Coordination of mono- and bi-articular muscles in multi-degree of freedom elbow movements

We investigated the coordination of mono- and bi-articular muscles during movements involving one or more degrees of freedom at the elbow. Subjects performed elbow flexion (or extension) alone, forearm pronation (or supination) alone, and combinations of the two. In bi-articular muscles such as biceps brachii and pronator teres, the amplitude of agonist electromyographic (EMG) activity was dependent on motion in the two degrees of freedom. Agonist burst amplitudes for combined movements were approximately the sum of the agonist burst amplitudes for movements in the individual degrees of freedom. Activity levels in individual degrees of freedom were, in turn, greater than activity levels observed when a muscle acted as agonist in one degree of freedom and antagonist in the other. Other muscles such as triceps, brachialis, and pronator quadratus acted primarily during motion in a single degree of freedom. The relative magnitude and the timing of activity between sets of muscles also changed with motion in a second degree of freedom. These patterns are comparable with those reported previously in isometric studies.     

Shoulder and elbow muscle activity in goal-directed arm movements

 This research examined the electromyographic (EMG) activity of shoulder and elbow muscles during reaching movements of the upper limb. Subjects performed goal-directed arm movements in the horizontal plane. Movements which varied in amplitude, speed, and direction were performed in different sections of the workspace. EMG activity was recorded from the pectoralis major, posterior deltoid, biceps brachii short head, brachioradialis, triceps brachii long head, and triceps brachii lateral head; motion recordings were obtained with an optoelectric system. The analysis focused on the magnitude and timing of opposing muscle groups at the shoulder and elbow joints. For hand movements within any given direction of the workspace direction, kinematic manipulations changed agonist and antagonist EMG magnitude and intermuscle timing in a manner consistent with previous single-joint findings. To produce reaching movements in different directions and areas of the workspace, shoulder and elbow agonist EMG magnitude increased for those hand motions which required higher angular velocities, while the timing between opposing muscle groups at each joint was invariant. Received: 11 January 1996 / Accepted: 24 February 1997     

Role of agonist and antagonist muscles in fast arm movements in man

Summary Fast goal-directed voluntary movements of the human upper extremity are known to be associated with three distinct bursts of EMG activity in antagonistic muscles. The role of each burst (AG1, ANT, AG2) in controlling motion is not fully understood, largely because overall limb response is a complex function of the entire sequence of bursts recorded during experimental trials. In order to investigate the role of each burst of muscle activity in controlling motion, we studied fast voluntary arm movements and also developed two simulation techniques, one employing a mathematical model of the limb and the other using electrical stimulation of human arm muscles. These techniques show that two important movement parameters (peak displacement, time to reach peak displacement) are non-linear functions of the magnitude of the antagonist input (torque and stimulation voltage, respectively, in our two simulations). In the fastest movements, the agonist muscle is primarily responsible for the distance moved, while the antagonist muscle provides an effective means of reducing movement time. The third component of the triphasic pattern moderates the antagonist braking forces and redirects the movement back to the target.     

EMG patterns in antagonist muscles during isometric contraction in man: Relations to response dynamics

Summary We studied the EMG activity of biceps and triceps in human subjects during isometric force adjustments at the elbow. Rapid targeted force pulses exhibited stereotyped trajectories in which peak force was a linear function of the derivatives of force and the time to peak force was largely independent of its amplitude. These responses were associated with an alternating triphasic pattern of EMG bursts in agonist and antagonist muscles similar to that previously described for rapid limb movements. When the instructions demanded rapid force pulses, initial agonist bursts were of constant duration, and their magnitude was strongly related to peak force achieved. The timing of EMG bursts in antagonist pairs was closely coupled to the dynamics of the force trajectory, and the rising phase of the force was determined by both agonist and antagonist bursts. When peak force was kept constant and rise time systematically varied, the presence and magnitude of antagonist and late agonist bursts were dependent on the rate of rise of force, appearing at a threshold value and then increasing in proportion to this parameter. It is proposed that antagonist activity compensates for nonlinearity in muscle properties to enable the linear scaling of targeted forces which characterizes performance in this task.Supported by the Dystonia Medical Research Foundation and NS 19205     

Timing and magnitude of electromyographic activity for two-joint arm movements in different directions.

