Human subjects performed step-tracking movements of the wrist in the radial direction. Movement amplitude, external load, and accuracy instructions were varied. We used surface electrodes to record muscle activity from an agonist, extensor carpi radialis longus, and an antagonist, extensor carpi ulnaris. When subjects performed movements ''as fast as possible'' that were opposed by different external loads, we observed two distinct patterns of modulation of the agonist burst. In one pattern, termed pulse-height modulation, the force of the agonist muscle was graded by varying the peak amplitude of a short-duration agonist burst. This pattern occurred when subjects performed movements of different amplitudes with a lightweight manipulandum. In the other pattern, termed pulse-width modulation, the force of the agonist muscle was graded by varying the duration of an agonist burst of nearly maximal amplitude. When the agonist burst was prolonged, the onset of antagonist activity was delayed. This pattern occurred when subjects performed movements of different amplitudes that were opposed by elastic or viscoelastic loads applied to a heavy manipulandum. The strongest subject exhibited more pulse-height modulation and less pulse-width modulation of the agonist burst than other subjects. Conversely, the weakest subject displayed more pulse-width modulation of the agonist burst than other subjects. These observations indicate that the force requirements of a task, relative to the force generating capacity of a subject's agonist muscle(s), have a significant influence on the pattern of agonist modulation. In a second experiment using three nonhuman primates, we observed that agonist bursts in wrist flexor and extensor muscles exhibited strikingly different patterns of modulation. For wrist flexion, agonist bursts in wrist flexors were brief and displayed pulse-height modulation when movement amplitude was varied. For wrist extension, agonist bursts in wrist extensors were prolonged and displayed largely pulse-width modulation when movement amplitude was varied. We suggest that the distinct patterns of modulation observed in the wrist muscles of monkeys were due to differences in the strength of wrist flexors and extensors, rather than to alterations in movement strategy. In a third experiment, we instructed human subjects to be ''accurate'' when they made step-tracking movements. When subjects performed movements with a lightweight manipulandum, most displayed short-duration agonist bursts that were pulse-height modulated. When subjects performed ''accurate'' movements that were opposed by elastic loads, they displayed pulse-width modulation of a small-amplitude agonist burst. This result indicates that the duration of the agonist burst can be modulated even when the amplitude of the burst is not at its maximum. These findings, together with those of our prior study (Hoffman and Strick, 1990), demonstrate that the nervous system can independently specify three parameters of agonist and antagonist muscle activity: (1) the amplitude of an agonist burst, (2) the duration of an agonist burst, and (3) the amplitude of an antagonist burst. This flexibility over the control of agonist and antagonist activity enables the nervous system to shape precisely the magnitude and time course of the force needed to accomplish a specific task.
