Antagonist EMG Activity Research Articles

Differences in counter-movement jump between boys with and without intellectual disability.

The purpose of this study was to describe the performance and biomechanical parameters of the counter-movement jump for young people with ID, in comparison with age matched individuals without ID. Volunteers with ID (n=13; age=15.3 ± 1.6 years; Wisk III intelligence quotient 55.6 ± 11.2) and without ID (n=13; age=15.4 ± 1.2 years) performed maximal counter-movement jumps, while knee kinematics, vertical ground reaction forces and electromyographic activity of the vastus lateralis and biceps femoris were captured. Individuals without ID jumped higher than their counterparts with ID and had lower take-off velocity, lower knee joint power and stiffness, lower knee joint extension angle and angular velocity, longer braking and propulsion phase, lower agonist and higher antagonist EMG activity. These results give an insight on possible causes for the performance deficit in CMJ in persons with ID and give the potential for such individuals to improve their ability to jump higher and more efficiently.

Marked reduction of cerebellar deficits in upper limbs following transcranial cerebello-cerebral DC stimulation: tremor reduction and re-programming of the timing of antagonist commands

Cerebellar ataxias represent a very heterogeneous group of disabling disorders for which we lack effective symptomatic therapies in most cases. There is currently an intense interest in the use of non-invasive transcranial DC stimulation (tDCS) to modulate the activity of the cerebellum in ataxic disorders. We performed a detailed laboratory assessment of the effects of transcranial cerebello-cerebral DC stimulation (tCCDCS, including a sham procedure) on upper limb tremor and dysmetria in 2 patients presenting a dominant spinocerebellar ataxia (SCA) type 2, one of the most common SCAs encountered during practice. Both patients had a very similar triplet expansion size in the ATXN2 gene (respectively, 39 and 40 triplets). tCCDCS reduced both postural tremor and action tremor, as confirmed by spectral analysis. Quadratical PSD (power spectral density) of postural tremor dropped to 38.63 and 41.42% of baseline values in patient 1 and 2, respectively. The integral of the subband 4–20 Hz dropped to 46.9 and 62.3% of baseline values, respectively. Remarkably, tCCDCS canceled hypermetria and reduced dramatically the onset latency of the antagonist EMG activity associated with fast goal-directed movements toward 3 aimed targets (0.2, 0.3, and 0.4 rad). Following tCCDCS, the latency dropped from 108–98 to 63–57 ms in patient 1, and from 74–87 to 41–46 ms in patient 2 (mean control values ± SD: 36 ± 8 to 45 ± 11 ms), corresponding to a major drop of z scores for the 2 patients from 7.12 ± 0.69 to 1.28 ± 1.27 (sham procedure: 6.79 ± 0.71). This is the first demonstration that tCCDCS improves upper limb tremor and hypermetria in SCA type 2. In particular, this is the first report of a favorable effect on the onset latency of the antagonist EMG activity, a neurophysiological marker of the defect in programming of timing of motor commands. Our results indicate that tCCDCS should be considered in the symptomatic management of upper limb motor deficits in cerebellar ataxias. Future studies addressing a tDCS-based neuromodulation to improve motor control of upper limbs are required (a) in a large group of cerebellar disorders, and (b) in different subgroups of ataxic patients. The anatomical location of the cerebellum below the skull is particularly well suited for such studies.

Agonist and antagonist EMG activity of neck muscles during maximal isometric flexion and extension at different positions in young healthy men and women

The aim of this study was to compare maximal isometric torque and EMG activity of neck flexors and extensors in flexed and extended positions between men and women. Twenty four non-trained young healthy subjects (12 men vs. 12 women) performed maximal isometric neck flexion and extension within 30° around the neutral position in a sitting posture using a modified isokinetic dynamometer. Surface EMG activity of sternocleidomastoid, scalenus, paraspinal and upper trapezius muscles was recorded bilaterally. Men exhibited higher normalized-to-lean body weight torque than women mainly during neck flexion (44%, P < 0.001) compared to extension (18%, P < 0.05). In addition, torque increased from extended to flexed positions in women only (+17%, P < 0.001). This was associated with a decrease in EMG of neck extensors and upper trapezius muscles (from 35% to 20% and from 18% to 7%, P < 0.001, respectively) without changes in agonistic activity of neck flexors with neck position. In contrast, men displayed similar torque and muscle activation level within 30° of range of motion around the neutral position for both directions. These findings demonstrate gender-specific differences in neck function that was probably linked to higher coactivation level in antagonist muscles (neck extensors) and stabilizers (upper trapezius muscles).