1. We studied electromyographic (EMG) and kinematic features of self-paced human arm movements involving rotations about the shoulder and elbow joints. Movements were initiated from various positions and covered much of the reachable work space in the horizontal plane. The attempt was to characterize robust features of the relative timing and magnitude of the EMG activity at the two joints, and to correlate them with variables related to the initial and final positions. 2. The pattern of muscle activity at each joint was typically characterized by bursts of alternating agonist and antagonist activity, comparable with the three-burst pattern associated with single-joint movements. As the spatial direction of the target was altered, the magnitude of each burst was modulated over a continuous range. Modulation down to zero activity was observed, not only for later bursts, as has been shown in some cases of single-joint movements, but for the first agonist burst as well. 3. In the preceding paper we showed that the choice of agonists (i.e., flexors or extensors) at each joint is predictable on the basis of the target direction relative to the distal segment (psi). Here, we present quantitative analyses of initial agonist EMG activity at the shoulder and elbow, which reveal that the onset-time difference between agonists at the two joints also varied systematically with psi, and so did their relative magnitude. 4. For most target directions, initial EMG activity at the shoulder preceded that at the elbow by 5-40 ms. Exceptions were observed mainly for target directions near the transitions between initial flexor and initial extensor activity at the shoulder. In these cases the initial agonist activity at the shoulder was greatly reduced or, in some cases, appeared entirely suppressed, although the later bursts were present in their usual temporal alignment with the corresponding bursts at the elbow. 5. Antagonist onset at the elbow tended to precede antagonist onset at the shoulder, but the difference in timing did not vary consistently with psi. 6. Despite the consistency of initial agonist timing between the two joints, the agonist onset-time difference was poorly correlated with the apparent difference in the onset times of shoulder and elbow joint rotations. The latter difference, which is affected by mechanics, cannot therefore be imputed directly to the CNS.(ABSTRACT TRUNCATED AT 400 WORDS)     

The effect of muscle pain on elbow flexion and coactivation tasks

The effects of muscle pain on movement can easily be observed in daily life routines. However, the influence of muscle pain on motor control strategies has not been fully clarified. In this human experimental study it was hypothesized that muscle pain affects the motor control of elbow flexion movements, in different combinations of range of motion and target size, by decreased agonistic muscle activity and increased antagonistic muscle activity with consequent implications on kinematic parameters. The effects of experimentally induced muscle pain on movement strategy for: (1) small and large range of motion (ROM) elbow flexion movements towards a wide target, (2) large ROM flexion movements towards a narrow and wide target, and (3) subsequent coactivation of agonistic and antagonistic muscles to elbow flexion were assessed. Muscle pain induced by injections of hypertonic saline (1 ml, 5.8%) in either m. biceps brachii or m. triceps brachii caused similar effects on the movements. For low accurate movements the initial (100 ms) integrated electromyographic (EMG) activity of m. biceps brachii was decreased during muscle pain. In contrast, integrated EMG of the entire m. biceps brachii burst was decreased by muscle pain only for small ROM at a low accuracy, which also showed decreased EMG activity of m. triceps brachii and m. brachioradialis, together with increased activity of m. trapezius. Finally, high accurate movements and post-movement coactivation were generally not modulated by muscle pain. In summary, the present study shows that acute muscle pain can perturb the motor control strategy, which might be highly important in occupational settings where such a change may need compensatory actions from other muscles and thereby eventually contribute to the development of musculoskeletal pain problems.     

Elbow torques and EMG patterns of flexor muscles during different isometric tasks.

This paper examines the torque responses and EMG activity levels in four muscles acting at the elbow joint during different combinations of one- and two- degree of freedom isometric torque production (single and dual tasks, respectively). Flexor and supinator/pronator torques and surface EMG signals from m. biceps brachii, m. brachialis, m. brachioradialis and m. triceps brachii were measured in 16 male subjects while they performed maximal effort isometric contractions of pure flexion, pure supination, pure pronation, combined flexion and supination and combined flexion and pronation. In the single tasks, the torque responses were consistent with task requirements, but the dual task results were surprising in that flexor torque levels were reduced as compared to pure flexion, while supinator/pronator torque levels were as high or higher than in pure supination or pronation. Muscle activity levels varied with task, and could not always explain the differences observed in torque responses. These data are discussed within the framework of subpopulations of task-specific motor units within each muscle. The implications of such task-specific muscle units are related to musculoskeletal modelling and previous EMG - torque relationships found at the elbow.     

