Role of cocontraction in arm movement accuracy

Cocontraction (the simultaneous activation of antagonist muscles around a joint) provides the nervous system with a way to adapt the mechanical properties of the limb to changing task requirements-both in statics and during movement. However, relatively little is known about the conditions under which the motor system modulates limb impedance through cocontraction. The goal of this study was to test for a possible relationship between cocontraction and movement accuracy in multi-joint limb movements. The electromyographic activity of seven single- and double-joint shoulder and elbow muscles was recorded using surface electrodes while subjects performed a pointing task in a horizontal plane to targets that varied randomly in size. Movement speed was controlled by providing subjects with feedback on a trial-to-trial basis. Measures of cocontraction were estimated both during movement and during a 200-ms window immediately following movement end. We observed an inverse relationship between target size and cocontraction: as target size was reduced, cocontraction activity increased. In addition, trajectory variability decreased and endpoint accuracy improved. This suggests that, although energetically expensive, cocontraction may be a strategy used by the motor system to facilitate multi-joint arm movement accuracy. We also observed a general trend for cocontraction levels to decrease over time, supporting the idea that cocontraction and associated limb stiffness are reduced over the course of practice.     

Repetitive arm motion-induced fatigue affects shoulder but not endpoint position sense

Neck/shoulder pain has previously been linked to repetitive work and muscle fatigue. We have shown that asymptomatic people performing repetitive upper limb tasks display signs of shoulder fatigue and of whole-body compensatory strategies. However, the role played by the proprioceptive system in the production of these compensatory strategies has not been studied. A group of asymptomatic adults (n = 18) performed a repetitive pointing task at shoulder height to fatigue. Before and after fatigue, they performed two position sense tasks, eyes closed: a single-joint task where they abducted their shoulder to the perceived horizontal and a multi-joint task, where they stood and placed their finger at the perceived location of a target in front of them at shoulder height. After fatigue, subjects made larger shoulder errors by raising their elbow higher above the horizontal (~+1.3 cm) than before fatigue; however, their finger position accuracy was not changed, despite all subjects performing the movement in less time (~−0.18 s) while fatigued. There were no gender differences in shoulder or finger position accuracy before or after fatigue; however, there were gender differences in the perceived finger-target location and in the temporal characteristics of the finger movement toward the target. Results suggest that healthy individuals are able to develop strategies to compensate for fatigue-induced deficits at one joint to maintain the endpoint accuracy of a multi-joint task constant. Gender differences in movement strategies and perception of endpoint location may play parts in the previously reported gender differences in work-related neck/shoulder symptoms.     

Fatigue-induced adaptive changes of anticipatory postural adjustments

To examine the fatigue-induced adaptive changes (e.g., timing) of anticipatory postural adjustments (APAs), APAs of 30 research participants were recorded before (baseline) and after (post-test) conditions of either rest (control group, n = 15) or fatigue (fatigue group, n = 15). Muscle fatigue was generated using a dead-lift exercise performed to exhaustion. Self-initiated postural perturbations were induced using a rapid unilateral arm-raising maneuver (focal movement), and APAs were obtained using electromyography (EMG) recorded bilaterally in the lumbar and thoracic paraspinal muscles as well as the hamstring muscles. Postural stability during the focal movement was assessed using a force plate. Results showed that fatigue had no effect on postural stability during the focal movement, and yet caused earlier APA onsets in three of the six muscles evaluated. In spite of early APA activation, the APA EMG integrals of two of the three postural control muscles which exhibited fatigue-induced early APA onsets (T9 and L4 contralateral paraspinals) did not differ between baseline and post-test measures. The findings suggest that early APA onset may enhance postural stability by permitting a longer duration APA which can counteract fatigue-induced decreases in the force-producing capability of muscles that contribute to postural stability.     

Adaptation of motor behavior to preserve task success in the presence of muscle fatigue

To achieve task goals in the various contexts of everyday life, the CNS has to adapt to short time scale changes in the properties of the neuromuscular system, such as those induced by fatigue. Here we investigated how humans preserve task success despite fatigue-induced changes within the neuromuscular system, when they have to aim at a target as fast and as accurately as possible. In such a task, subjects generally choose a compromise between speed and accuracy that has been formalized as Fitts's law. We first characterized the effect of fatigue on Fitts's law in an experiment where participants had to perform fast but accurate elbow movements aimed at targets of different sizes, before and after a fatiguing exercise that reduced maximal voluntary force by ∼30%. We found that movements were slower to guarantee task success in the presence of fatigue. We then used an optimal control model to determine how fatigue-induced changes in variables such as noise in motor commands, muscle contraction and relaxation times, and the gain between neural activation and muscle force may contribute to changes in Fitts's law with fatigue. We concluded that the observed behavior was not due to the lack of available force, but very likely reflected the fact that the CNS uses the same optimal strategy with a fatigued neuromuscular plant that notably exhibits increased signal-dependent noise in motor commands. This strategy appears necessary to preserve task success in the presence of acute changes in the neuromuscular system.     