Neural Adaptations to Resistive Exercise

It is generally accepted that neural factors play an important role in muscle strength gains. This article reviews the neural adaptations in strength, with the goal of laying the foundations for practical applications in sports medicine and rehabilitation. An increase in muscular strength without noticeable hypertrophy is the first line of evidence for neural involvement in acquisition of muscular strength. The use of surface electromyographic (SEMG) techniques reveal that strength gains in the early phase of a training regimen are associated with an increase in the amplitude of SEMG activity. This has been interpreted as an increase in neural drive, which denotes the magnitude of efferent neural output from the CNS to active muscle fibres. However, SEMG activity is a global measure of muscle activity. Underlying alterations in SEMG activity are changes in motor unit firing patterns as measured by indwelling (wire or needle) electrodes. Some studies have reported a transient increase in motor unit firing rate. Training-related increases in the rate of tension development have also been linked with an increased probability of doublet firing in individual motor units. A doublet is a very short interspike interval in a motor unit train, and usually occurs at the onset of a muscular contraction. Motor unit synchronisation is another possible mechanism for increases in muscle strength, but has yet to be definitely demonstrated. There are several lines of evidence for central control of training-related adaptation to resistive exercise. Mental practice using imagined contractions has been shown to increase the excitability of the cortical areas involved in movement and motion planning. However, training using imagined contractions is unlikely to be as effective as physical training, and it may be more applicable to rehabilitation. Retention of strength gains after dissipation of physiological effects demonstrates a strong practice effect. Bilateral contractions are associated with lower SEMG and strength compared with unilateral contractions of the same muscle group. SEMG magnitude is lower for eccentric contractions than for concentric contractions. However, resistive training can reverse these trends. The last line of evidence presented involves the notion that unilateral resistive exercise of a specific limb will also result in training effects in the unexercised contralateral limb (cross-transfer or cross-education). Peripheral involvement in training-related strength increases is much more uncertain. Changes in the sensory receptors (i.e. Golgi tendon organs) may lead to disinhibition and an increased expression of muscular force. Agonist muscle activity results in limb movement in the desired direction, while antagonist activity opposes that motion. Both decreases and increases in co-activation of the antagonist have been demonstrated. A reduction in antagonist co-activation would allow increased expression of agonist muscle force, while an increase in antagonist co-activation is important for maintaining the integrity of the joint. Thus far, it is not clear what the CNS will optimise: force production or joint integrity. The following recommendations are made by the authors based on the existing literature. Motor learning theory and imagined contractions should be incorporated into strength-training practice. Static contractions at greater muscle lengths will transfer across more joint angles. Submaximal eccentric contractions should be used when there are issues of muscle pain, detraining or limb immobilisation. The reversal of antagonists (antagonist-to-agonist) proprioceptive neuromuscular facilitation contraction pattern would be useful to increase the rate of tension development in older adults, thus serving as an important prophylactic in preventing falls. When evaluating the neural changes induced by strength training using EMG recording, antagonist EMG activity should always be measured and evaluated.

Shift from hypermetria to hypometria in multiple system atrophy: Analysis of distal and proximal movements

Dysmetria is a classical sign which designates the overshoot, also called hypermetria, and the undershoot, or hypometria, when the patient attempts to reach rapidly an aimed target. Dysmetria is typically observed in patients presenting a cerebellar dysfunction. Dysmetria of distal movements is associated with an imbalance between the timing and/or the intensity of agonist and antagonist EMG activities. So far, 1. there is only one description in human of a shift from hypermetria to hypometria for fast goal-directed single-joint movements during an aberrant recovery following a cerebellar infarction, and 2. such a shift has not been described for proximal movements. We report a patient presenting a multiple system atrophy (MSA). Initially, he exhibited a marked cerebellar syndrome. Fast wrist flexions and fast upper limb reaches in the sagittal plane were hypermetric. The distal hypermetria was associated with a delayed onset latency of the antagonist EMG activity and reduced intensities of both the agonist and the antagonist EMG activities. The proximal hypermetria was associated with a defect in the phasic spatial tuning of the EMG activities. He developed progressively severe extra-pyramidal signs. Distal hypermetria turned into hypometria, as a result of a decrease in the intensity of the agonist muscle. Proximal hypermetria turned into hypometria, as a result of the loss of directional preference of the EMG activities in proximal muscles. MSA is the second human model of a shift from hypermetria to hypometria. [Neurol Res 2002; 24: 249-258]

