Agonist Burst Research Articles

Progressive resistance exercise restores some properties of the triphasic EMG pattern and improves bradykinesia: the PRET-PD randomized clinical trial.

In Parkinson's disease (PD), the characteristic triphasic agonist and antagonist muscle activation pattern during ballistic movement is impaired: the number of agonist muscle bursts is increased, and the amplitudes of the agonist and antagonist bursts are reduced. The breakdown of the triphasic electromyographic (EMG) pattern has been hypothesized to underlie bradykinesia in PD. Progressive resistance exercise has been shown to improve clinical measures of bradykinesia, but it is not clear whether the benefits for bradykinesia are accompanied by changes in agonist and antagonist muscle activity. This study examined the spatiotemporal changes in agonist and antagonist muscle activity following 24 mo of progressive resistance exercise and the combined relationship between spatiotemporal muscle activity and strength measures and upper limb bradykinesia. We compared the effects of progressive resistance exercise training (PRET) with a nonprogressive exercise intervention, modified Fitness Counts (mFC), in patients with PD. We randomized 48 participants with mild-to-moderate PD to mFC or PRET. At the study endpoint of 24 mo, participants randomized to PRET compared with mFC had significantly faster movement velocity, accompanied by significant increases in the duration, magnitude, and magnitude normalized to duration of the 1st agonist burst and fewer number of agonist bursts before peak velocity. The antagonist muscle activity was increased relative to baseline but did not differ between groups. Spatiotemporal EMG muscle activity and muscle strength were significantly associated with upper limb bradykinesia. These findings demonstrate that progressive resistance exercise improves upper limb movement velocity and restores some aspects of the triphasic EMG pattern.

A physiological neural controller of a muscle fiber oculomotor plant in horizontal monkey saccades.

A neural network model of biophysical neurons in the midbrain is presented to drive a muscle fiber oculomotor plant during horizontal monkey saccades. Neural circuitry, including omnipause neuron, premotor excitatory and inhibitory burst neurons, long lead burst neuron, tonic neuron, interneuron, abducens nucleus, and oculomotor nucleus, is developed to examine saccade dynamics. The time-optimal control strategy by realization of agonist and antagonist controller models is investigated. In consequence, each agonist muscle fiber is stimulated by an agonist neuron, while an antagonist muscle fiber is unstimulated by a pause and step from the antagonist neuron. It is concluded that the neural network is constrained by a minimum duration of the agonist pulse and that the most dominant factor in determining the saccade magnitude is the number of active neurons for the small saccades. For the large saccades, however, the duration of agonist burst firing significantly affects the control of saccades. The proposed saccadic circuitry establishes a complete model of saccade generation since it not only includes the neural circuits at both the premotor and motor stages of the saccade generator, but also uses a time-optimal controller to yield the desired saccade magnitude.

Control of Arm Movements for Quick Change of Movement Direction

ABSTRACT The authors investigated the control strategy for changing movement direction during arm movements by analyzing the changes in a triphasic electromyographic pattern. Subjects performed a 40° flexion (basic) and a 40° flexion-extension to return to the start position (return) under two conditions: performing a predetermined task (SF) and performing each task in response to a signal (ST). The results revealed the agonist burst for the return task under the ST condition resembled that of the basic task under the SF condition, and the antagonist burst increased after presenting the modification signal. In conclusion, the strategy for quick change of movement direction was to increase the antagonist burst by an additional command from the central nervous system without cancelling the planned movement.

