated with the difference between the spindle activity occurring in the agonist and antagonist muscles. These neurophysiological data are in agreement with the results of previous psychophysical studies showing for example that a sensation of illusory movement can be elicited only when there exists an imbalance between the agonist versus antagonist vibration-induced Ia inputs. In addition, the greater the difference between the vibration frequencies applied to the two antagonist muscles, the higher the perceived movement velocity was found to be. All in all, joint movement perception seems to result from the co-processing by the central nervous system of the multiple spindle feedbacks originating from the whole set of muscles involved in the performance of a movement.
Copyright 1998 Elsevier Science B.V.
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