Muscle coactivation: definitions, mechanisms, and functions

Abstract

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.

Stochastic optimal open-loop control as a theory of force and impedance planning via muscle co-contraction

“…In this vein, several studies on deafferented monkeys (without feedback circuitry at all) suggested that an equilibrium point/trajectory resulting from the co-contraction of agonist and antagonist mus- Similar conclusions were drawn with deafferented patients who were able to perform relatively accurate reaching movements without on-line vision -if allowed to see their arm transiently prior to movement execution- [41]. Furthermore, neurophysiological studies seem to agree that co-contraction commands have a central origin with little contribution from spinal mechanisms [14,19,42]. Noticeably, during cocontraction of opposing muscles, disynaptic reciprocal inhibition has been shown to be reduced by central signals [43,44].…”

“…On the one hand, one may consider an end-effector or joint level description of the stiffness-like property of the neuromusculoskeletal system (e.g. [46] or the r-and 190 c-commands in [14]). On the other hand, one may consider more advanced models representing the multiple muscles crossing each joint, the activation of which will modulate both the apparent stiffness of the musculoskeletal system and net joint torques (e.g.…”

“…[51]). This choice is related to the hierarchical control hypothesis, as discussed in [4,14] for instance. As this choice is still elusive, we will consider both joint and muscle levels of description.…”

“…1. To simplify the derivations, we note that the state of a joint can be modified only in two ways: it can either (1) be moved to another position via changes of net torques or 200 (2) be stiffened with no apparent motion via co-contraction [14]. Accordingly, the forearm dynamics can be rewritten as…”

“…However, these two prominent approaches have in common that they fail to simply account for a fundamental motor control strategy used by the central nervous system (CNS) and often referred to as muscle 20 co-contraction or co-activation of antagonist muscles (see [14] for a recent review). This frequent phenomenon is known since more than a century and the work of Demenÿ [15], and has been investigated extensively since then.…”