Adjustments of fast goal-directed movements in response to an unexpected inertial load

Summary Subjects made fast goal-directed elbow flexion movements against an inertial load. Target distance was 8 or 16 cm, randomly chosen. To exert a force in the direction of the movement subjects had to activate flexors of both shoulder and elbow, but shoulder flexors did not change appreciably in length during the movement. In 20% of the trials the inertial load was increased or decreased without knowledge of the subjects. Until 90–110 ms after the onset of the agonist muscle activity (about 65–85 ms after the start of movement) EMG activity was very similar in all conditions tested. The changes that occured in the EMG from that moment on were effectively a later cessation of the agonist activity and a later start of the antagonist activity if the load was increased unexpectedly. If the load was reduced unexpectedly, the agonist activity ceased earlier and the antagonist activity began earlier. The latency at which EMGs started to change was the same for muscles around shoulder and elbow, for agonists and antagonists and for both distances. All adjustments had the same latency (37 ms) relative to the point where the angular velocity of the elbow in the unexpectedly loaded movements differed by 0.6 rad/s from the expected value. We discuss why simple reflex- or servo-mechanisms cannot account for the measured EMG changes. We conclude that appropriate adjustments of motor programmes for fast goal-directed arm movements start within 40 ms of the detection of misjudgment of load.     

Vibration-induced changes in movement-related EMG activity in humans

The effect of muscle tendon vibration during voluntary arm movement was studied in normal humans. Subjects made alternating step flexion and extension movements about the elbow. A small vibrator was mounted over either the biceps or the triceps muscle and vibration was applied during flexion or extension movements. The vibrator was turned off between movements. After a period of practice, subjects learned the required movements and were able to make them with their eyes closed. Application of vibration to the muscle antagonist to the movement being performed produced an undershoot of the required end-movement position. The undershoot was 20-30% of the total movement amplitude. In contrast, vibration of the muscle agonist to the movement resulted in no change in movement end position. The vibration-induced undershoot was associated with an increase in the EMG activity of the vibrated (antagonist) muscle and a resultant increase in the ratio of the antagonist to agonist EMG activity. The increase in antagonist EMG produced by the vibration occurred with a latency of approximately 60 ms from vibration onset. The observed results are consistent with vibration-induced activation of muscle spindle receptors in the lengthening muscle during movement. It is suggested that, during movement, the sensitivity of the spindle receptors in the shortening muscle is decreased and the information concerning limb position during movement comes primarily from the lengthening muscle.     

A comparison of the effects of agonist and antagonist muscle fatigue on performance of rapid movements

The aim of this study was to investigate the effects of agonist and antagonist muscle fatigue on the performance of rapid, self-terminating movements. Six subjects performed rapid, consecutive elbow flexion and extension movements between two targets prior to and after fatiguing either the elbow flexor or elbow extensor muscles. The experiments demonstrated consistent results. Agonist muscle fatigue was associated with a decrease in peak velocity and peak deceleration, while a decrease in peak acceleration was particularly prominent. Antagonist muscle fatigue, however, was associated with a decrease in peak deceleration, while a decrease in both the peak velocity and peak acceleration was modest and, in some tests, non-significant. The relative acceleration time (i.e. acceleration time as a proportion of the total movement time) increased when agonists were fatigued, but decreased when antagonists were fatigued. Taken together, these results emphasize the mechanical roles of the agonist and antagonist muscles; namely, the fatigue of each muscle group particularly affected the movement phase in which that group accelerated a limb, while changes of the movement kinematics pattern provided more time for action of the fatigued muscles. In addition, the results presented suggest that agonist muscle fatigue affects movement velocity more than antagonist muscle fatigue, even in movements that demonstrate prominently both mechanical and myoelectric activity of the antagonist muscles, such as rapid, self-terminating movements.     

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.     

Rapid goal-directed elbow flexion movements: limitations of the speed control system due to neural constraints