Transition from slow to ballistic movement: development of triphasic electromyogram patterns

Summary The purpose of this investigation was to determine how the triphasic electromyogram (EMG) pattern of muscle activation developed from the agonist muscle only pattern as movement time (t _mov) decreased. Six adult women produced a series of 30° elbow extension movements in the horizontal plane at speeds ranging from ballistic (< 400-ms t _mov) to very slow (> 800-ms t _mov). Surface EMG from triceps brachii (agonist) and biceps brachii (antagonist) muscles were recorded, together with elbow angle, on a microcomputer. The results showed that triphasic EMG patterns developed systematically as t _mov decreased from 1000 ms to < 200 ms. In trials with very long t _mov, many elbow extension movements were produced by a single continuous activation of the agonist triceps brachii muscle. As t _mov decreased however, agonist activation became predominantly burst-like and other components of the triphasic EMG pattern [activation of the antagonist (Ant) and second agonist activation (Ag₂)] began to appear. At the fastest movement speeds, triphasic EMG patterns (Ag₁-Ant-Ag₂, Ag₁ being first activation of agonist muscle) were always present. This data indicated that the triphasic pattern of muscle activation was not switched on when a particular t _mov was achieved. Rather, each component systematically developed until all were present, as distinctive bursts of activity, in most trials with t _mov less than 400 ms.     

Strategies for muscle activation during isometric torque generation at the human elbow

1. We studied the patterns of electromyographic (EMG) activity in elbow muscles of 14 normal human subjects. The activity of five muscles that act in flexion-extension and forearm supination-pronation was simultaneously recorded during isometric voluntary torque generation, in which torques generated in a plane orthogonal to the long axis of the forearm were voluntarily coupled with torques generated about the long axis of the forearm (i.e., supination-pronation). 2. When forearm supination torques were superimposed on a background of elbow flexion torque, biceps brachii activity increased substantially, as expected; however, brachioradialis and brachialis EMG levels decreased modestly, a less predictable outcome. The pronator teres was also active during pure flexion and flexion coupled with mild supination (even though no pronation torque was required). This was presumably to offset inappropriate torque contributions of other muscles, such as the biceps brachii. 3. When forearm supination torque was superimposed on elbow extension torque, again the biceps brachii was strongly active. The pronator teres also became mildly active during extension with added pronation torque. These changes occurred despite the fact that both the pronator and biceps muscles induce elbow flexion. 4. In these same elbow extension tasks, triceps brachii activity was also modulated with both pronation or supination loads. It was most active during either supination or pronation loads, again despite the fact that it has no mechanical role in producing forearm supination-pronation torque. 5. Recordings of EMG activity during changes in forearm supination-pronation angle demonstrated that activation of the biceps brachii followed classic length-tension predictions, in that less EMG activity was required to achieve a given supination torque when the forearm was pronated (where biceps brachii is relatively longer). On the other hand, EMG activity of the pronator teres did not decrease when the pronator was lengthened. Triceps EMG was also more active when the forearm was supinated, despite its having no direct functional role in this movement. 6. Plots relating EMG activity in biceps brachii, brachialis, and brachioradialis at three different forearm positions revealed that there was a consistent positive near-linear relationship between brachialis and brachioradialis and that biceps brachii is often most active when brachioradialis and brachialis are least active. 7. We argue that, for the human elbow joint at least, fixed muscle synergies are rather uncommon and that relationships between muscle activities are situation dependent.(ABSTRACT TRUNCATED AT 400 WORDS)     

Centrally programmed patterns of muscle activity in voluntary motor behavior of humans