Startle reveals independent preparation and initiation of triphasic EMG burst components in targeted ballistic movements

Muscles involved in rapid, targeted movements about a single joint often display a triphasic [agonist (AG1)-antagonist (ANT)-agonist (AG2)] electromyographic (EMG) pattern. Early work using movement perturbations suggested that for short movements, the entire EMG pattern was prepared and initiated in advance (Wadman WJ, Dernier van der Gon JJ, Geuze RH, Mol CR. J Hum Mov Stud 5: 3-17, 1979), whereas more recent transcranial magnetic stimulation evidence indicates that the ANT may be programmed separately (MacKinnon CD, Rothwell JC. J Physiol 528: 633-645, 2000) with execution of the bursts occurring serially (Irlbacher K, Voss M, Meyer BU, Rothwell JC. J Physiol 574: 917-928, 2006). The purpose of the current study was to investigate the generation of triphasic EMG bursts for movements of different amplitudes. In experiment 1, participants performed rapid elbow extension movements to 20° and 60° targets, and on some trials, a startling acoustic stimulus (SAS), which is thought to trigger prepared motor commands at short latency, was delivered at the onset of AG1. For short movements, this perturbation elicited ANT and AG2 early, suggesting the agonist and antagonist bursts may have been programmed independently. In contrast, the same manipulation did not disrupt EMG timing parameters for the long movements, raising the possibility that ANT and AG2 were not fully programmed in advance of movement onset. In experiment 2, an SAS was delivered later in the movement, which produced early onset of both ANT and AG2. We propose that the triphasic pattern is executed serially but believe the trigger signal for initiating the ANT burst occurs not in relation to the AG1 burst, but rather in close temporal proximity to the expected onset of ANT.

Multi-neuronal recordings in the Basal Ganglia in normal and dystonic rats.

Classical rate-based pathway models are invaluable for conceptualizing direct/indirect basal ganglia pathways, but cannot account for many aspects of normal and abnormal motor control. To better understand the contribution of patterned basal ganglia signaling to normal and pathological motor control, we simultaneously recorded multi-neuronal and EMG activity in normal and dystonic rats. We used the jaundiced Gunn rat model of kernicterus as our experimental model of dystonia. Stainless steel head fixtures were implanted on the skulls and EMG wires were inserted into antagonistic hip muscles in nine dystonic and nine control rats. Under awake, head-restrained conditions, neuronal activity was collected from up to three microelectrodes inserted in the principal motor regions of the globus pallidus (GP), subthalamic nucleus, and entopeduncular nucleus (EP). In normal animals, most neurons discharged in regular or irregular patterns, without appreciable bursting. In contrast, in dystonic animals, neurons discharged in slow bursty or irregular, less bursty patterns. In normal rats, a subset of neurons showed brief discharge bursts coinciding with individual agonist or antagonist EMG bursts. In contrast, in dystonics, movement related discharges were characterized by more prolonged bursts which persist over multiple dystonic co-contraction epics. The pattern of movement related decreases in discharge activity however did not differ in dystonics compared to controls. In severely dystonic rats, exclusively, simultaneously recorded units often showed abnormally synchronized movement related pauses in GP and bursts in EP. In conclusion, our findings support that slow, abnormally patterned neuronal signaling is a fundamental pathophysiological feature of intrinsic basal ganglia nuclei in dystonia. Moreover, from our findings, we suggest that excessive movement related silencing of neuronal signaling in GP profoundly disinhibits EP and in turn contributes to sustained, unfocused dystonic muscle contractions.

Muscle activity patterns during quick increase of movement amplitude in rapid elbow extensions

In this study, we investigated a motor strategy for increasing the amplitude of movement in rapid extensions at the elbow joint. This study focused on the changes in a triphasic electromyographic (EMG) pattern, i.e., the first agonist burst (AG1), the second agonist burst (AG2) and the antagonist burst (ANT), for increasing the amplitude of movement required after the initiation of movement. Subjects performed 40° (Basic task) and 80° of extension (Wide task). These tasks were performed under two conditions; performing a predetermined task (SF condition) and performing a task in response to a visual stimulus immediately after movement commencement (ST condition). Kinematic parameters and EMG activity from the agonist (triceps brachii) and the antagonist (biceps brachii) muscles were recorded. As a result, the onset latency of AG1 and AG2 and the duration of AG1 were longer under the ST condition than the SF condition. No difference was observed between the SF and ST condition with respect to ANT activity. It is concluded that the motor strategy for increasing the amplitude of movement after the initiation of movement was to control the movement velocity and the timing to stop movement by the coactivation duration of AG1 and ANT and to stop the desired position accurately by AG2 activity.