Fatigue Mechanisms in Trained and Untrained Plantar Flexors

The effect of an isometric intermittent submaximal fatigue protocol on the voluntary and evoked contractile properties of 14 trained and 14 untrained plantar flexor muscles was investigated at pre-, postfatigue, and recovery. The greater force output of trained subjects at rest was not attributed to differences in muscle activation or evoked contractile properties. At prefatigue, trained subjects had 40.3% less antagonist EMG activity than untrained subjects, which may have contributed to their increased strength. They also performed more contractions till fatigue and had significantly (p < 0.01) smaller decrements in maximum voluntary contraction force immediately postfatigue. The greater fatiguability of untrained subjects was accompanied by significant decreases in M-wave amplitude and peak twitch torque immediately postfatigue. Fatigue-induced decreases in untrained agonist EMG, combined with similar decreases in antagonist EMG for both groups, resulted in relatively less antagonist activity for the trained subjects. It appears that trained-state differences in plantar flexor fatiguability are related to peripheral and motor control changes rather than to central impairments.

Different types of cerebellar hypometria associated with a distinct topography of the lesion in cerebellum.

We recorded ballistic wrist flexion movements in fifteen cerebellar patients exhibiting hypometria. The movement and the associated agonist and antagonist EMG activities were analysed. On the basis of the topography of the cerebellar lesion, our patients were divided into three groups. In the first group including five patients, lesions involved the efferent dentato-thalamo-cortical pathway and hypometria was associated with an imbalance between the rate of rise of the agonist EMG activity and the rate of rise of the antagonist EMG activity. In the three patients of group II, lesions were located at the level of the middle cerebellar peduncle, disrupting the crossed ponto-cerebellar projections. In these patients, the intensity of the agonist EMG activity was reduced and the duration of the antagonist EMG activity was increased. In the third group including seven patients presenting either a diffuse cerebellar atrophy or a stroke involving a large parenchymatous area, the agonist-antagonist EMG pattern showed a prolongation of the duration of the antagonist burst. Our results show that discrete mechanisms of cerebellar hypometria are associated with different anatomical lesions.

Shift from hypermetria to hypometria in an aberrant recovery following cerebellar infarction

Cerebellar hypermetria, a classical sign designating the overshoot when the patient attempts to reach rapidly an aimed target, is associated with an imbalance between timing and/or intensity of agonist and antagonist EMG activities. Recovery of hypermetria following a cerebellar ischemia or hemorrhage has been demonstrated to take place in a multistage process, but aberrant recovery following a cerebellar stroke has not been described previously. We report an 85-year-old woman presenting an abnormal recovery following a cerebellar infarction. We identified three successive stages. At stage 1, fast wrist flexion movements were severely hypermetric and associated with three EMG defects: a delayed onset latency of antagonist EMG activity, a reduction of intensity of the agonist EMG activity and a depression of intensity of antagonist EMG activity. At stage 2, movements were characterized by terminal oscillations around the target and the onset latency of the antagonist activity had returned to normal. At stage 3, movements were markedly hypometric, the intensity of the antagonist EMG activity had returned to normal, while the intensity of the agonist EMG activity remained abnormally low. This case illustrates an abnormal reprogramming of the EMG triphasic pattern, resulting in the shift from severe hypermetria to severe hypometria.

Influences of muscle stretch reflexes on voluntary, velocity-controlled movements in spastic paraparesis.

We studied voluntary, velocity-controlled knee movements in 22 patients with spastic paraparesis (11 male, 11 female) and 22 healthy controls (11 male, 11 female). Torque and EMG activity of the quadriceps and the hamstring muscles were determined in maximal voluntary concentric (shortening) and eccentric (lengthening) actions of knee extensor and flexor muscles at constant movement velocities of 30, 60, 120 and 180 degrees/s, using an active, isokinetic dynamometer. In the spastic patients, the voluntary strength and the agonist EMG activity were reduced in all movements. The reduction was largest in concentric actions at high velocity. The antagonist EMG activity was reduced in the same proportion as the agonist EMG activity in eccentric actions. In concentric actions when stretch is imposed upon antagonists, the antagonist EMG activity increased with the velocity of stretch, indicating stretch reflex activation. In parallel with the stretch reflex activation of antagonists, there was reduced activation of the agonists compatible with Ia reciprocal inhibition of agonist motoneurons. When agonists were stretched in eccentric actions, stretch reflexes appeared to support the voluntary, agonist activation of knee flexor muscles but not knee extensors.

