Normal human subjects made discrete elbow flexions and extensions in the horizontal plane from a stationary initial position to visually defined targets at different distances with a constant inertial load or made flexions to a visually defined target with different inertial loads. We measured joint angle, acceleration, and electromyograms (EMGs) from two agonist and two antagonist muscles. Subjects were instructed to move their limbs accurately but quickly to the targets. Movements of greater distances or lesser loads were performed at higher velocities. Peak inertial torque, acceleration and velocity, movement time, and integrated, rectified EMG were all highly correlated with the task variables, distance and intertial load. We show that peak inertial torque can be used as a linking variable that is almost sufficient to explain all correlations between the tasks, the EMG, and movement kinematics. The rate at which subjects initially developed torque to accelerate their movements was invariant over changes in the value of either task variable. The rising phase of the agonist EMG was also independent of the distance or load moved. Two components were distinguished in the antagonist EMG. The first had a relatively constant latency and amplitude. It terminated on the onset of the second and larger component at a latency that was delayed as both distance and load increased. The integrated, rectified antagonist EMG was proportional to inertial load and peak decelerating torque for changes in inertial load. When target distance varied, proportionality between peak decelerating torque and antagonist EMG could be found if correction was made for the effects of muscle length on the torque-EMG relationship. We propose organizing principles for the control of single-joint human movements in which tasks are performed by one of two strategies. These are called speed-insensitive and speed-sensitive strategies. A model is described in which movements made under a speed-insensitive strategy are executed by controlling the duration and the relative timing of amplitude invariant patterns of activation to the spinal motoneuron pools.
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