肘関節における素早い伸展動作切り換え時の筋活動

In this study, we investigated a motor strategy for changing the amplitude or direction of movement during rapid extensions of the elbow joint. We focused on changes in the triphasic electromyographic (EMG) pattern, i.e. the first agonist burst (AG1), the second agonist burst (AG2) and the antagonist burst (ANT), in relation to changes in the amplitude and direction of movement required after the initiation of movement. Ten seated subjects extended the elbow 40 degrees in the Basic task and 80 degrees in the Wide task, and then returned to the starting position after reaching for a target in the Basic task (Return task). The tasks were performed under two conditions: while performing a predetermined task (SF condition), and while performing a task in response to a visual stimulus after movement commencement (ST-BW condition—the subject performed either the Basic task or the Wide task; ST-BR condition—the subject performed either the Basic task or the Return task). Kinematic and temporal parameters, and EMG activity from the agonist (triceps brachii) and the antagonist (biceps brachii) muscles were recorded. Comparing the Wide task with the Basic task, the onset latency of AG2 increased, and the duration in all bursts increased. In the ST-BW condition, the onset latency of AG1 and AG2 and the duration of AG1 increased compared with the SF condition. Comparing the Return task with the Basic task, the onset latency of ANT and AG2 increased. The duration of all bursts and the average EMG (a-EMG) of ANT in the Return task increased compared with the Basic task. There was no difference between the SF and ST-BR conditions. It is concluded that the motor strategy for changing the amplitude of initiated movement is to control the duration of AG1 depending on the amplitude of movement in order to change the timing to stop movement, and that the motor strategy for changing the direction of initiated movement is to increase the duration and amplitude of ANT in order to stop at the target and flex continuously.

Effects of Transcranial Magnetic Stimulation Over the Cerebellum on Triphasic Electromyographic Pattern

The purpose of this study was to investigate the effects of transcranial magnetic stimulation (TMS) over the cerebellum on the triphasic electromyographic (EMG) pattern. Eight healthy subjects extended the left wrist as fast as possible in response to a start cue. TMS was delivered over the cerebellum 50 ms after the start cue. TMS over the cerebellum produced shortening of the latency in the first agonist burst, and an increase in the EMG activity of the antagonist burst. The triphasic EMG pattern may be partially under the control of the cerebellum.

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 α 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 α 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.

Influence of ipsilateral transcranial magnetic stimulation on the triphasic EMG pattern accompanying fast ballistic movements in humans

Fast ballistic flexion movements of the wrist are produced by a triphasic pattern of electromyographic (EMG) activity in flexor and extensor muscle. Whereas it is generally accepted that the primary motor cortex generates the first agonist burst (AG1), its contribution to the following antagonist burst (ANT) and second agonist burst (AG2) is unresolved. We applied single pulses of suprathreshold transcranial magnetic stimulation (TMS) at different times to the motor cortex ipsilateral to wrist flexion. This produced interhemispheric inhibition of the opposite motor cortex and a silent period in the ballistic EMG pattern that started about 30 ms after the stimulus and lasted for a further 30 ms. If the silence was timed to start within the first 30 ms of AG1, then timing of the subsequent ANT and AG2 bursts was delayed. However, if the silence began later, then the timing of the ANT burst was not changed. A similar effect on the onset latency of the AG2 was seen if the silence began in the first part of the ANT burst. The results are compatible with a model in which the triphasic pattern is not triggered as a single entity. Instead we suggest that each burst has its own trigger that occurs about 30-40 ms after the start of AG1 (or ANT). If AG1 (or ANT) is interrupted within this time period then this trigger, and hence later bursts, are delayed. If the interruption occurs after 30-40 ms it has no effect on the onset of later bursts since they have already been triggered.