An evaluation of knee extensor and knee flexor torques and EMGs in patients with patellofemoral pain syndrome in comparison with matched controls.

The relationship between concentric and eccentric isokinetic torques and EMGs of quadriceps and hamstring muscles in patients with unilateral patellofemoral pain was studied in 27 patients (13 males, 14 females). The patients and a group of controls matched for age, gender, and physical activity were tested on a Kin-Com dynamometer at 60 degrees/s and 180 degrees/s angular velocity. EMGs were recorded for eight of the patients and their matched controls. In addition, the reproducibility of isokinetic measurements made under the same conditions but on different occasions in patients with patellofemoral pain was evaluated. Twenty-one patients (11 males, 10 females) underwent testing of their quadriceps and hamstring muscles two or three times on a Kin-Com dynamometer. This was performed both concentrically and eccentrically in their painful leg while the patients evaluated their knee pain using Borg's pain scale. The data show that the patients had a significantly lower agonist as well as antagonist EMG activity during knee extension measurements in their painful leg compared with the controls. However, there were no differences in either agonist or antagonist EMG activities during knee flexion measurements between the patients and the controls. The quadriceps muscle torque was considerably weaker in the patients' painful leg compared with both their asymptomatic leg and with the controls. Peak torque for knee extension was reached at a mean of 66 degrees of knee flexion for both patients and controls. However, the patients showed a considerably wider range within which they produced their peak torque in their painful leg than in their asymptomatic and also in comparison with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain mechanisms of the mind: information synthesis in dominant cortical areas

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°–80° were made under two instructions: “move at own speed” and “move fast and accurate.” In a second experiment, 5 elderly subjects practiced 30° 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. This greater movement variability may result from: 1) changes in motor neuron population and motor unit properties with aging and the associated effects on muscle force output and joint torques and 2) abnormal control of phasic and tonic antagonist muscle activity. The ability to improve performance with practice, however, is clearly not lost in the elderly.

Cerebellar Dysfunction of Movement and Perception

This review describes some characteristics of patients with cerebellar lesions, including limb movements, changes in motor planning and disturbances in time-dependent perception. The delay in movement initiation can be explained by a delay in onset of movement-related discharge of neurons in motor cortex. Disorders of movement termination (hypermetria) are accompanied by asymmetric velocity profiles and by prolonged agonist and delayed antagonist EMG activity necessary to brake the movement. During complex movements in three-dimensional space, the cerebellum contributes to timing between single components of a movement, scales the size of muscular action, and coordinates the sequence of agonists and antagonists. The basic structure of motor programs is not generated exclusively within the cerebellum and patients with cerebellar lesions can use precuing information to improve their motor performance. Time-dependent perception in the auditory and visual domains are disturbed in patients with cerebellar lesions.

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°–80° were made under two instructions: “move at own speed” and “move fast and accurate.” In a second experiment, 5 elderly subjects practiced 30° 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. This greater movement variability may result from: 1) changes in motor neuron population and motor unit properties with aging and the associated effects on muscle force output and joint torques and 2) abnormal control of phasic and tonic antagonist muscle activity. The ability to improve performance with practice, however, is clearly not lost in the elderly.

Modification in movement accuracy in the triphasic pattern during a rapid forearm-flexion task.

The present study was designed to investigate modifications in the triphasic EMG pattern during a forearm-flexion task at maximum speed which required three levels of movement accuracy. 36 subjects participated in 4 training sessions, performing a total of 200 repetitions of each movement. The fastest movement time was associated with the least accurate movement task. Likewise, the slowest movement time was found for the movement requiring the greatest accuracy. Differences in the duration and amplitude of agonist 1 activity, the start of agonist 2 activity, and the start and amplitude of antagonist activity were observed for the three movements. The results indicate that agonist 1 provides a propulsive force to initiate limb movement. The antagonist EMG activity was thought responsible for braking and correcting limb movement. Modifications in agonist 2 activity suggest this burst is related to movement velocity.

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.