Summary Rapid voluntary limb movements are accompanied by a triphasic electromyogram (EMG): the agonist muscle discharges briefly to generate the initial limb displacement and then, in sequence, an antagonist and second agonist burst occur. The origins of these bursts of EMG have been attributed to both peripheral and central sources. We attempted to determine in human subjects whether somesthetic afferent inputs related to passive muscle stretch or joint rotation were necessary for the appearance of the three bursts. EMGs were recorded while subjects performed rapid isotonic movements before and after forearm afferent function was blocked by ischemia. EMG patterns were also studied during phasic and sustained isometric contractions of forearm muscles.When the forearm was ischemically deafferented the triphasic EMG pattern persisted though the amplitudes of the three bursts were modified. In separate experiments, a similar three burst pattern was also observed while phasic isometric contractions were performed, but not when rapid-onset sustained isometric contractions were executed.These data support the view that somesthetic afferent information related to muscle length or joint rotation is not necessary for the occurrence of the three burst pattern during rapid motor behaviors. Since bursts of EMG activity were observed when torque rose and fell quickly during fast isotonic movements and phasic isometric contractions, the triphasic pattern appears to be a fundamental property of the central program underlying such rapid motor behaviors.     

Basic features of phasic activation for reaching in vertical planes

The purpose of this study was to fully characterize the timing and intensity of the phasic portion of the electromyographic (EMG) waveform for reaching movements in vertical planes. Electromyographic activity was simultaneously recorded from nine superficial elbow and/or shoulder muscles while human subjects made rapid arm movements. Hand paths comprised 20 directions in a sagittal plane and 20 directions in a frontal plane. In order to focus on the more phasic aspects of muscle activation, estimates of postural EMG activity were subtracted from the EMG traces recorded during rapid reaches. These postural estimates were obtained from activity recorded during very slow reaches to the same targets. After subtraction of this postural activity, agonist or antagonist burst patterns were often observed in the phasic EMG traces. For nearly all muscles and all subjects, the relation between phasic EMG intensity and movement direction was a function with multiple peaks. For all muscles, the timing of phasic EMG bursts varied as a function of movement direction: the data from each muscle exhibited a gradual temporal shift of activity over a certain range of directions. This gradual temporal shift has no obvious correspondence to the mechanical requirements of the task and might represent a neuromuscular control strategy in which burst timing contributes to the specification of movement direction.     

Movement and electromyographic disorders associated with cerebellar dysmetria

The objective of these experiments was to determine whether dysmetric elbow flexions, which occurred during cerebellar dysfunction, had the same kinematic and electromyographic characteristics as movements of the same amplitude and velocity performed under normal conditions. Reversible cerebellar lesions were produced by cooling through two probes implanted on either side of the dentate nucleus in five Cebus albifrons monkeys. Normal, fast, and accurate elbow flexions had single-peaked velocities and a bi- or triphasic EMG pattern in agonist and antagonist muscles. During cerebellar dysfunction movements became ataxic. Ataxic movements were classified into two categories: those with oscillations (tremor) during the movement and those without oscillations. A terminal tremor occurred after both types of movements. Oscillations during movements were more likely to occur when a constant force loaded the antagonist. Addition of mass to the handle attenuated or abolished the oscillations. Movements with oscillations reached the target with increased variability of end position, whereas movements without oscillations were often hypermetric. The movement parameters and EMG patterns associated with flexions without oscillations during the movement were studied in detail. A characteristic of these movements was that the acceleration and deceleration phases were asymmetric. Compared with control movements of the same peak velocity, they had smaller magnitudes of acceleration and larger magnitudes of deceleration. The large deceleration was abnormal because it initiated the terminal tremor. The disorder in acceleration was associated with agonist EMG activity that was less abrupt in onset, smaller in magnitude, and more prolonged in duration. The disorder in deceleration was associated with delayed onset of phasic antagonist EMG activity. The results show that hypermetric arm movements without oscillations have different properties than those of normal movements of similar velocity and amplitude. Thus it is unlikely that dysmetria results from inappropriate selection or triggering of an otherwise normal motor program. We conclude that normal function of the cerebellum is necessary for the generation of agonist and antagonist muscle activity that is both of the appropriate magnitude and timing to control the dynamic phase of arm movements.     

