Relation between EMG activation patterns and kinematic properties of aimed arm movements

Aimed flexion movements of the arm of different amplitude and duration were studied. Velocity and acceleration traces of movements with equal duration but different amplitude were equal, apart from a scaling factor (ratio between movement amplitudes). After appropriate scaling, EMG activity of the first agonist burst for these movements superimposed. This was not true for EMG activity in the antagonist muscle. For movements with equal amplitude, but different duration, the time to peak acceleration was constant for all MT'. Except for this fact, traces of acceleration, velocity, and agonist activity following the time of peak acceleration were about equal after appropriate scaling in time and amplitude. The integral of EMG activity in the first agonist burst increased linearly with peak velocity. For the antagonist burst, the integrated EMG activity increased more than proportionally. During movements made as fast as possible, subjects used a different strategy by varying the duration of the accelerating phase for movements of different amplitude. Movement amplitude was achieved by adjusting the duration of the agonist burst and the onset time for the antagonist muscle. Amplitude of the antagonist burst was constant within a narrow range for movements of different amplitude. These results did not change when the inertial mass was doubled by loading the arm with an additional mass.     

Relation Between EMG Activation Patterns and Kinematic Properties of Aimed Arm Movements

Aimed flexion movements of the arm of different amplitude and duration were studied. Velocity and acceleration traces of movements with equal duration but different amplitude were equal, apart from a scaling factor (ratio between movement amplitudes). After appropriate scaling, EMG activity of the first agonist burst for these movements superimposed. This was not true for EMG activity in the antagonist muscle.

For movements with equal amplitude, but different duration, the time to peak acceleration was constant for all MT’s. Except for this fact, traces of acceleration, velocity, and agonist activity following the time of peak acceleration were about equal after appropriate scaling in time and amplitude. The integral of EMG activity in the first agonist burst increased linearly with peak velocity. For the antagonist burst, the integrated EMG activity increased more than proportionally.

During movements made as fast as possible, subjects used a different strategy by varying the duration of the accelerating phase for movements of different amplitude. Movement amplitude was achieved by adjusting the duration of the agonist burst and the onset time for the antagonist muscle. Amplitude of the antagonist burst was constant within a narrow range for movements of different amplitude.

These results did not change when the inertial mass was doubled by loading the arm with an additional mass.     

Temporal modulations of agonist and antagonist muscle activities accompanying improved performance of ballistic movements

Although many studies have examined performance improvements of ballistic movement through practice, it is still unclear how performance advances while maintaining maximum velocity, and how the accompanying triphasic electromyographic (EMG) activity is modified. The present study focused on the changes in triphasic EMG activity, i.e., the first agonist burst (AG1), the second agonist burst (AG2), and the antagonist burst (ANT), that accompanied decreases in movement time and error. Twelve healthy volunteers performed 100 ballistic wrist flexion movements in ten 10-trial sessions under the instruction to "maintain maximum velocity throughout the experiment and to stop the limb at the target as fast and accurately as possible". Kinematic parameters (position and velocity) and triphasic EMG activities from the agonist (flexor carpi radialis) and antagonist (extensor carpi radialis) muscles were recorded. Comparison of the results obtained from the first and the last 10 trials, revealed that movement time, movement error, and variability of amplitudes reduced with practice, and that maximum velocity and time to maximum velocity remained constant. EMG activities showed that AG1 and AG2 durations were reduced, whereas ANT duration did not change. Additionally, ANT and AG2 latencies were reduced. Integrated EMG of AG1 was significantly reduced as well. Analysis of the alpha angle (an index of the rate of recruitment of the motoneurons) showed that there was no change in either AG1 or AG2. Correlation analysis of alpha angles between these two bursts further revealed that the close relationship of AG1 and AG2 was kept constant through practice. These findings led to the conclusion that performance improvement in ballistic movement is mainly due to the temporal modulations of agonist and antagonist muscle activities when maximum velocity is kept constant. Presumably, a specific strategy is consistently applied during practice.     