Effect of combined variation of force amplitude and rate of force development on the modulation characteristics of muscle activation during rapid isometric aiming force production

Studies of rapid target-directed limb movements have suggested that various control schemes can be defined by the modulation pattern of the muscle activity. The present study was aimed to address the question regarding the extent to which a simultaneous control of force amplitude, and rate of force development influences the modulation characteristics of muscle activation associated with producing rapid isometric aiming forces at the elbow joint. The subjects were instructed to produce rapid isometric force pulses to three different force amplitudes (15, 35, and 55% of their maximal voluntary contractions) under systematically varied force-rate conditions ranging from a fast and accurate force-rate to the fastest force-rate possible. The results showed that larger force amplitudes were achieved by increasing the rate of force development (d F/d t) while the time to peak force remained relatively constant. The magnitude of the electromyographic (EMG) burst systematically increased as a function of force amplitude at all force-rate conditions. The primary finding was that the characteristic of the EMG burst duration associated with different force amplitudes showed a significant difference among force-rate conditions. Under a fast and accurate force-rate condition, the duration of the agonist burst increased linearly with force amplitude. A gradual transition into a fixed duration of the agonist burst then was observed over the remaining three force-rate requirements. With increasingly faster force-rates, there were no changes in the agonist burst duration over three force amplitudes. These results indicate that the combined variations in force amplitude and force-rate examined relative to the most rapid force-rate influence the control patterns for the muscle activation during the fast isometric force production. Changes in the EMG modulation patterns observed are likely due to the constraints imposed by muscle contractile properties.

Effects of deep brain stimulation and medication on strength, bradykinesia, and electromyographic patterns of the ankle joint in Parkinson's disease

We investigated the control of movement in 12 patients with Parkinson's disease (PD) after they received surgically implanted high-frequency stimulating electrodes in the subthalamic nucleus (STN). The experiment studied ankle strength, movement velocity, and the associated electromyographic patterns in PD patients, six of whom had tremor at the ankle. The patients were studied off treatment, ON STN deep brain stimulation (DBS), on medication, and on medication plus STN DBS. Twelve matched control subjects were also examined. Medication alone and STN DBS alone increased patients' ankle strength, ankle velocity, agonist muscle burst amplitude, and agonist burst duration, while reducing the number of agonist bursts during movement. These findings were similar for PD patients with and without tremor. The combination of medication plus STN DBS normalized maximal strength at the ankle joint, but ankle movement velocity and electromyographic patterns were not normalized. The findings are the first to demonstrate that STN DBS and medication increase strength and movement velocity at the ankle joint.

Optimal Control of Redundant Muscles in Step-Tracking Wrist Movements

An important question in motor neuroscience is how the nervous system controls the spatiotemporal activation patterns of redundant muscles in generating accurate movements. The redundant muscles may not only underlie the flexibility of our movements but also pose the challenging problem of how to select a specific sequence of muscle activation from the huge number of possible activations. Here, we propose that noise in the motor command that has an influence on task achievement should be considered in determining the optimal motor commands over redundant muscles. We propose an optimal control model for step-tracking wrist movements with redundant muscles that minimizes the end-point variance under signal-dependent noise. Step-tracking wrist movements of human and nonhuman primates provide a detailed data set to investigate the control mechanisms in movements with redundant muscles. The experimental EMG data can be summarized by two eminent features: 1) amplitude-graded EMG pattern, where the timing of the activity of the agonist and antagonist bursts show slight variations with changes in movement directions, and only the amplitude of activity is modulated; and 2) cosine tuning for movement directions exhibited by the agonist and antagonist bursts, and the discrepancy found between a muscle's agonist preferred direction and its pulling direction. In addition, it is also an important observation that subjects often overshoot the target. We demonstrate that the proposed model captures not only the spatiotemporal activation patterns of wrist muscles but also trajectory overshooting. This suggests that when recruiting redundant muscles, the nervous system may optimize the motor commands across the muscles to reduce the negative effects of motor noise.

Postural strategy to keep balance on the seesaw

This work investigates the kinematic and electromyography (EMG) strategy used by the central nervous system (CNS) to keep equilibrium during anterior-posterior balance on seesaws with different degrees of instability. The movement of hip, knee, and ankle were reconstructed using a 3D motion-analysis system and the EMG activities of selected ankle, knee, and hip muscles were recorded. Balance was kept mainly at the ankle joint. The EMG patterns of the gastrocnemius and anterior tibialis alternated between agonist and antagonist bursts. The agonist burst started before the end of the lengthening phase and was prolonged until the end of the shortening phase. The EMG activities of the muscles crossing the knee and hip joints were characterized by a pattern of generalized co-activation. The movements at these two joints were very small, suggesting a neural or biomechanical constraint underlying the operations of the equilibrium control. Our results also indicate that the strategy to keep balance on the seesaw is qualitatively the same for the different levels of mechanical demands in terms of the seesaw's instability.

Signs of muscle thixotropy during human ballistic wrist joint movements

A study was conducted on healthy subjects to determine whether voluntary ballistic wrist flexion movements are influenced by immediately preceding conditioning of the forearm muscles. Single rapid wrist flexion movements were made in response to an auditory "Go" signal. Rectified surface EMG was recorded from wrist flexors and extensors, and joint position was measured by a goniometer. The movements were preceded (2-3 s) by four different conditioning routines: 40-s rest (Rest), 10-s voluntary alternating wrist joint flexion and extension movements (Osc), and 10 s of 25 degrees weak isometric wrist extensor (Ext) or flexor contractions (Flex). When subjects made ballistic movements after Osc compared with Rest, peak velocity was higher (P = 0.02) and movement time shorter (P = 0.06), but there was no difference (P = 0.83) in motor reaction time (time between the onset of the first agonist burst and movement onset). If the movements were preceded by Ext compared with Flex, motor reaction time was longer (P = 0.01), indicating a longer electromechanical delay. There were no indications that postconditioning differences in agonist or antagonist muscle activity could explain the results. It was also demonstrated that, after Rest, peak velocity was lower (P < 0.01) for the first than for the second of a series of repetitive ballistic movements. The observations corresponded to results from passive experiments in which the median nerve was electrically stimulated. In conclusion, history-dependent (thixotropic) changes in skeletal muscle resistance seem to have implications for voluntary ballistic wrist movements. The study also provided evidence that muscle conditioning influences the central nervous reaction time preceding ballistic contractions.

Effect of medication in Parkinson’s disease: a wavelet analysis of EMG signals

The improvements in the motor ability in patients with Parkinson’s disease due to antiparkinsonian medication is well-known and widely documented. Recent results, based both on kinematic parameters and standard electromyographic (EMG) signal analysis, clearly indicated that the medication reduced, as expected, the clinical signs of Parkinson’s disease, but did not restore agonist burst duration modulation with distance in elbow flexion movements. The main aim of the present work is to shed more light on this medication effect using a wavelet analysis approach on multiple EMG signals recorded both on shoulder and elbow muscles in ballistic or rapid movements. The wavelet cross-correlation information allows us to evidence some important quantitative features of the EMG signals due to medication.

Greater impairment of extension movements as compared to flexion movements in Parkinson?s disease

Research on isometric contractions in subjects with Parkinson's disease (PD) has shown that anti-parkinsonian medication results in a greater increase in extensor strength than flexor strength. This finding is consistent with the hypothesis that there is a greater impairment in neural activation of extensor muscles as compared to flexor muscles in subjects with PD. Such a hypothesis is physiologically feasible given the known differences in the neural control of flexor and extensor muscles. If the above hypothesis is true for both phasic and tonic muscle activation, then differences between performance of rapid single-joint flexion and extension movements should exist in subjects with PD. Twelve subjects with PD, "off" and "on" medication, and 12 age-and sex-matched healthy control subjects performed rapid single-joint movements in flexion and extension over three distances. For neurologically healthy subjects, we did not identify any significant differences in either kinematic or EMG parameters between flexion and extension movements. In contrast, in the PD subjects extension movements were slower and associated with more agonist bursts when compared to flexion movements. The results are consistent with the hypothesis that there is a differential impairment of neural activation of extensor muscles of the arm as compared to flexor muscles in subjects with PD.

Effects of deep brain stimulation and medication on bradykinesia and muscle activation in Parkinson's disease.

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and antiparkinsonian medication (Meds) have proved to be effective therapies for treating bradykinesia in Parkinson's disease. However, it is not currently known how or to what extent STN stimulation alters the control signals to agonist and antagonist muscles to change movement speed. Our objective was to investigate movement speed along with the amplitude and temporal features of EMG activity to determine how and to what extent these parameters are changed by DBS and medication. Nine patients with Parkinson's disease were studied following neurosurgery that implanted high-frequency stimulating electrodes in the STN. The experiments for the patients were performed in each of four treatment conditions: (i) OFF treatment; (ii) STN DBS; (iii) Meds; and (iv) Meds plus STN DBS. Also, a group of age- and gender-matched control subjects were examined. Medication and DBS had similar effects in that both treatments increased movement speed, increased the amplitude of the first agonist burst, increased burst duration, reduced the number of agonist bursts, reduced cocontraction, increased the size of the antagonist EMG, and reduced the centroid time of the antagonist EMG. When DBS and medication were combined, only temporal measures of burst duration and the number of agonist bursts were different from the medication alone condition. There was a positive association between the level of bradykinesia OFF treatment and the level of bradykinesia following DBS and medication. The movement speed of neurologically normal control subjects' was over 40% higher during both flexion and extension movements when compared with the patients during Meds plus STN DBS. The changes in the muscle activation patterns provide a mechanism of action for the pharmacological and surgical interventions used to treat bradykinesia in Parkinson's disease. However, despite the success of medication and DBS at improving bradykinesia in patients with Parkinson's disease, patients' movement speed was not restored to normal due to limitations in the amplitude and temporal scaling of the agonist and antagonist bursting pattern. These findings suggest a link between basal ganglia function in scaling both the amplitude and temporal parameters of the input to the motor neuron pool.

Shoulder muscle activity in Parkinson's disease during multijoint arm movements across a range of speeds.

Bradykinesia is one of the primary symptoms of Parkinson disease and leads to significant functional limitations for patients. Single joint movement studies, that have investigated the mechanism of bradykinesia, suggest that several features of muscle activity are disrupted, including modulation of burst amplitude and duration, and the number of bursts. It has been proposed that it is the blending of these different burst deficits that collectively defines bradykinesia. This study adds two new approaches to the study of bradykinesia. First, we examined the features of shoulder muscle activities during multijoint arm movement in bradykinetic and control subjects, such that previously reported single joint hypotheses could be tested for generalized arm movement. Second, we directly manipulated speed while keeping distance constant for a large range of speeds. In this manner, we could compare individual trials of muscle activity between controls and subjects with Parkinson's disease (PD) for movements matched for both speed and movement duration. Our results showed that while a multiple burst pattern of shoulder muscles was a common strategy for all subjects (young, elderly controls and PD), subjects with PD showed several burst abnormalities, including deficits in initial agonist burst amplitude and duration at both fast and slow speeds. Subjects with PD also (1) failed to produce a one-burst pattern at fast speeds and, instead, produced a predominance of multiple burst patterns and (2) showed a relationship between the number of burst deficits and the severity of disease. These results extend the findings of single joint studies to multi-joint and similarly indicate that a combination of burst modulation abnormalities correlate with bradykinesia and disease severity.

The neural control of single degree-of-freedom elbow movements. Effect of starting joint position.

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 degrees, 40 degrees, 70 degrees, 100 degrees, and 130 degrees, where 0 degrees 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 degrees elbow flexion movements from each of four starting elbow positions (10 degrees, 40 degrees, 70 degrees, and 100 degrees). 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.