Movement-related phasic muscle activation. II. Generation and functional role of the triphasic pattern

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)     

Characteristics of synergic relations during isometric contractions of human elbow muscles

We studied the patterns of EMG activity in elbow muscles in three normal human subjects. The myoelectrical activity of 7-10 muscles that act across the human elbow joint was simultaneously recorded with intramuscular electrodes during isometric joint torques exerted over a range of directions. These directions included flexion, extension, varus (internal humeral rotation), valgus (external humeral rotation), and several intermediate directions. The forces developed at the wrist covered a range of 360 degrees, all orthogonal to the long axis of the forearm. The levels of EMG activity were observed to increase with increasing joint torque in an approximately linear manner. All muscles were active for ranges less than 360 degrees and most were active for less than 180 degrees. The EMG activity was observed to vary in a systematic manner with changes in torque direction and, when examined over the full angular range at a variety of torque levels, is simply scaled with increasing torque magnitude. There were no torque directions or torque magnitudes for which a single muscle was observed to be active alone. In all cases, joint torque appeared to be produced by a combination of muscles. The direction for which the EMG of a muscle reached a maximum value was observed to correspond to the direction of greatest mechanical advantage as predicted by a simple mechanical model of the elbow and relevant muscles. Muscles were relatively inactive during varus torques. This implies that the muscles were not acting to stabilize the joint in this direction and could have been allowing ligaments to carry the load. Plots of EMG activity in one muscle against EMG activity in another demonstrate some instances of pure synergies, but patterns of coactivation for most muscles are more complicated and vary with torque direction. The complexity of these patterns raises the possibility that synergies are determined by the task and may have no independent existence. Activity in two heads of triceps brachii (medial head--a single-joint muscle and long head--a two-joint muscle) covaried closely for a range of torque magnitudes and directions, though shoulder torque and hence the forces experienced by the long head of the triceps undoubtedly varied. The similarity of activation patterns indicates that elbow torque was the principal determining factor. The origins of muscle synergies are discussed. It is suggested that they are best understood on the basis of a model which encodes limb torque in premotor neurons.(ABSTRACT TRUNCATED AT 400 WORDS)     

Neural control: novel evaluation of stretch reflex sensitivity

We evaluated the stretch reflex activities of the elbow flexor and extensor muscles considering the relationship between the reflex electromyographic (EMG) responses and their corresponding standardized muscle stretch velocities. Specifically, muscular stretch velocity was estimated by using ultrasonograms. Stretch reflex EMG responses were elicited in the biceps brachii, brachioradialis and triceps brachii with a ramp-and-hold rotation at the elbow joint, which consisted of various angular velocities for the extension- or flexion-direction. The whole muscle stretch velocity induced by each ramp-and-hold rotation was calculated on the basis of fibre length changes associated with the elbow joint angle. A linear regression equation was fitted to the relation between the whole muscle stretch velocity and the reflex EMG responses, and the variables from the equation were used to quantify sensitivity of each reflex EMG component. The reflex EMG responses were increased as the ramp-and-hold rotational velocity increased. There were no significant differences in the recorded magnitudes of reflex EMG responses with equivalent joint rotational velocity between the brachioradialis and the triceps brachii medial head. These muscles showed the highest reflex responses in the flexor and extensor muscles, respectively. To the contrary, the reflex EMG response elicited by the standardized muscle stretches was significantly greater in the extensor muscles, indicating a higher reflex sensitivity. This was because of the lower muscle stretch velocity of the triceps brachii with an equivalent elbow joint rotation. The stretch reflex sensitivity in both the elbow flexor and extensor muscles might be regulated so as to make the reflex responses the same when the equivalent joint rotational velocity is applied to these muscles.     