Movement related EMGs become more variable during learning of fast accurate movements

Human subjects performed simple flexion and extension movements about the elbow in a visual step-tracking paradigm. Movements were self-terminated. Subjects were instructed to increase movement velocity while maintaining end-point accuracy during practice. The effects of practice on the pattern and variability of EMG activity of the biceps and triceps muscles were studied. Initial movements were performed using reciprocal phasic activation of agonist and antagonist muscles as indicated by surface EMGs. With practice, increases in movement speed were associated with larger agonist and antagonist bursts and an earlier onset of the antagonist burst. Decreased duration of the premovement antagonist silence was also observed during practice. Decreases in variability of movements during practice were not accompanied by equivalent decreases in variability of the associated EMGs. Surprisingly, both agonist and antagonist EMGs were more variable in faster, practiced movements. The combined agonist-antagonist EMG variability depended on both movement speed and trajectory variability. Lower variability in movements in the presence of greater variability in the related EMGs occurred because of linked variations in agonist and antagonist muscle activities. Variations in the first agonist burst were often compensated for by associated variations in the antagonist and late agonist bursts. These linked variations maintained the limb trajectory relatively constant in spite of large variations in the first agonist burst. Modifications to impulse-variability models are therefore needed to explain compensations for variability in accelerative impulses (produced by the first agonist burst) by linked variations in impulses for deceleration (produced by the antagonist and late agonist bursts).     

Movement Related EMGs Become More Variable During Learning of Fast Accurate Movements

Human subjects performed simple flexion and extension movements about the elbow in a visual step-tracking paradigm. Movements were self-terminated. Subjects were instructed to increase movement velocity while maintaining end-point accuracy during practice. The effects of practice on the pattern and variability of EMG activity of the biceps and triceps muscles were studied. Initial movements were performed using reciprocal phasic activation of agonist and antagonist muscles as indicated by surface EMGs. With practice, increases in movement speed were associated with larger agonist and antagonist bursts and an earlier onset of the antagonist burst. Decreased duration of the premovement antagonist silence was also observed during practice.

Decreases in variability of movements during practice were not accompanied by equivalent decreases in variability of the associated EMGs. Surprisingly, both agonist and antagonist EMGs were more variable in faster, practiced movements. The combined agonist-antagonist EMG variability depended on both movement speed and trajectory variability. Lower variability in movements in the presence of greater variability in the related EMGs occurred because of linked variations in agonist and antagonist muscle activities. Variations in the first agonist burst were often compensated for by associated variations in the antagonist and late agonist bursts. These linked variations maintained the limb trajectory relatively constant in spite of large variations in the first agonist burst. Modifications to impulse-variability models are therefore needed to explain compensations for variability in accelerative impulses (produced by the first agonist burst) by linked variations in impulses for deceleration (produced by the antagonist and late agonist bursts).     

Distance and Movement Time Effects on the Timing of Agonist and Antagonist Muscles

The experiment examined the effects of movement time (MT) and distance on the timing of electromyographic (EMG) activity from an agonist and antagonist muscle during rapid, discrete elbow movements in the horizontal plane. According to impulse-timing theory (Wallace, 1981) MT, not distance moved, should have a pronounced effect on the timing of EMG activity (duration of initial agonist and antagonist burst and time to onset of initial antagonist burst). The levels of MT were 100 and 160 msec and the levels of distance were 27° and 45° of elbow flexion. In general support of impulse-timing theory, the results of the three EMG timing measures showed that MT had a more pronounced effect on these measures than distance. In addition, the timing of EMG activity in relation to total MT remained fairly consistent across the four MT-distance conditions.     

Distance and movement time effects on the timing of agonist and antagonist muscles: a test of the impulse-timing theory

The experiment examined the effects of movement time (MT) and distance on the timing at electromyographic (EMG) activity from an agonist and antagonist muscle during rapid, discrete elbow movements in the horizontal plane. According to impulse-timing theory (Wallace, 1981) MT, not distance moved, should have a pronounced effect on the timing of EMG activity (duration of initial agonist and antagonist burst and time to onset of initial antagonist burst). The levels of MT were 100 and 160 msec and the levels of distance were 27 degrees and 45 degrees of elbow flexion. In general support of impulse-timing theory, the results of the three EMG timing measures showed that MT had a more pronounced effect on these measures than distance. In addition, the timing of EMG activity in relation to total MT remained fairly consistent across the four MT-distance conditions.     

Response timing variability: coherence of kinematic and EMG parameters

A detailed kinematic and electromyographic (EMG) analysis of single degree of freedom timing responses is reported to (a) determine the coherence of kinematic and EMG variability to the reduced timing error variability exhibited with amplitude increments within a given criterion movement time and (b) understand the temporal organization of various movement parameters in simple responses. The data reveal that the variability of kinematic (time to peak acceleration, duration of acceleration phase, time to peak deceleration) and EMG (duration of agonist burst, duration of antagonist burst, time to antagonist burst) timing parameters decreased with increments of average velocity in a manner consistent with the variable timing error. In addition, the coefficient of variation for peak acceleration, peak deceleration, and integrated EMG of the agonist burst followed the same trend. Increasing average movement velocity also led to decreases in premotor and motor reaction times. Overall, the findings suggest a strong coherence between the variability of response outcome, kinematic, and EMG parameters.     