Effects of muscle fatigue on mechanically sensitive afferents of slow conduction velocity in the cat triceps surae

1. Group III and IV muscle afferents have been shown to be sensitive to both mechanical stimuli and metabolic and thermal changes in muscle. To establish the potential role of slowly conducting muscle afferents in regulating motor output during fatigue, we recorded from mechanically sensitive group III and nonspindle group II afferents originating in the triceps surae in barbiturate-anesthetized cats. We evaluated the response of these afferents to tetanic muscle contraction, stretch, and surface pressure, before, during, and after fatigue. 2. Our results show that muscle fatigue both increases spontaneous discharge in these mechanically sensitive afferents and sensitizes their response to muscle stretch, surface pressure, and, in a few instances, muscle contraction. These fatigue-induced changes typically occurred after 5-10 min of submaximal fatiguing stimulation. 3. During recovery from muscle fatigue, several contraction-sensitive free nerve endings, which had become sensitized to contractions during fatigue, remained sensitized after 20-30 min of rest. 4. The results of this study provide support for the hypothesis that fatigue-induced excitation of slowly conducting afferents is significant in mediating fatigue-induced inhibition of motoneuron output. However, our finding that the discharge of many slowly conducting mechanoreceptor afferents declines during the initial phase of fatigue argues against a primary role for these afferents in mediating the initial decline in motoneuron rate that is so prominent in fatiguing maximum voluntary muscular contraction.     

Effect of isolated hip abductor fatigue on single-leg landing mechanics and simulated ACL loading

BackgroundAltered movement biomechanics are a risk factor for ACL injury. While hip abductor weakness has been shown to negatively impact landing biomechanics, the role of this musculature and injury risk is not clear. The aim of this musculoskeletal simulation study was to determine the effect of hip abductor fatigue-induced weakness on ACL loading, force production of lower extremity muscles, and lower extremity biomechanics during single-leg landing.MethodsBiomechanical data from ten healthy adults were collected before and after a fatigue protocol and used to derive subject-specific estimates of muscle forces and ACL loading using a 5-degree of freedom (DOF) model.ResultsThere were no significant differences in knee joint angles and ACL loading between pre and post-fatigue. However, there were significant differences, due to fatigue, in lateral trunk flexion angle, total excursion of trunk, muscle forces, and joint moments.ConclusionAltered landing mechanics, due to hip abductor fatigue-induced weakness, may be associated with increased risk of ACL injury during single-leg landings. Clinical assessment or screening of ACL injury risk will benefit from subject-specific musculoskeletal models during dynamic movements. Future study considering the type of the fatigue protocols, cognitive loads, and various tasks is needed to further identify the effect of hip abductor weakness on lower extremity landing biomechanics.     

Muscle fatigue: from observations in humans to underlying mechanisms studied in intact single muscle fibres

Prolonged dynamic exercise and sustained isometric contractions induce muscle fatigue, as manifested by decreased performance and a reduction in the maximum voluntary contraction force. Studies with non-invasive measurements in exercising humans show that mechanisms located beyond the sarcolemma are important in the fatigue process. In this review, we describe probable cellular mechanisms underlying fatigue-induced changes in excitation–contraction (E–C) coupling occurring in human muscle fibres during strenuous exercise. We use fatigue-induced changes observed in intact single muscle fibres, where force and cellular Ca²⁺ handling can be directly measured, to explain changes in E–C coupling observed in human muscle during exercise.     