Compensation for interaction torques during single- and multijoint limb movement

During multijoint limb movements such as reaching, rotational forces arise at one joint due to the motions of limb segments about other joints. We report the results of three experiments in which we assessed the extent to which control signals to muscles are adjusted to counteract these "interaction torques." Human subjects performed single- and multijoint pointing movements involving shoulder and elbow motion, and movement parameters related to the magnitude and direction of interaction torques were manipulated systematically. We examined electromyographic (EMG) activity of shoulder and elbow muscles and, specifically, the relationship between EMG activity and joint interaction torque. A first set of experiments examined single-joint movements. During both single-joint elbow (experiment 1) and shoulder (experiment 2) movements, phasic EMG activity was observed in muscles spanning the stationary joint (shoulder muscles in experiment 1 and elbow muscles in experiment 2). This muscle activity preceded movement and varied in amplitude with the magnitude of upcoming interaction torque (the load resulting from motion of the nonstationary limb segment). In a third experiment, subjects performed multijoint movements involving simultaneous motion at the shoulder and elbow. Movement amplitude and velocity at one joint were held constant, while the direction of movement about the other joint was varied. When the direction of elbow motion was varied (flexion vs. extension) and shoulder kinematics were held constant, EMG activity in shoulder muscles varied depending on the direction of elbow motion (and hence the sign of the interaction torque arising at the shoulder). Similarly, EMG activity in elbow muscles varied depending on the direction of shoulder motion for movements in which elbow kinematics were held constant. The results from all three experiments support the idea that central control signals to muscles are adjusted, in a predictive manner, to compensate for interaction torques-loads arising at one joint that depend on motion about other joints.     

Electromyographic responses to constant position errors imposed during voluntary elbow joint movement in human

The role of reflexes in the control of stiffness during human elbow joint movement was investigated for a wide range of movement speeds (1.5–6 rad/s). The electromyographic (EMG) responses of the elbow joint muscles to step position errors (step amplitude 0.15 rad; rise time 100 ms) imposed at the onset of targeted flexion movements (1.0 rad amplitude) were recorded. For all speeds of movement, the step position disturbance produced large modulations of the usual triphasic EMG activity, both excitatory and inhibitory, with an onset latency of 25 ms. In the muscles stretched by the perturbation, the early EMG response (25–60 ms latency) magnitude was greater than 50% of the activity during the unperturbed movements (background activity). In all muscles the EMG responses integrated over the entire movement were greater than 25% of the background activity. The responses were relatively greater for slower movements. Perturbations assisting the movement caused a short-latency (25–60 ms) reflex response (in the antagonist muscle) that increased with movement speed and was constant as a percentage of the background EMG activity. In contrast, perturbations resisting the movement caused a reflex response (in the agonist muscle) that was of the same absolute magnitude at all movement speeds, and thus decreased with movement speed as a percentage of the background EMG activity. There was a directional asymmetry in the reflex response, which produced an asymmetry in the mechanical response during slow movements. When the step perturbation occurred in a direction assisting the flexion movement, the antagonist muscle activity increased, but the main component of this response was delayed until the normal time of onset of the antagonist burst. When the step perturbation resisted the movement the agonist muscles responded briskly at short latency (25 ms). A reflex reversal occurred in two of six subjects. A fixed reflex response occurred in the antagonist muscle, regardless of the perturbation direction. For the extension direction perturbations (resisting movement), this response represented a reflex reversal (50 ms onset latency) and it caused the torque resisting the imposed step (stiffness) to drop markedly (below zero for one subject). Reflex responses were larger when the subject was prevented from reaching the target. That is, when the perturbation remained on until after the normal time of reaching the target, the EMG activity increased, with a parallel increase in stiffness. Similarly, when the perturbations prevented the subject from reaching the target during a 1-rad voluntary cyclic movement, the EMG and stiffness increased markedly. Coactivation of the antagonist muscle with the agonist muscle was not prominent (<30% of antagonist activity) during unperturbed movements. The perturbations were resisted with reciprocal activity, and thus reflex action did not increase the coactivation. However, as a result of the low-pass properties of muscle, substantial cocontraction of the agonist and antagonists muscle forces may have occurred during rapid movements, thus leading to increased stiffness. As the relative changes in normal EMG activity produced by the perturbation were often comparable with the changes in mean muscle torque (stiffness) reported in the first paper of this series, we conclude that the action of reflexes produced a significant portion of the resistance to perturbations. This reflexive portion was greater for slower movements, it was greater when the subject neared the target, and it was variable according to the perturbation direction and the particular subject. Given that the perturbations were of similar frequency content to the movement itself (though of smaller amplitude) and that the reflexes contributed substantially to the resistance to these perturbations, we suggest that in normal unperturbed movements the observed EMG is likewise substantially determined by the reflex activity.     

