The control of rapid limb movement in the cat

Summary Electromyographic (EMG) activity associated with rapid voluntary limb movements exhibits a characteristic three burst pattern. The first burst is in the agonist muscle (AG1), the second is in the antagonist (ANT) and the third is again in the agonist (AG2). The present study was undertaken to determine whether ANT and AG2 reflect preprogrammed commands or responses to stretch consequent upon limb displacement. To answer this question EMG activity of agonist and antagonist muscles was examined in cats performing a tracking task. To dissociate centrally programmed muscular events from their intended mechanical consequences, isometric and anisometric conditions were presented in either a predictable or unpredictable sequence. A torque motor was used to control limb trajectory and to impose passive angular displacements.Whereas AG1 was present under both isometric and anisometric conditions, ANT and AG2 required limb displacement and were time locked to movement parameters. ANT occurred within 15 ms following the onset of acceleration. Its magnitude varied linearly with this parameter and inversely with AG1. Passive displacements stretching the antagonist elicited responses with similar latencies and greatest magnitude for a given acceleration. AG2 was only present in underdamped movements with terminal oscillations and typically occurred when the position reached its peak and the velocity recrossed zero. Its magnitude was a function of both limb deceleration and of intended force.The data indicate that both ANT and AG2 represent responses to muscles stretch whose amplitudes are modulated by descending commands. Reciprocal mechanisms operating at a spinal level could account for the reduction of the antagonist response as a function of intended force. The increased sensitivity of late stretch responses in the agonist with higher intended forces is compatible with motoneuron facilitation by tonic descending commands. It is proposed that the stretch evoked responses function to dampen terminal oscillations which ensue from rapid displacement of the mass of the limb against elastic forces of muscle and soft tissue.Supported by NIH Grant NS 15750