The phenomenon of agonist-antagonist muscle coactivation is discussed with respect to its consequences for movement mechanics (such as increasing joint apparent stiffness, facilitating faster movements, and effects on action stability), implication for movement optimization, and involvement of different neurophysiological structures. Effects of coactivation on movement stability are ambiguous and depend on the effector representing a kinematic chain with a fixed origin or free origin. Furthermore, coactivation is discussed within the framework of the equilibrium-point hypothesis and the idea of hierarchical control with spatial referent coordinates. Relations of muscle coactivation to changes in one of the basic commands, the c-command, are discussed and illustrated. A hypothesis is suggested that agonist-antagonist coactivation reflects a deliberate neural control strategy to preserve effector-level control and avoid making it degenerate and facing the necessity to control at the level of signals to individual muscles. This strategy, in particular, allows stabilizing motor actions by covaried adjustments in spaces of control variables. This hypothesis is able to account for higher levels of coactivation in young healthy persons performing challenging tasks and across various populations with movement impairments.
All Science Journal Classification (ASJC) codes