Response Timing Variability

A detailed kinematic and electromyographic (EMG) analysis of single degree of freedom timing responses is reported to (a) determine the coherence of kinematic and EMG variability to the reduced timing error variability exhibited with amplitude increments within a given criterion movement time and (b) understand the temporal organization of various movement parameters in simple responses. The data reveal that the variability of kinematic (time to peak acceleration, duration of acceleration phase, time to peak deceleration) and EMG (duration of agonist burst, duration of antagonist burst, time to antagonist burst) timing parameters decreased with increments of average velocity in a manner consistent with the variable timing error. In addition, the coefficient of variation for peak acceleration, peak deceleration, and integrated EMG of the agonist burst followed the same trend. Increasing average movement velocity also led to decreases in premotor and motor reaction times. Overall, the findings suggest a strong coherence between the variability of response outcome, kinematic, and EMG parameters.     

A Computational Model of the Simplest Motor Program

A computational procedure (program) is defined to generate control signals for the motoneuron pools of agonist and antagonist muscles that will move a limb segment from one stationary position to another. The program accounts for the ability to move different distances with different inertial loads and for the influence of instructions concerning movement speed and accuracy. These motor commands allow the program to produce EMG patterns as well as force and kinematic trajectories that are consistent with much of the data found in the literature of these movements. The program is premised on the notion that kinematically defined tasks are accomplished by programming commands to the motoneuron pools, based on only a few cognitively recognized kinematic and dynamic features of the task. Most of the features found in EMG and kinematic patterns can be considered consequences of the program's algorithmic procedures rather than specifically planned features of those movements.     

Facilitation of corticospinal excitability during motor imagery of wrist movement with visual or quantitative inspection of EMG activity

The present study investigated facilitation of corticospinal excitability during motor imagery of wrist movement with visual or quantitative inspection of background electromyographic (EMG) activity. Ten healthy participants imagined wrist extension from a first-person perspective in response to a start cue. Transcranial magnetic stimulation was delivered to the motor cortex 2 sec. after the start cue. EMG signals were recorded from the extensor carpi radialis muscle. Trials with background EMG activity were discarded based on visual inspection. Both motor-evoked potential (MEP) and background EMG amplitudes increased during motor imagery. The amount of increase in MEP amplitude was positively correlated with the amount of increase in background EMG amplitude during motor imagery. The statistically significant increase in MEP amplitude during motor imagery disappeared when the effect of muscle activity was statistically eliminated or after trials with background EMG activity were discarded based on strict quantitative criteria. Facilitation of corticospinal excitability during motor imagery of wrist movement depends partially on muscle activity. Discarding background EMG activity during motor imagery based on visual inspection is not sufficient to equalize background EMG amplitude between resting and motor imagery. Discarding trials with background EMG activity through strict quantitative criteria is useful to equalize background EMG amplitude between at rest and during motor imagery.     

Effects of initial limb position on the accuracy, reaction time and electromyographic patterns of rapid movements

An experiment was performed to determine the effects of initial limb condition on final accuracy of rapid, elbow flexion movements in the horizontal plane. Electromyographic (EMG) recordings were also taken from an agonist (biceps) and antagonist (triceps) muscle by means of bipolar surface electrodes. In the experiment the subject's forearm was passively oscillated by means of an electric motor, and when an auditory buzzer sounded, the subject was required to react as quickly as possible and rapidly move to the previously learned target angle. Thus, movements could be initiated from either static or moving starting positions. The results indicated that general accuracy was not greatly affected by these manipulations, however, constant error and pre-motor reaction time suggested that subjects may have been utilizing initial limb condition information contrary to a mass-spring view. EMG data showed that the timing characteristics of the agonist and antagonist muscles were modulated, depending on the type of movement produced, supporting an impulse-timing model (Wallace 1981).     

Time-dependence between upper arm muscles activity during rapid movements: Observation of the proportional effects predicted by the kinematic theory

Rapid human movements can be assimilated to the output of a neuromuscular system with an impulse response modeled by a Delta-Lognormal equation. In such a model, the main assumption concerns the cumulative time delays of the response as it propagates toward the effector following a command. To verify the validity of this assumption, delays between bursts in electromyographic (EMG) signals of agonist and antagonist muscles activated during a rapid hand movement were investigated. Delays were measured between the surface EMG signals of six muscles of the upper limb during single rapid handwriting strokes. From EMG envelopes, regressions were obtained between the timing of the burst of activity produced by each monitored muscle. High correlation coefficients were obtained supporting the proportionality of the cumulative time delays, the basic hypothesis of the Delta-Lognormal model. A paradigm governing the sequence of muscle activities in a rapid movement could, in the long run, be useful for applications dealing with the analysis and synthesis of human movements.     

Amplitude and target diameter in motor programming of discrete, rapid aimed movements: Fitts and Peterson (1964) and Klapp (1975) revisited

The reports by Fitts and Peterson [J. Exp. Psychol. 67(2) (1964) 103-113] and Klapp [J. Exp. Psychol. Hum. Percept. Perform. 104(2) (1975) 147-153] concerning the effects of movement amplitude and target diameter on reaction time present conflicting results. Fitts and Peterson reported that reaction time increased when movement amplitude was lengthened. Klapp reported an interaction in which target diameter effect on reaction time was moderated by movement length: for small targets, reaction time decreased with increasing movement length but reaction time remained unchanged (or increased modestly) when target diameter was large. Two experiments were conducted to replicate and examine the inconsistency in the reaction time results. For both experiments movement time results were in agreement with the predictions of Fitts' law. However, the results for reaction time were mixed: support was obtained for Klapp (1975) but not for Fitts and Peterson (1964). Further analysis identified several potential variables that could have influenced reaction time and explained the different effects on reaction time reported by Fitts and Peterson (1964) and Klapp (1975). The potential variables could include: limb posture at the start of a response; number of limb segments required to perform the task; and the effect of pooling reaction time data from targets located right and left of the start point, and from near and far targets.     

Rapid Error Correction During Human Arm Movements

Studies were made of rapid error correction movements in eight subjects performing a visually guided tracking task involving flexion-extension movements about the elbow. Subjects were required to minimize reaction times in this two-choice task. Errors in initial movement direction occurred in about 3% of the trials. Error correction times (time from initiation to reversal of movement in incorrect direction) ranged from 30-150 ms. The first sign of correction of the error movement was a suppression of the electromyographic (EMG) activity in the muscle producing the error movement. This suppression started as early as 20-40 ms after the initiation of the error-related EMG activity and as much as 50 ms before any overt sign of limb movement. The correction of the error movement was also accompanied by an increase in the drive to the muscle which moved the arm in the correct direction. This increased activity always occurred after the initiation of the error movement. It is concluded that the first step in the error correction, suppression of drive to the muscle producing the error movement, cannot be based on information from the moving limb. It is thus suggested that this earliest response to the error movement is based on central monitoring of the commands for movement.     

Rapid error correction during human arm movements: evidence for central monitoring

Studies were made of rapid error correction movements in eight subjects performing a visually guided tracking task involving flexion-extension movements about the elbow. Subjects were required to minimize reaction times in this two-choice task. Errors in initial movement direction occurred in about 3% of the trials. Error correction times (time from initiation to reversal of movement in incorrect direction) ranged from 30-150 ms. The first sing of correction of the error movement was a suppression of the electromyographic (EMG) activity in the muscle producing the error movement. This suppression started as early as 20-40 ms after the initiation of the error-related EMG activity and as much as 50 ms before any overt sign of limb movement. The correction of the error movement was also accompanied by an increase in the drive to the muscle which moved the arm in the correct direction. This increased activity always occurred after the initiation of the error movement. it is concluded that the first step in the error correction, suppression of drive to the muscle producing the error movement, cannot be based on information from the moving limb. It is thus suggested that this earliest response to the error movement is based on central monitoring of the commands for movement.     

