|
|
||||||||
Journal of Neurophysiology, Vol 63, Issue 3 465-472, Copyright © 1990 by APS
ARTICLES |
J. D. Cooke and S. H. Brown
Department of Physiology, University of Western Ontario, London, Canada.
1. Electromyographic (EMG) activity of arm movements made at constant velocity was studied in humans. In these movements, acceleration was temporally separated from deceleration by a period of constant velocity (zero acceleration) lasting up to 600 ms. 2. Agonist (AG1) and antagonist (ANT1) bursts were associated with acceleration. AG1 began before acceleration onset. ANT1 started after the onset of AG1 and was often partially coextensive with AG1. The initial phasic activity was followed by tonic EMG activity during the constant-velocity phase of the movements. Movement deceleration was associated with an antagonist burst (ANT2) and an agonist (AG2) burst. 3. Subjects could alter the magnitudes of the acceleration- and deceleration-related activities independently, with resulting independent changes in the movement acceleration and deceleration. 4. When the duration of the constant-velocity phase was decreased, the agonist/antagonist burst pairs occurred progressively closer in time. When movement duration was decreased to the point at which the velocity profile resembled that of step-tracking movements, the four periods of phasic EMG activity formed the classic triphasic pattern. 5. Triphasic EMG patterns were occasionally seen at the beginning or end of long-duration, constant-velocity movements. When they occurred, these triphasic patterns were associated with an acceleration/deceleration pattern similar to that seen in step-tracking movements. 6. The data indicate that paired agonist/antagonist activation is the basic unit of movement control. The AG1/ANT1 burst pair determines the increase and decrease of acceleration, respectively, and the ANT2/AG2 burst pair the increase and decrease of deceleration. These muscle activation pairs can be combined as needed to produce movements having different temporal characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)
This article has been cited by other articles:
![]() |
S. Y. Schaefer, K. Y. Haaland, and R. L. Sainburg Ipsilesional motor deficits following stroke reflect hemispheric specializations for movement control Brain, August 1, 2007; 130(8): 2146 - 2158. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. E. Sergio, C. Hamel-Paquet, and J. F. Kalaska Motor Cortex Neural Correlates of Output Kinematics and Kinetics During Isometric-Force and Arm-Reaching Tasks J Neurophysiol, October 1, 2005; 94(4): 2353 - 2378. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. S. A. Graziano, K. T. Patel, and C. S. R. Taylor Mapping From Motor Cortex to Biceps and Triceps Altered By Elbow Angle J Neurophysiol, July 1, 2004; 92(1): 395 - 407. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. A. Doeringer and N. Hogan Intermittency in Preplanned Elbow Movements Persists in the Absence of Visual Feedback J Neurophysiol, October 1, 1998; 80(4): 1787 - 1799. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |