• C Ghez and J Gordon.
• Exp Brain Res. 1987 Jan 1;67(2):225-40.

AbstractThe functional role of opposing muscles in the production of isometric force trajectories was studied in six adult subjects producing impulses and steps of elbow flexor force, with different rise times and amplitudes. Rapidly rising forces were invariably associated with an alternating pattern of EMG activity in agonist and antagonist muscles: an agonist burst (AG1) initiated the development of force in the desired direction while a reciprocal burst in the antagonist (ANT-R) led to the deceleration of the force trajectory prior to the peak force. The temporal pattern of agonist and antagonist activation was dependent on force rise time. Force trajectories with long rise times (greater than 200 ms) were entirely controlled by the agonist, and EMG activity closely followed the contours of the rising force trajectory. For rise times of about 120 to 200 ms, agonist activation formed a discrete EMG burst, and force continued to rise during the subsequent silent period. For brief force rise times (less than 120 ms), reciprocal activation of the antagonist muscle occurred at about the time of the peak dF/dt. The integrated magnitude of AG1 was dependent on peak force but was independent of force rise time. AG1 duration varied directly with both peak force and force rise time. The integrated value of ANT-R varied as an inverse function of force rise time and was minimally influenced by peak force. ANT-R was present with the same magnitude and timing in both force impulses and steps when rise times were equal; therefore it did not serve to return force to baseline. Rather it served to truncate the rising force when very brief rise times were required, thus compensating for the low-pass filter properties of the agonist muscle. Subjects were able to voluntarily suppress ANT-R in rapidly accelerated force trajectories, indicating that the linkage between the commands controlling agonist and antagonist is not obligatory; however AG1 was then prolonged. Our findings emphasize that neuronal commands to opposing muscles acting at a joint must be adapted to constraints imposed by the properties of the neuromuscular plant.

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