摘要：The movement in a joint is facilitated by a pair of muscles that pull in opposite directions. The difference in the pair’s muscle force or reciprocal activity results in joint torque, while the overlapping muscle force or the cocontraction is related to the joint’s stiffness. Cocontraction knowingly adapts implicitly over a number of movements, but it is unclear whether the central nervous system can actively regulate cocontraction in a goal-directed manner in a short span of time. We developed a muscle interface where a cursor’s horizontal position was determined by the reciprocal activity of the shoulder flexion–extension muscle pair, while the vertical position was controlled by its cocontraction. Participants made goal-directed movements to single and via-point targets in the two-dimensional muscle space, learning to move the cursor along the shortest path. Simulations using an optimal control framework suggest that the reciprocal activity and the cocontraction may be controlled independently by the CNS, albeit at a rate orders of magnitude slower than the muscle’s maximal activation speed.
其他摘要：Abstract The movement in a joint is facilitated by a pair of muscles that pull in opposite directions. The difference in the pair’s muscle force or reciprocal activity results in joint torque, while the overlapping muscle force or the cocontraction is related to the joint’s stiffness. Cocontraction knowingly adapts implicitly over a number of movements, but it is unclear whether the central nervous system can actively regulate cocontraction in a goal-directed manner in a short span of time. We developed a muscle interface where a cursor’s horizontal position was determined by the reciprocal activity of the shoulder flexion–extension muscle pair, while the vertical position was controlled by its cocontraction. Participants made goal-directed movements to single and via-point targets in the two-dimensional muscle space, learning to move the cursor along the shortest path. Simulations using an optimal control framework suggest that the reciprocal activity and the cocontraction may be controlled independently by the CNS, albeit at a rate orders of magnitude slower than the muscle’s maximal activation speed.