Relationship between EMG patterns and kinematic properties for flexion movements at the human wrist

Summary EMG patterns associated with voluntary wrist flexion movements were studied in normal human subjects. Initially, subjects were trained to produce movements within five specified velocity ranges while the amplitude of the movement and the opposing load remained constant. In a second set of experiments, subjects were required to produce movements at four different amplitudes, moving as rapidly as possible against a constant load. Finally, with movement velocity and amplitude kept constant, the external load was varied so that different forces were required to generate the movements. The slowest movements were associated with a prolonged burst of EMG activity from the agonist muscle with little or no antagonist activity. With increasing movement velocity, there was a gradual evolution to the characteristic triphasic pattern associated with rapid voluntary movements. As velocity of movement increased further, the amplitude and area of the EMG bursts increased while burst duration and interburst intervals decreased. Increases in movement amplitude were accomplished mainly by changing the timing of the EMG bursts; with larger amplitude movements the antagonist burst occurred later. With movements against larger loads there was an increase in the size of the agonist burst and a decrease in the antagonist burst, but no change in the relative timing of the EMG bursts. These systematic changes in EMG patterns associated with different types of movement provide an indirect method of obtaining information concerning the motor programs which generate the movements.     

Control of simple arm movements in elderly humans

Eight elderly subjects (aged 68-95 years) and 6 young adults (aged 21-24 years) performed elbow flexion and extension movements in a visual step-tracking paradigm. Movement amplitudes ranging from 10 degrees-80 degrees were made under two instructions: "move at own speed" and "move fast and accurate." In a second experiment, 5 elderly subjects practiced 30 degrees movements for a total of 180 flexion and 180 extension movements under the instruction to increase movement speed, while maintaining accuracy, during practice. Movement trajectories became more variable as both movement amplitude and speed increased. Trajectory variability was greater in the elderly subjects for both the acceleratory and deceleratory phases of movements. This was due primarily to a greater rate of increase in trajectory variability during the acceleration phase in the elderly. With practice, elderly subjects could substantially reduce trajectory variability with little change in movement speed. The agonist burst initiating movements was qualitatively normal in the elderly subjects. However, there was considerable tonic cocontraction of agonist and antagonist muscles prior to and during movement. Phasic antagonist EMG activity was obviously abnormal in many elderly subjects. There was often no clear antagonist burst associated with deceleration of the movements or, if present, it was timed inappropriately early. With practice, combined agonist-antagonist EMG variability decreased. A clear antagonist burst also developed during practice in most elderly subjects, but its inappropriate timing remained in all but one subject. The results show that movement trajectories are less accurately controlled in the elderly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evidence that a disordered servo-like mechanism contributes to tremor in movements during cerebellar dysfunction

The characteristics of discontinuities and tremor that occurred in elbow flexions during cooling of the lateral cerebellar nuclei were investigated in five Cebus monkeys. Discontinuities in movements appeared as rhythmical oscillations (kinetic tremor) when movements were slow or when movements were made with a constant force that loaded the antagonist. These oscillations had similar properties to cerebellar terminal tremor following movements; e.g., their amplitude and frequency were decreased by addition of mass to the handle and they occurred in the absence of visual feedback. The abnormal initial decrease in velocity that initiated oscillations in flexion movements was associated with abnormally early or large antagonist (triceps) electromyogram (EMG) activity. This abnormal EMG activity did not follow the normal inverse relation between initial velocity and antagonist latency from onset of movement. The initial deflection from the expected trajectory was opposed by a second burst of EMG activity in the agonist (biceps). This second burst was not the continuation of a step of EMG activity because its amplitude was often larger than the amplitude of the first agonist burst. The second agonist burst had the properties of a servo-like response: it occurred when biceps shortening was slowed (but biceps was not stretched), its magnitude was proportional to the magnitude or the deflection in velocity, its latency was 50-80 ms from onset of the abnormal decrease in velocity, and it occurred in the absence of visual feedback. However, this servo-like response was disordered because it did not return the limb accurately to the expected trajectory. The servo-like mechanism was studied further by applying torque pulse perturbations during elbow flexions. When the cerebellar nuclei were cooled, agonist responses to the perturbation were proportional to the size of the velocity deflection, but they were prolonged and onset of antagonist activity was delayed. It is suggested that discontinuities and tremor in movements during cerebellar dysfunction result from the same mechanism: alternation between disordered stretch reflexes and disordered servo-assistance mechanisms, both partly involving transcortical pathways.