运动性疲劳的生物力学评价及其与损伤关系研究进展

综述国内外有关运动性疲劳的研究文献,对运动性疲劳诱导方案、下肢生物力学特征及其与损伤关系进行总结。现阶段,实验室条件下诱导运动性疲劳主要可分为传统型疲劳方案和功能型疲劳方案两种,传统型疲劳方案的模型主要有功率自行车、跑台及台阶实验模型等;功能型疲劳方案更贴近运动实际或比赛中所发生的情况,通常表现为多运动平面相结合的运动形式。此外,对运动性疲劳的生物力学评价主要从运动学、地面反作用力、关节力矩、肌电图指标等方面展开,不同疲劳方案会对研究结果产生影响。未来的研究中需要考虑将疲劳诱导方案和评价指标进行标准化,以便将不同疲劳方案的诱导效果进行比较,为疲劳方案选择提供参考;同时,针对具体动作结构特征,更多地关注不同疲劳方案诱导后大脑-神经活化反馈及肌肉-骨骼激活效应的内在联系,理解不同疲劳方案间的生物力学机制差异,更深层次地探讨疲劳对运动损伤的影响。     

Muscular fatigue increases signal-dependent noise during isometric force production

This study was designed to characterize the effect of fatigue on the relationship between muscular force and its variability over a broad range of submaximal forces. Eight participants had to match 4 levels of isometric force from 7 to 53% of their maximal capabilities. This task was repeated before and after a fatigue protocol that induced a loss of maximal force of 31%. We found that, despite an increase in force variability that was proportional to the force level, the linear scaling of force variability with mean force was preserved during fatigue. Because this linear scaling is a prerequisite for optimal sensorimotor control models, our results broaden the explanatory power of these models to the fatigue case, while at the same time offering new routes towards understanding how the central nervous system adapts to fatigue.     

Reactive oxygen species and fatigue-induced prolonged low-frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice

Skeletal muscle often shows a delayed force recovery after fatiguing stimulation, especially at low stimulation frequencies. In this study we focus on the role of reactive oxygen species (ROS) in this fatigue-induced prolonged low-frequency force depression. Intact, single muscle fibres were dissected from flexor digitorum brevis (FDB) muscles of rats and wild-type and superoxide dismutase 2 (SOD2) overexpressing mice. Force and myoplasmic free [Ca(2+)] ([Ca(2+)](i)) were measured. Fibres were stimulated at different frequencies before and 30 min after fatigue induced by repeated tetani. The results show a marked force decrease at low stimulation frequencies 30 min after fatiguing stimulation in all fibres. This decrease was associated with reduced tetanic [Ca(2+)](i) in wild-type mouse fibres, whereas rat fibres and mouse SOD2 overexpressing fibres instead displayed a decreased myofibrillar Ca(2+) sensitivity. The SOD activity was approximately 50% lower in wild-type mouse than in rat FDB muscles. Myoplasmic ROS increased during repeated tetanic stimulation in rat fibres but not in wild-type mouse fibres. The decreased Ca(2+) sensitivity in rat fibres could be partially reversed by application of the reducing agent dithiothreitol, whereas the decrease in tetanic [Ca(2+)](i) in wild-type mouse fibres was not affected by dithiothreitol or the antioxidant N-acetylcysteine. In conclusion, we describe two different causes of fatigue-induced prolonged low-frequency force depression, which correlate to differences in SOD activity and ROS metabolism. These findings may have clinical implications since ROS-mediated impairments in myofibrillar function can be counteracted by reductants and antioxidants, whereas changes in SR Ca(2+) handling appear more resistant to interventions.     

Interaction of fibre type,potentiation and fatigue in human knee extensor muscles

AIM: To examine the effect of fibre type on potentiation and fatigue. METHODS: Young men (n = 4 per group) with a predominance of type I [61.4 +/- 6.9% (SD), group I (GI)] or type II [71.8 +/- 9.2%, group II (GII)] fibres in vastus lateralis, performed a fatigue protocol of sixteen 5-s maximal voluntary isometric contractions (MVCs) of the right knee extensors. Maximal twitches and corresponding muscle action potentials (M-waves) were evoked before the first MVC, during the 3-s rest period after each MVC and at intervals during the 5-min recovery period after the last MVC. RESULTS: Group II [49.3 +/- 2.6% (SE)] had a greater decrease in MVC force than GI (22.8 +/- 6.2%) during the fatigue protocol. Group II (126.4 +/- 13.6%) showed greater twitch force potentiation early in the fatigue protocol than GI (38.2 +/- 2.3%), but greater depression at the end (33.7 +/- 13.7% vs.17.4 +/- 3.4%). Twitch time-to-peak torque (TPT) and half relaxation time (HRT) initially decreased but then increased as the fatigue protocol progressed; GII had a greater increase in HRT. During a 5-min recovery period twitch force increased above the prefatigue level and remained so until the end of the recovery period; the pattern was similar in GI and GII. Twitch TPT and HRT remained elevated during recovery. M-wave area increased throughout the fatigue protocol and the first part of recovery before returning to baseline values in GII, whereas there were no significant changes in GI. The interaction between potentiation and fatigue was amplified in GII early in the fatigue protocol with concurrently greater twitch and M-wave potentiation, and greater MVC force decrease and HRT increase. Late in the protocol, GII had a greater decrease in twitch and MVC force combined with greater M-wave potentiation. CONCLUSION: It is concluded that fibre type distribution influences potentiation and fatigue of the twitch, and potentiation of the M-wave during fatiguing exercise.     