Summary In rapid goal-directed elbow flexion movements the influence of both movement amplitude and inertial load on the three-burst pattern and the consequences on movement time were studied. Subjects performed visually guided, self-paced movements as rapidly and as accurately as possible. An increase of both the movement amplitude and the inertial load were found to be interacting factors for the modulation of the three-burst-pattern and movement time. The first biceps burst progressively increased in duration and amplitude for larger movements, resulting in prolonged movement times. Surplus inertial loads further prolonged the agonist burst for large, but not for small movement amplitudes. The activity of the antagonist burst, in contrast, was largest in small movements and successively decreased at increasing movement amplitudes. Its duration, however, remained fairly constant. As was similarly observed for the agonist burst, surplus inertial loads lead to a prolongation of antagonist burst duration and an increase of the activity integral for large, but not for small movement amplitudes. It is suggested that in elbow flexion movements the programming of fastest goal-directed movements must take into account neural constraints and biomechanical characteristics of the agonist muscle and the antagonist muscle. Due to neural constraints of the biceps muscle, in contrast to finger movements, the concept of movement time invariance does not hold for elbow movements. Furthermore, neural constraints of the antagonist muscle lead to a limited force production of the agonist muscle at small movement amplitudes in order to avoid an overload of the braking process. The complexity of the relationship between neural and mechanical factors indicate that the size and timing of the three-burst-pattern has to be subtly adjusted to the precise nature of the task and its biomechanical characteristics.Supported by the Deutsche Forschungsgemeinschaft (SFB 33)     

Effective utilization of gravity during arm downswing in keystrokes by expert pianists

The present study investigated a skill-level-dependent interaction between gravity and muscular force when striking piano keys. Kinetic analysis of the arm during the downswing motion performed by expert and novice piano players was made using an inverse dynamic technique. The corresponding activities of the elbow agonist and antagonist muscles were simultaneously recorded using electromyography (EMG). Muscular torque at the elbow joint was computed while excluding the effects of gravitational and motion-dependent interaction torques. During descending the forearm to strike the keys, the experts kept the activation of the triceps (movement agonist) muscle close to the resting level, and decreased anti-gravity activity of the biceps muscle across all loudness levels. This suggested that elbow extension torque was produced by gravity without the contribution of agonist muscular work. For the novices, on the other hand, a distinct activity in the triceps muscle appeared during the middle of the downswing, and its amount and duration were increased with increasing loudness. Therefore, for the novices, agonist muscular force was the predominant contributor to the acceleration of elbow extension during the downswing. We concluded that a balance shift from muscular force dependency to gravity dependency for the generation of a target joint torque occurs with long-term piano training. This shift would support the notion of non-muscular force utilization for improving physiological efficiency of limb movement with respect to the effective use of gravity.     

Reprogramming of muscle activation patterns at the wrist in compensation for elbow reaction torques during planar two-joint arm movements

The relationship between wrist kinematics, dynamics and the pattern of muscle activation were examined during a two-joint planar movement in which the two joints moved in opposite directions, i.e. elbow flexion/wrist extension and elbow extension/wrist flexion. Elbow movements (ranging from 10 to 70 deg) and wrist movements (ranging from 10 to 50 deg) were performed during a visual, step-tracking task in which subjects were required to attend to the initial and final angles at each joint. As the elbow amplitude increased, wrist movement duration increased and the wrist movement trajectories became quite variable. Analysis of the torques acting at the wrist joint showed that elbow movements produced reaction torques acting in the same direction as the intended wrist movement. Distinct patterns of muscle activation were observed at the wrist joint that were dependent on the relative magnitude of the elbow reaction torque in relation to the net wrist torque. When the magnitude of the elbow reaction torque was quite small, the wrist agonist was activated first. As the magnitude of the elbow reaction torque increased, activity in the wrist agonist decreased significantly. In conditions where the elbow reaction torque was much larger than the net wrist torque, the wrist muscle torque reversed direction to oppose the intended movement. This reversal of wrist muscle torque was directly associated with a change in the pattern of muscle activation where the wrist antagonist was activated prior to the wrist agonist. Our findings indicate that motion of the elbow joint is an important consideration in planning wrist movement. Specifically, the selection of muscle activation patterns at the wrist is dependent on the relative magnitude and direction of the elbow reaction torque in relation to the direction of wrist motion.     

Cerebellar nuclear activity in relation to simple movements

Summary Single unit activity in the fastigial, interpositus and dentate cerebellar nuclei was recorded in relation to simple elbow flexion and extension movements in two macaque monkeys. In common with proximal muscle activity, 94% of the task-related neurons had qualitatively similar discharge patterns for both directions of forearm movement. In many cases the flexion and extension discharge was virtually identical, but some cells had a distinct directional bias. The very few neurons which were directionally specific were located in the dentate and interpositus. Two had tonic activity well correlated to elbow angle. Task-related changes in discharge rate occurred earliest in dentate and latest in fastigial, but almost always during the period of concomitant proximal and elbow EMG changes. Correlations of phasic activity with movement velocity were uniformly weak. Many eye movement-related neurons were encountered in the fastigial, dentate and y-group nuclei. Fastigial eye cells, both bursting and tonic, tended to be highly direction specific, whereas dentate eye cells were usually omnidirectional and variable. For both arm and eye cerebellar cells, the directional preferences of phasic and tonic discharge, in the same neuron, could be opposed to one another.     

