Cortical Mechanisms of Central Fatigue and Sense of Effort

The purpose of this study was to investigate cortical mechanisms upstream to the corticospinal motor neuron that may be associated with central fatigue and sense of effort during and after a fatigue task. We used two different isometric finger abduction protocols to examine the effects of muscle activation and fatigue the right first dorsal interosseous (FDI) of 12 participants. One protocol was intended to assess the effects of muscle activation with minimal fatigue (control) and the other was intended to elicit central fatigue (fatigue). We hypothesized that high frequency repetitive transcranial magnetic stimulation (rTMS) of the supplementary motor area (SMA) would hasten recovery from central fatigue and offset a fatigue-induced increase in sense of effort by facilitating the primary motor cortex (M1). Constant force-sensation contractions were used to assess sense of effort associated with muscle contraction. Paired-pulse TMS was used to assess intracortical inhibition (ICI) and facilitation (ICF) in the active M1 and interhemispheric inhibitory (IHI) was assessed to determine if compensation occurs via the resting M1. These measures were made during and after the muscle contraction protocols. Corticospinal excitability progressively declined with fatigue in the active hemisphere. ICF increased at task failure and ICI was also reduced at task failure with no changes in IHI found. Although fatigue is associated with progressive reductions in corticospinal excitability, compensatory changes in inhibition and facilitation may act within, but not between hemispheres of the M1. rTMS of the SMA following fatigue enhanced recovery of maximal voluntary force and higher levels of ICF were associated with lower sense of effort following stimulation. rTMS of the SMA may have reduced the amount of upstream drive required to maintain motor output, thus contributing to a lower sense of effort and increased rate of recovery of maximal force.     

A dynamical model of muscle activation, fatigue, and recovery

A dynamical model is presented as a framework for muscle activation, fatigue, and recovery. By describing the effects of muscle fatigue and recovery in terms of two phenomenological parameters (F, R), we develop a set of dynamical equations to describe the behavior of muscles as a group of motor units activated by voluntary effort. This model provides a macroscopic view for understanding biophysical mechanisms of voluntary drive, fatigue effect, and recovery in stimulating, limiting, and modulating the force output from muscles. The model is investigated under the condition in which brain effort is assumed to be constant. Experimental validation of the model is performed by fitting force data measured from healthy human subjects during a 3-min sustained maximal voluntary handgrip contraction. The experimental results confirm a theoretical inference from the model regarding the possibility of maximal muscle force production, and suggest that only 97% of the true maximal force can be reached under maximal voluntary effort, assuming that all motor units can be recruited voluntarily. The effects of different motor unit types, time-dependent brain effort, sources of artifacts, and other factors that could affect the model are discussed. The applications of the model are also discussed.     

Sustained contraction at very low forces produces prominent supraspinal fatigue in human elbow flexor muscles.

During sustained maximal voluntary contractions (MVCs), most fatigue occurs within the muscle, but some occurs because voluntary activation of the muscle declines (central fatigue), and some of this reflects suboptimal output from the motor cortex (supraspinal fatigue). This study examines whether supraspinal fatigue occurs during a sustained submaximal contraction of 5% MVC. Eight subjects sustained an isometric elbow flexion of 5% MVC for 70 min. Brief MVCs were performed every 3 min, with stimulation of the motor point, motor cortex, and brachial plexus. Perceived effort and pain, elbow flexion torque, and surface EMGs from biceps and brachioradialis were recorded. During the sustained 5% contraction, perceived effort increased from 0.5 to 3.9 (out of 10), and elbow flexor EMG increased steadily by approximately 60-80%. Torque during brief MVCs fell to 72% of control values, while both the resting twitch and EMG declined progressively. Thus the sustained weak contraction caused fatigue, some of which was due to peripheral mechanisms. Voluntary activation measured by motor point and motor cortex stimulation methods fell to 90% and 80%, respectively. Thus some of the fatigue was central. Calculations based on the fall in voluntary activation measured with cortical stimulation indicate that about two-thirds of the fatigue was due to supraspinal mechanisms. Therefore, sustained performance of a very low-force contraction produces a progressive inability to drive the motor cortex optimally during brief MVCs. The effect of central fatigue on performance of the weak contraction is less clear, but it may contribute to the increase in perceived effort.     