Interaction of fibre type,potentiation and fatigue in human knee extensor muscles

Aim: To examine the effect of fibre type on potentiation and fatigue. Methods: Young men (n = 4 per group) with a predominance of type I [61.4 ± 6.9% (SD), group I (GI)] or type II [71.8 ± 9.2%, group II (GII)] fibres in vastus lateralis, performed a fatigue protocol of sixteen 5‐s maximal voluntary isometric contractions (MVCs) of the right knee extensors. Maximal twitches and corresponding muscle action potentials (M‐waves) were evoked before the first MVC, during the 3‐s rest period after each MVC and at intervals during the 5‐min recovery period after the last MVC. Results: Group II [49.3 ± 2.6% (SE)] had a greater decrease in MVC force than GI (22.8 ± 6.2%) during the fatigue protocol. Group II (126.4 ± 13.6%) showed greater twitch force potentiation early in the fatigue protocol than GI (38.2 ± 2.3%), but greater depression at the end (33.7 ± 13.7% vs.17.4 ± 3.4%). Twitch time‐to‐peak torque (TPT) and half relaxation time (HRT) initially decreased but then increased as the fatigue protocol progressed; GII had a greater increase in HRT. During a 5‐min recovery period twitch force increased above the prefatigue level and remained so until the end of the recovery period; the pattern was similar in GI and GII. Twitch TPT and HRT remained elevated during recovery. M‐wave area increased throughout the fatigue protocol and the first part of recovery before returning to baseline values in GII, whereas there were no significant changes in GI. The interaction between potentiation and fatigue was amplified in GII early in the fatigue protocol with concurrently greater twitch and M‐wave potentiation, and greater MVC force decrease and HRT increase. Late in the protocol, GII had a greater decrease in twitch and MVC force combined with greater M‐wave potentiation. Conclusion: It is concluded that fibre type distribution influences potentiation and fatigue of the twitch, and potentiation of the M‐wave during fatiguing exercise.     

Fatigue-induced changes of impedance and performance in target tracking

Kinematic variability is caused, in part, by force fluctuations. It has been shown empirically and numerically that the effects of force fluctuations on kinematics can be suppressed by increasing joint impedance. Given that force variability increases with muscular fatigue, we hypothesized that joint impedance would increase with fatigue to retain a prescribed accuracy level. To test this hypothesis, subjects tracked a target by elbow flexion and extension both with fatigued and unfatigued elbow flexor and extensor muscles. Joint impedance was estimated from controlled perturbations to the elbow. Contrary to the hypothesis, elbow impedance decreased, whereas performance, expressed as the time-on-target, was unaffected by fatigue. Further analysis of the data revealed that subjects changed their control strategy with increasing fatigue. Although their overall kinematic variability increased, task performance was retained by staying closer to the center of the target when fatigued. In conclusion, the present study reveals a limitation of impedance modulation in the control of movement variability.     

Muscle cocontraction following dynamics learning

Coactivation of antagonist muscles is readily observed early in motor learning, in interactions with unstable mechanical environments and in motor system pathologies. Here we present evidence that the nervous system uses coactivation control far more extensively and that patterns of cocontraction during movement are closely tied to the specific requirements of the task. We have examined the changes in cocontraction that follow dynamics learning in tasks that are thought to involve finely sculpted feedforward adjustments to motor commands. We find that, even following substantial training, cocontraction varies in a systematic way that depends on both movement direction and the strength of the external load. The proportion of total activity that is due to cocontraction nevertheless remains remarkably constant. Moreover, long after indices of motor learning and electromyographic measures have reached asymptotic levels, cocontraction still accounts for a significant proportion of total muscle activity in all phases of movement and in all load conditions. These results show that even following dynamics learning in predictable and stable environments, cocontraction forms a central part of the means by which the nervous system regulates movement.     

