The regulation of disynaptic reciprocal Ia inhibition during co‐contraction of antagonistic muscles in man.

Abstract

1. The disynaptic reciprocal inhibition from ankle dorsiflexors to ankle plantarflexors was investigated at rest, during tonic plantar‐ and dorsiflexion and during co‐contraction. In relation to rest, it was found to be decreased during plantarflexion and co‐contraction, but unchanged during dorsiflexion. 2. When increasing the strength of plantarflexion the amount of inhibition became progressively smaller. Already during weak co‐contraction, the amount of inhibition was very small and it did not become smaller during stronger contraction. The decrease of inhibition during co‐contraction could not be explained by an addition of the changes of inhibition observed during plantar‐ and dorsiflexion individually. 3. The disynaptic reciprocal inhibition was also found to be decreased when the peripheral feedback from the muscles was blocked by inducing ischaemia in the leg and at the beginning of a dynamic co‐contraction before sensory feedback could interfere. This implies that the observed decrease is caused by a central inhibition of the transmission in the pathway. 4. The amount of disynaptic reciprocal inhibition was also investigated during standing. No significant difference in the amount of inhibition was found when the subjects were standing up at rest as compared to sitting down at rest. When the subjects were forced to make a co‐contraction in order to maintain balance, i.e. when they were standing on one leg, leaning backwards or standing on an unstable platform, a decrease of disynaptic reciprocal inhibition was seen. When the subjects leaned forward, thus forcing a contraction of the soleus muscle, a decrease was also seen, but it was smaller than in the co‐contraction tasks. Finally, when the subjects lifted the examined leg, thus contracting the tibialis anterior muscle, either no change or a small increase of inhibition was seen. 5. A similar control of the disynaptic reciprocal inhibition as described for the pathway from ankle dorsiflexors to ankle plantarflexors was also observed for the pathway from ankle plantarflexors to dorsiflexors and from wrist extensors to wrist flexors. 6. It is concluded that when co‐contraction is used in order to stabilize a joint, i.e. to maintain posture, a specific co‐contraction motor programme is activated that depresses the transmission in the disynaptic reciprocal pathway thereby ensuring a high excitability level in the motoneurones of both antagonistic muscles.