Antagonist muscle activity during human forearm movements under varying kinematic and loading conditions.

During the performance of unidirectional, single-joint movements it is known that muscle activation is not confined to the agonist, but is generally seen in the antagonist as well, appearing as a burst of antagonist activity if the movement is quite rapid. We have studied the integral over time of antagonist electromyographic activity (Eant) during forearm movements encompassing a wide range of movement speeds, amplitudes and inertial loads, with two intents: first, to provide an empirical description of the dependence of Eant on kinematic and loading parameters which would be valid over a several hundred-fold range of Eant; and second, to test the hypothesis that Eant is related to the torque necessary for braking the movement. With respect to the first aim, we found that for all subjects Eant was correlated with a simple algebraic expression dependent upon peak velocity, movement amplitude and total moment of inertia, when each of these movement parameters was varied either singly or in combination. Although a more complex algebraic expression, in which exponents for each parameter were optimized for a given subject, provided marginally better correlations with Eant, we prefer the simpler expression on the grounds that it provides similar correlations without requiring a different form for each subject. With respect to the second aim of the study, the braking hypothesis was supported by the fact that the simple expression could be interpreted as representing the average net torque required for braking. However, in experiments in which an external torque was provided to assist in braking, antagonist muscle activity was not reduced as much as would be expected if provision of braking torque was the sole function of antagonist activity. We conclude that: (1) antagonist activity varies with kinematic parameters and inertial load in accordance with the requirements for braking the limb, but (2) the activity may in fact provide a multiple of the torque that is required for braking alone, with excess activity presumably offset by concurrent agonist activity. Possible roles of such cocontraction are discussed.