Contralateral muscle fatigue in human quadriceps muscle: evidence for a centrally mediated fatigue response and cross-over effect

The purpose of this investigation was to examine the effects of voluntary muscular fatigue in one lower limb and determine whether a ‘cross-over’ of fatigue is evident in the contralateral limb. Twenty-eight subjects (13 males and 15 females) performed a series of voluntary and evoked isometric contractions of both the dominant (exercised) and non-dominant (non-exercised) leg extensor muscles, prior to and after a fatigue protocol consisting of a 100-s sustained maximal isometric contraction (MVC) performed by the dominant limb only. Force values and surface electromyography (EMG) from the vastus lateralis muscle were obtained allowing for the determination of twitch and compound action potential (M-wave) values. Maximal twitch tension and peak-to-peak amplitude were significantly decreased after the fatigue test in the dominant limb, as was maximal voluntary force (∼65 N reduction), EMG activity (∼0.1 mV decrease) and voluntary activation (∼17% decline). However, no significant changes were observed in the non-dominant limb with respect to twitch and M-wave properties nor in MVC force. The voluntary activation of the non-dominant limb decreased significantly by 8.7% after the fatigue test, which was performed only on the dominant limb. The results of the present study suggest that the decrease in force production in the exercised limb was primarily related to peripheral fatigue mechanisms, with central fatigue making a lesser contribution. Centrally mediated mechanisms appear to be the sole contributor to fatigue in the non-exercised limb suggesting an anticipatory fatigue response and a ‘cross-over’ of central fatigue between the exercised and non-exercised contralateral limb.     

Adaptation to destabilizing dynamics by means of muscle cocontraction

Adaptive control of wrist mechanics was investigated by means of destabilizing dynamics created by a torque motor. Subjects performed a 20 degrees movement to a 3 degrees target under the constraint that no motion should occur outside of the target zone once 800 ms had elapsed from movement onset. This constraint served as the minimum acceptable level of postural stability. The ability of subjects to modify their muscle activation patterns in order to successfully achieve this stability was investigated by creating three types of destabilizing dynamics with markedly different features: negative stiffness, negative damping, and square-wave vibration. Subjects performed sets of trials with the first type of destabilizing dynamics and were then required to adapt to the second and third. The adaptive response was quantified in terms of the rms electromyographic (EMG) activity recorded during various phases of the task. Surface EMG activity was recorded from three muscles contributing to wrist flexion and three muscles contributing to wrist extension. With negative stiffness, a significant compensatory increase in cocontraction of wrist flexor and extensor muscles was observed for slow movements, but there was little change in the muscle activity for rapid movements. With negative damping, muscle cocontraction was elevated to stabilize rapid movements, declining only gradually after the target was reached. For slow movements, cocontraction occurred only when negative damping was high. The response to square-wave vibration (10 Hz, +/-0.5 Nm), beginning at movement onset, was similar to that of negative damping, in that it resulted in elevated cocontraction. However, because the vibration persisted after the target was reached, there was no subsequent decrease in muscle activity. When the frequency was reduced to 5.5 Hz, but with the same torque impulse, cocontraction increased. This is consistent with greater mechanical instability. In summary, agonist-antagonist cocontraction was adapted to the stability of the task. This generally resulted in less of a change in muscle activity during the movement phase, when the task was performed quickly compared with slowly. On the other hand, the change in muscle activity during stabilization depended more on the nature of the instability than the movement speed.     

Effect of a fatiguing protocol on motor imagery accuracy

This study was devised to evaluate the influence of muscle fatigue on athletes ability to perform motor imagery. Performance impairment is a consequence of fatigue, but alterations on perception and mental activity may also occur. To test whether peripheral fatigue affects mental processes, ten sports students imagined three consecutive countermovement jumps before and after a fatiguing protocol, through repetition of upright movements, at 70% of maximal voluntary contraction, until exhaustion. Autonomic nervous system responses and imagined movement durations were considered the dependent variables. Actual duration was systematically overestimated during both visual and kinesthetic imagery, but motor imagery duration and autonomic responses were similar without and under fatigue. Results suggest that muscle fatigue, unlike fatigue induced by prolonged exercise, does not elicit mental fatigue and therefore does not alter motor imagery accuracy.     