Relationship between cocontraction, movement kinematics and phasic muscle activity in single-joint arm movement

Patterns of muscle coactivation provide a window into mechanisms of limb stabilization. In the present paper we have examined muscle coactivation in single-joint elbow and single-joint shoulder movements and explored its relationship to movement velocity and amplitude, as well as phasic muscle activation patterns. Movements were produced at several speeds and different amplitudes, and muscle activity and movement kinematics were recorded. Tonic levels of electromyographic (EMG) activity following movement provided a measure of muscle cocontraction. It was found that coactivation following movement increased with maximum joint velocity at each of two amplitudes. Phasic EMG activity in agonist and antagonist muscles showed a similar correlation that was observable even during the first 30 ms of muscle activation. All subjects but one showed statistically significant correlations on a trial-by-trial basis between tonic and phasic activity levels, including the phasic activity measure taken at the initiation of movement. Our findings provide direct evidence that muscle coactivation varies with movement velocity. The data also suggest that cocontraction is linked in a simple manner to phasic muscle activity. The similarity in the patterns of tonic and phasic activation suggests that the nervous system may use a simple strategy to adjust coactivation and presumably limb impedance in association with changes in movement speed. Moreover, since the pattern of tonic activity varies with the first 30 ms of phasic activity, the control of cocontraction may be established prior to movement onset. Electronic Publication     

Target-dependent differences between free and constrained arm movements in chronic hemiparesis

This study compares the kinematic and kinetic characteristics of constrained and free upper limb movements in eight subjects with chronic hemiparesis. Movements of the dominant and nondominant limbs were also examined in five control subjects. Rapid movements were performed in the horizontal plane from a central starting point to five targets located to require various combinations of flexion/extension rotations at the elbow and shoulder. Support of the upper limb against gravity loading was provided either by a low-friction air-bearing apparatus (constrained condition) or by voluntary generation of abduction and external rotation torques at the shoulder (free condition). Data analysis focused on the peak joint torques generated during the acceleratory phase of movement, and on the net change in joint angles at the elbow and shoulder. We found that movement parameters were broadly invariant with support condition for either limb of control subjects, as well as for the nonparetic limb of hemiparetic subjects. In contrast, support condition had a target-dependent effect on movements of the paretic limb. Relative to the constrained condition, peak torques for free arm movements were significantly reduced for distal targets requiring elbow extension and/or shoulder flexion torques. However, peak elbow flexion and shoulder extension joint torques for proximal targets were relatively unaffected by support condition. Of perhaps more functional importance, free movements were characterized by a target-dependent restriction in the hands work area that reflected a reduced range of active elbow extension, relative to constrained movements. The target-dependent effects of support condition on movements of the paretic limb are consistent with the existence of abnormal constraints on muscle activation patterns in subjects with chronic hemiparesis, namely an abnormal linkage between activation of the elbow flexors and shoulder extensors, abductors, and external rotators.     

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.     

The neural control of single degree-of-freedom elbow movements

It is known that muscle activation patterns are changed when the force requirements of a task are increased (e.g., moving a heavier inertial load) or when the available muscle force is reduced (e.g., by inducing muscle fatigue). It is not known whether this is true when the torque-producing capability of a muscle is altered. Eight neurologically healthy subjects performed flexion and extension maximum voluntary isometric contractions (MVC) at five different joint positions (10°, 40°, 70°, 100°, and 130°, where 0° is full elbow extension). Flexion MVC increased by 138% and extension MVC increased by 74% as the elbow joint position changed from the most extended to the most flexed position tested. The same subjects then made rapid, 30° elbow flexion movements from each of four starting elbow positions (10°, 40°, 70°, and 100°). Muscle activation patterns for movements made from the more extended positions showed an increased first agonist burst duration and increased latency of the antagonist burst. There was no change in the initial rate of rise of the agonist burst across starting joint positions. Movements made from the most extended starting position were significantly slower and had longer acceleration and deceleration times than did movements made from the more flexed starting positions. The changes in muscle activation patterns were consistent with those seen when the force requirements of a task are increased or the available muscle force is reduced. We hypothesize that a fall in the ratio of available to required muscle forces causes the nervous system to change muscle activation patterns, to increase the ratio. Our results are consistent with this hypothesis.     

