Optimal control of antagonistic muscle stiffness during voluntary movements.
This paper presents a study on the control of antagonist muscle stiffness during single-joint arm movements by optimal control theory with a minimal effort criterion. A hierarchical model is developed based on the physiology of the neuromuscular control system and the equilibrium point hypothesis. For point-to-point movements, the model provides predictions on (1) movement trajectory, (2) equilibrium trajectory, (3) muscle control inputs, and (4) antagonist muscle stiffness, as well as other variables. We compared these model predictions to the behavior observed in normal human subjects. The optimal movements capture the major invariant characteristics of voluntary movements, such as a sigmoidal movement trajectory with a bell-shaped velocity profile, an 'N'-shaped equilibrium trajectory, a triphasic burst pattern of muscle control inputs, and a dynamically modulated joint stiffness. The joint stiffness is found to increase in the middle of the movement as a consequence of the triphasic muscle activities. We have also investigated the effects of changes in model parameters on movement control. We found that the movement kinematics and muscle control inputs are strongly influenced by the upper bound of the descending excitation signal that activates motoneuron pools in the spinal cord. Furthermore, a class of movements with scaled velocity profiles can be achieved by tuning the amplitude and duration of this excitation signal. These model predictions agree with a wide body of experimental data obtained from normal human subjects. The results suggest that the control of fast arm movements involves explicit planning for both the equilibrium trajectory and joint stiffness, and that the minimal effort criterion best characterizes the objective of movement planning and control.
Lan
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Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106.
Crago
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D001132:Arm; D003198:Computer Simulation; D003491:Cybernetics; D006801:Humans; D008954:Models, Biological; D009046:Motor Neurons / Q000502:physiology; D009068:Movement / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology; D009132:Muscles / Q000502:physiology*; D017711:Nonlinear Dynamics