Metabolic factors contributing to altered Ca2+ regulation in skeletal muscle fatigue

AIM: Skeletal muscle fatigue is characterized by a failure to maintain force production or power output during intense exercise. Many recent studies on isolated fibres have used brief repetitive tetanic contractions to mimic fatigue resulting from intensive exercise and to investigate the underlying cellular mechanisms. Such studies have shown that characteristic changes in Ca2+ regulation occur during fatiguing stimulation. This includes prolongation of the 'Ca2+-tails' which follow each period of tetanic stimulation and a progressive rise in resting [Ca2+]. More importantly, the final stage of fatigue is associated with a rapid decrease in tetanic [Ca2+]i and force. These fatigue-induced changes in sarcoplasmic reticulum (SR) Ca2+ regulation are temporally associated with alterations in the intracellular levels of phosphate metabolites and a causal relationship has often been proposed. The aim of this review is to evaluate the evidence linking changes in the levels of phosphate metabolites and altered Ca2+ regulation during fatigue. RESULTS: The following current hypotheses will be discussed: (1) the early changes in Ca2+ regulation reflect alterations in the intracellular levels of phosphate metabolites, (2) inhibition of the SR Ca2+ release mechanism (e.g. caused by ATP depletion and increased [Mg2+]) contributes to the decrease in tetanic [Ca2+]i during the final stages of fatigue and (iii) delayed entry of inorganic phosphate ions (Pi) into the SR, followed by precipitation of calcium phosphate (Ca-Pi), can explain the fatigue-induced decrease in tetanic [Ca2+]i. CONCLUSION: There is strong evidence that changes in phosphate metabolite levels contribute to early changes in SR Ca2+ regulation during fatigue and that inhibition of the SR Ca2+ release mechanism can partially explain the rapid decrease in tetanic [Ca2+]i during the final stages of fatigue. While precipitation of Ca-Pi may occur within the SR during fatigue, there is currently insufficient evidence to establish whether this contributes to the late decline in tetanic [Ca2+]i.     

Effects of vitamin E deficiency on fatigue and muscle contractile properties

Radical-mediated oxidative damage of skeletal muscle membranes has been implicated in the fatigue process. Vitamin E (VE) is a major chain breaking antioxidant that has been shown to reduce contraction-mediated oxidative damage. We hypothesized that VE deficiency would adversely affect muscle contractile function, resulting in a more rapid development of muscular fatigue during exercise. To test this postulate, rats were fed either a VE-deficient (EDEF) diet or a control (CON) diet containing VE. Following a 12-week feeding period, animals were anesthetized and mechanically ventilated. Muscle endurance (fatigue) and contractile properties were evaluated using an in situ preparation of the tibialis anterior (TA) muscle. Contractile properties of the TA muscle were determined before and after a fatigue protocol. The muscle fatigue protocol consisted of 60 min of repetitive contractions (250 ms trains at 15 Hz; duty cycle=11%) of the TA muscle. Prior to the fatigue protocol, no significant differences existed in the force-frequency curves between EDEF and CON animals. At the completion of the fatigue protocol, muscular force production was significantly (P<0.05) lower in the EDEF group (reduced by 69%) compared to CON group (reduced by 38%). Following the fatigue protocol, a right shift existed in the force-frequency curve at low stimulation frequencies (≤40 Hz) in the EDEF animals compared to the CON animals (P<0.05). The stimulated and the contralateral TA muscle from the EDEF animals had significantly higher markers of lipid peroxidation compared to the same muscles in the CON animals (P<0.05). These data support the hypothesis that VE deficiency impairs muscular endurance and alters muscle contractile properties following a prolonged series of contractions. Electronic Publication     

Effects of fatigue of elbow extensor muscles voluntarily induced and induced by electromyostimulation on multi-joint movement organization

To investigate the capacity of the central nervous system to integrate and differentiate two different muscular fatigue states, the present study examines the changes on multi-joint movement organization following muscular fatigue of elbow extensor muscles (triceps brachii) induced by voluntary versus electrically induced contractions. Twenty right-handed male volunteers performed throws in the horizontal plane before and after two fatiguing procedures. First, success rate of throws was not affected by fatigue neither after voluntary contractions, nor after electrically induced contractions. Despite similar reductions of the maximal voluntary isometric force and the median frequency of the electromyographic signal following both fatiguing protocols, voluntary contractions induced greater changes in muscle activation, kinematics and kinetics during throws than electrically induced contractions. The changes observed following voluntary contractions are interpreted as a compensatory strategy involving a greater contribution of the wrist. In contrast, the greater activation of the triceps brachii could compensate the weakness of this muscle induced by fatigue without any modification of the initial multi-joint movement organization.