Changes in movement final position associated with agonist and antagonist muscle fatigue

We have tested the hypothesis that agonist and antagonist muscle fatigue could affect the final position of rapid, discrete movements. Six subjects performed consecutive elbow flexion and extension movements between two targets, with their eyes closed prior to, and after fatiguing the elbow extensor muscles. The results demonstrate that elbow extension movements performed in the post-test period systematically undershot the final position as compared to pre-test movements. However, attainment of the aimed final position in elbow flexion movements was unaffected by fatiguing of the extensor muscles. Undershoot of the final position obtained in extension movements was associated with agonist muscle fatigue, a result that was expected from the point of view of current motor control theories, and that could be explained by a reduced ability of the shortening muscle to exert force. On the other hand, the absence of the expected overshoot of the final position when the antagonist is fatigued, indicates the involvement of various reflex and/or central mechanisms operating around the stretched muscle that could contribute to returning the limb to the standard final position after a brief prominent overshoot.     

Effects of inactivation of the anterior interpositus nucleus on the kinematic and dynamic control of multijoint movement

We previously showed that inactivating the anterior interpositus nucleus in cats disrupts prehension; paw paths, normally straight and accurate, become curved, hypometric, and more variable. In the present study, we determined the joint kinematic and dynamic origins of this impairment. Animals were restrained in a hammock and trained to reach and grasp a cube of meat from a narrow food well at varied heights; movements were monitored using the MacReflex analysis system. The anterior interpositus nucleus was inactivated by microinjection of the GABA agonist muscimol (0.25-0.5 microgram in 0.5 microliter saline). For each joint, we computed the torque due to gravity, inertial resistance (termed self torque), interjoint interactions (termed interaction torque), and the combined effects of active muscle contraction and passive soft tissue stretch (termed generalized muscle torque). Inactivation produced significant reductions in the amplitude, velocity, and acceleration of elbow flexion. However, these movements continued to scale normally with target height. Shoulder extension was reduced by inactivation but wrist angular displacement and velocity were not. Inactivation also produced changes in the temporal coordination between elbow, shoulder, and wrist kinematics. Dynamic analysis showed that elbow flexion both before and during inactivation was produced by the combined action of muscle and interaction torque, but that the timing depended on muscle torque. Elbow interaction and muscle torques were scaled to target height both before and during inactivation. Inactivation produced significant reductions in elbow flexor interaction and muscle torques. The duration of elbow flexor muscle torque was prolonged to compensate for the reduction in flexor interaction torque. Shoulder extension was produced by extensor interaction and muscle torques both before and during inactivation. Inactivation produced a reduction in shoulder extension, primarily by reduced interaction torque, but without compensation. Wrist plantarflexion, which occurred during elbow flexion, was driven by plantarflexor interaction and gravitational torques both before and during inactivation. Muscle torque acted in the opposite direction with a phase lead to restrain the plantarflexor interaction torque. During inactivation, there was a reduction in plantarflexor interaction torque and a loss of the phase lead of the muscle torque. Our findings implicate the C1/C3 anterior interpositus zone of the cerebellum in the anticipatory control of intersegmental dynamics during reaching, which zone is required for coordinating the motions of the shoulder and wrist with those of the elbow. In contrast, this cerebellar zone does not play a role in scaling the movement to match a target.     

Fatigue induced changes in phasic muscle activation patterns for fast elbow flexion movements

The present study investigated how muscle fatigue influences single degree-of-freedom elbow flexion movements and their associated patterns of phasic muscle activation. Maximal unfatigued voluntary isometric elbow flexor and extensor joint torque was measured at the beginning of the experiment. Subjects then performed elbow flexion movements over two distances as fast as possible, and movements over the longer distance at an intentionally slower speed. The slower speed was close to what would become the maximal speed in the fatigued state. Subjects then performed a fatiguing protocol of 20 sustained isometric flexion contractions of 25 s duration with 5 s rest at 50% maximal unfatigued voluntary force. After a recovery period they repeated the movements. The fatigue protocol was successful in inducing muscle fatigue, the evidence being decreased isometric maximal joint torque of over 20%. Fatigued movements had lower peak muscle torque and speed. Our principal finding was of changes in the timing of the phasic patterns of fatigued muscle activation. There was an increase in the duration of the agonist burst and a delay in the timing of the antagonist muscle as measured by the centroid of the EMG signals. We conclude that these changes serve as partial but incomplete, centrally driven compensation for fatigue induced changes in muscle function. An additional, unexpected finding was how small an effect fatigue had on movement performance when using a recovery time of 10 min that is long enough to allow muscle membrane conduction velocity to return to normal. This raises questions concerning the behavioral significance of classical laboratory studies of human fatigue mechanisms.     