Kinematic and electromyographic changes that occur as a function of learning a time-constrained aiming task

The present study attempted to examine the changes associated with learning two time-constrained aiming movements at the neuromuscular and behavioral levels of analysis. Electromyographic data and movement kinematics were used to assess changes due to practice. Eight right-handed females were required to perform a 45 degrees horizontal forearm extension in either 200 ms or 500 ms for 100 trials on each of four consecutive days. Both groups demonstrated an improvement in performance and a decrease in within-subject variability in the endpoint response measures, movement trajectory, and myoelectric pattern. With practice, there was a decrease in the amount of cocontraction between the agonist and antagonist muscles during movement execution, which indicated an elimination of unwanted neural activity. For the 200 ms task, the acceleration profile became symmetrical and triphasic myoelectric pattern became evident. The deceleratory phase of the 500 ms task was longer than the acceleratory phase, and a biphasic pattern became apparent. The results suggest that two different control strategies were developed in the execution of the two movements examined. In addition, the relative invariance of the spatial-temporal dependent measures, as compared to the variability of the EMG, led us tot he conclusion that the movement planning hierarchy was concerned with the spatial-temporal domain, whereas the amplitude and timing of muscular activity were planned at a lower level and thus played a subordinate role in movement production.     

Kinematic and Electromyographic Changes That Occur as a Function of Learning a Time-constrained Aiming Task

The present study attempted to examine the changes associated with learning two time-constrained aiming movements at the neuromuscular and behavioral levels of analysis. Electromyographic data and movement kinematics were used to assess changes due to practice. Eight right-handed females were required to perform a 45° horizontal forearm extension in either 200 ms or 500 ms for 100 trials on each of four consecutive days. Both groups demonstrated an improvement in performance and a decrease in within-subject variability in the endpoint response measures, movement trajectory, and myoelectric pattern. With practice, there was a decrease in the amount of cocontraction between the agonist and antagonist muscles during movement execution, which indicated an elimination of unwanted neural activity. For the 200 ms task, the acceleration profile became symmetrical and a triphasic myoelectric pattern became evident. The deceleratory phase of the 500 ms task was longer than the acceleratory phase, and a biphasic pattern became apparent. The results suggest that two different control strategies were developed in the execution of the two movements examined. In addition, the relative invariance of the spatial-temporal dependent measures, as compared to the variability of the EMG, led us to the conclusion that the movement planning hierarchy was concerned with the spatial-temporal domain, whereas the amplitude and timing of muscular activity were planned at a lower level and thus played a subordinate role in movement production.     

The attentional cost of amplitude and directional requirements when pointing to targets

The aim of this study was to investigate the comparative cost of accuracy constraints in direction or amplitude for movement regulation. The attentional cost is operationally defined as the amount of disturbance created in a secondary task by the simultaneous execution of a pointing task in direction or amplitude. The cost is expressed in terms of modifications in response to a secondary task, consisting of a foot-pedal release in response to an auditory stimulus (probe). The probe was introduced during the programming portion or the first, middle, or last portion of the pointing movement. The independent variables were the requirements of the task: direction or amplitude, and the moments of occurrence of the probe. Subjects were submitted to eight experimental conditions: (1) simple foot reaction time to a buzzer; (2) single directional task; (3) single amplitude task; (4) dual directional task (i.e. directional task with probe); (5) dual amplitude task (i.e. amplitude task with probe); (6) retest of foot simple reaction time; (7) retest of single directional task; and (8) retest of single amplitude task. Regulation in direction was more attention-demanding than regulation in distance in terms of programming. During pointing in amplitude, probe RT increased monotonically from start to end of movement execution, whereas directional pointing did not lead to any significant probe RT changes. These results emphasize the specific attentional loads for directional and amplitude pointing tasks, hence the involvement of different central nervous system mechanisms for the programming and regulation of the directional and amplitude parameters of pointing movements.     

An Impulse-Timing Theory for Reciprocal Control of Muscular Activity in Rapid,Discrete Movements

Much remains to be learned about how agonist and antagonist muscles are controlled during the production of rapid, voluntary movements. In an effort to summarize a wide body of existing knowledge and stimulate future research on this subject, an impulse-timing theory is presented which attempts to predict the activity of reciprocal muscles based on certain characteristics of a movement. The basic tenet of the theory is that variables of movement time, movement distance, and inertial load have fairly predictable effects on the underlying muscular activity of the agonist and antagonist muscles during the production of rapid and discrete, voluntary movements. The theory is derived from the kinematic work of Schmidt, Zelaznik, Hawkins, Frank, and Quinn (1979) and supporting evidence from studies which have used electromyographic (EMG) recordings of agonist and antagonist muscles during rapid movements. Issues related to synergistic muscle control, central and peripheral control of reciprocal muscle activity, muscle control, and neurological disorder and the relationship between impulse-timing and mass-spring control are discussed in the final section.