Effects of weak antagonist on fast elbow flexion movements in man.
By using a mathematical model and experiments involving electrical simulation of antagonistic muscles, we have formed the hypothesis (Wierzbicka et al. 1986) that in one-joint movements the antagonist muscle not only provides braking torque but also controls movement time. To get additional experimental support for this hypothesis, we studied elbow flexion movements performed by patients with spinal cord injury at the C5-6 level who had relatively normal strength in their biceps muscle and little or no voluntary control of the triceps. Seven quadriplegic patients and six control subjects performed elbow flexion movements of 10 degrees, 20 degrees, and 30 degrees "as fast and accurately as possible". Despite the lack of antagonist, patients used the same "pulse height" strategy as control subjects to scale their responses with movement amplitude. However, patients' movement time was on average twice that of control subjects, and durations of both accelerative and decelerative phases of movement were increased. Movement speed and acceleration were reduced to 20-50% of the corresponding values of control subjects. Patients tended to overshoot the target to a larger extent than control subjects, particularly 10 degrees targets, with nearly twice the error. We performed the same experiments using an external torque motor to assist the weak triceps. When a constant extensor torque of 2.5 or 5 Nm was provided by the motor, patients were able to move faster, and movement accuracy improved to within the normal range. These results provide direct evidence that the lack of an antagonist has an important effect on completion time and accuracy of fast goal-directed movements.
Wierzbicka
M M
MM
Spinal Cord Injury Service, Brockton/West Roxbury VA Medical Center, Boston, MA 02132.
Wiegner
A W
AW
D000328:Adult; D004551:Elbow Joint / Q000294:innervation / Q000502:physiology*; D004558:Electric Stimulation; D004576:Electromyography; D006801:Humans; D008875:Middle Aged; D008959:Models, Neurological; D009068:Movement / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology; D009132:Muscles / Q000294:innervation / Q000502:physiology*; D011782:Quadriplegia / Q000503:physiopathology