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.     

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.     

A novel shoulder–elbow mechanism for increasing speed in a multijoint arm movement

The speed of arm movements is normally increased by increasing agonist muscle activity, but in overarm throwing, an additional effect on speed may come from exploitation of interaction torques (a passive torque associated with motion at adjacent joints). We investigated how the central nervous system (CNS) controls interaction torques at the shoulder and elbow to increase speed in 2-D overarm throwing. Twelve experienced throwers made slow, medium, and fast 2-D throws in a parasagittal plane. Joint motions were computed from recordings made with search coils; joint torques were calculated using inverse dynamics. For slow and medium-speed throws, elbow extension was primarily produced by elbow muscle torque. For fast throws, there was an additional late-occurring elbow extensor interaction torque. Parceling out this elbow extension interaction torque revealed that it primarily arose from shoulder extension deceleration. Surprisingly, shoulder deceleration before ball release was not caused by shoulder flexor (antagonist) muscle torque. Rather, shoulder deceleration was produced by passive elbow-to-shoulder interaction torques that were primarily associated with elbow extension acceleration and velocity. It is concluded that when generating fast 2-D throws, the CNS utilized the arm’s biomechanical properties to increase ball speed. It did this by coordinating shoulder and elbow motions such that an instantaneous mechanical positive feedback occurred of interaction torques between shoulder and elbow before ball release. To what extent this mechanism is utilized in other fast multijoint arm movements remains to be determined.     

Role of agonist and antagonist muscle strength in performance of rapid movements

Six subjects performed rapid self-terminated elbow movements under different mechanical conditions prior to, and 5 weeks after an elbow extensor strengthening programme. Despite the large difference in the strengths of elbow flexors and extensors, the pretest did not demonstrate significant differences between the movement time of flexion and extension movements performed under the same mechanical conditions. The results obtained in the posttest demonstrated a decrease in movement time (i.e. an increase in movement speed) in both elbow flexion and extension movements under some mechanical conditions. In addition, flexion movements demonstrated a relative increase in the acceleration time (acceleration time as a proportion of the movement time). It was concluded that the strength of both the agonist and antagonist muscles was important for the performance of rapid movements. Stronger agonists could increase the acceleration of the limb being moved, while stronger antagonists could facilitate the arrest of the limb movement in a shorter time, providing a longer time for acceleration.     

Cerebellar ataxia: torque deficiency or torque mismatch between joints?

Prior work has shown that cerebellar subjects have difficulty adjusting for interaction torques that occur during multi-jointed movements. The purpose of this study was to determine whether this deficit is due to a general inability to generate sufficient levels of phasic torque inability or due to an inability to generate muscle torques that predict and compensate for interaction torques. A second purpose was to determine whether reducing the number of moving joints by external mechanical fixation could improve cerebellar subjects' targeted limb movements. We studied control and cerebellar subjects making elbow flexion movements to touch a target under two conditions: 1) a shoulder free condition, which required only elbow flexion, although the shoulder joint was unconstrained and 2) a shoulder fixed condition, where the shoulder joint was mechanically stabilized so it could not move. We measured joint positions of the arm in the sagittal plane and electromyograms (EMGs) of shoulder and elbow muscles. Elbow and shoulder torques were estimated using inverse dynamics equations. In the shoulder free condition, cerebellar subjects made greater endpoint errors (primarily overshoots) than did controls. Cerebellar subjects' overshoot errors were largely due to unwanted flexion at the shoulder. The excessive shoulder flexion resulted from a torque mismatch, where larger shoulder muscle torques were produced at higher rates than would be appropriate for a given elbow movement. In the shoulder fixed condition, endpoint errors of cerebellar subjects and controls were comparable. The improved accuracy of cerebellar subjects was accompanied by reduced shoulder flexor muscle activity. Most of the correct cerebellar trials in the shoulder fixed condition were movements made using only muscles that flex the elbow. Our findings suggest that cerebellar subjects' poor shoulder control is due to an inability to generate muscle torques that predict and compensate for interaction torques, and not due to a general inability to generate sufficient levels of phasic torque. In addition, reducing the number of muscles to be controlled improved cerebellar ataxia.