Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis

Abstract

In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments. 1. To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave amplitude for ECR brevis. Stimuli were delivered during both isometric wrist flexions and radial deviation actions with an equivalent EMG amplitude in FCR (approximately 5% wrist flexion MVC). 2. To explore the homonymous Ia afferent pathway to FCR motoneurons, 50 stimuli were delivered to the median nerve at intensities ranging from below motor threshold to at least two times that which evoked a maximal M-wave during wrist flexion and radial deviation (matched FCR EMG at approximately 5% wrist flexion MVC). 3. EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) greater during MVCs in wrist flexion and extension (respectively) than radial deviation. ECR longus EMG was significantly greater during MVCs in radial deviation than extension. These results indicate that the gain of the Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex pathway to FCR is greater during wrist flexion than radial deviation. Transmission through both of these pathways probably contributes to the inability of individuals to maximally activate FCR during radial deviation MVCs.