Effect of muscle fatigue on internal model formation and retention during reaching with the arm.

The motor system adapts to novel dynamic environments by forming internal models that predict the muscle forces needed to move skillfully. The goal of this study was to determine how muscle fatigue affects internal model formation during arm movement and whether an internal model acquired while fatigued could be recalled accurately after rest. Twelve subjects adapted to a viscous force field applied by a lightweight robot as they reached to a target. They then reached while being resisted by elastic bands until they could no longer touch the target. This protocol reduced the strength of the muscles used to resist the force field by approximately 20%. The bands were removed, and subjects adapted again to the viscous force field. Their adaptive ability, quantified by the amount and time constant of adaptation, was not significantly impaired following fatigue. The subjects then rested, recovering approximately 70% of their lost force-generation ability. When they reached in the force field again, their prediction of the force field strength was different than in a nonfatigued state. This alteration was consistent with the use of a higher level of effort than normally used to counteract the force field. These results suggest that recovery from fatigue can affect recall of an internal model, even when the fatigue did not substantially affect the motor system's ability to form the model. Recovery from fatigue apparently affects recall because the motor system represents internal models as a mapping between effort and movement and relies on practice to recalibrate this mapping.     

Locomotor muscle fatigue increases cardiorespiratory responses and reduces performance during intense cycling exercise independently from metabolic stress

Locomotor muscle fatigue, defined as an exercise-induced reduction in maximal voluntary force, occurs during prolonged exercise, but its effects on cardiorespiratory responses and exercise performance are unknown. In this investigation, a significant reduction in locomotor muscle force (-18%, P < 0.05) was isolated from the metabolic stress usually associated with fatiguing exercise using a 100-drop-jumps protocol consisting of one jump every 20 s from a 40-cm-high platform. The effect of this treatment on time to exhaustion during high-intensity constant-power cycling was measured in study 1 (n = 10). In study 2 (n = 14), test duration (871 +/- 280 s) was matched between fatigue and control condition (rest). In study 1, locomotor muscle fatigue caused a significant curtailment in time to exhaustion (636 +/- 278 s) compared with control (750 +/- 281 s) (P = 0.003) and increased cardiac output. Breathing frequency was significantly higher in the fatigue condition in both studies despite similar oxygen consumption and blood lactate accumulation. In study 2, high-intensity cycling did not induce further fatigue to eccentrically-fatigued locomotor muscles. In both studies, there was a significant increase in heart rate in the fatigue condition, and perceived exertion was significantly increased in study 2 compared with control. These results suggest that locomotor muscle fatigue has a significant influence on cardiorespiratory responses and exercise performance during high-intensity cycling independently from metabolic stress. These effects seem to be mediated by the increased central motor command and perception of effort required to exercise with weaker locomotor muscles.     

A model for neural control of gradation of muscle force

A mathematical muscle model is presented that relates neural control signals linearly to muscle force without violating important known physiological constraints, such as the size-principle (Henneman and Mendell 1981) and non-linear twitch summation (Burke et al. 1976). This linearity implies that the neural control signals (defined as a weighted sum of activities in a nerve bundle) can be interpreted as the internal representation of total muscle force. The model allows for different relative contributions from the two force-grading mechanisms, i.e. the recruitment of motor units and the modulation of their firing frequency. It can therefore be applied to a variety of (distal and proximal) muscles. Furthermore, it permits simple mechanisms for controlling muscle force, e.g. in superposed motor tasks. The model confirms our intuitive notion that a weighted sum of activities in a nerve bundle can directly represent an external controlled variable, which in this case is exerted muscle force.     

Optimization of muscle activity for task-level goals predicts complex changes in limb forces across biomechanical contexts

Optimality principles have been proposed as a general framework for understanding motor control in animals and humans largely based on their ability to predict general features movement in idealized motor tasks. However, generalizing these concepts past proof-of-principle to understand the neuromechanical transformation from task-level control to detailed execution-level muscle activity and forces during behaviorally-relevant motor tasks has proved difficult. In an unrestrained balance task in cats, we demonstrate that achieving task-level constraints center of mass forces and moments while minimizing control effort predicts detailed patterns of muscle activity and ground reaction forces in an anatomically-realistic musculoskeletal model. Whereas optimization is typically used to resolve redundancy at a single level of the motor hierarchy, we simultaneously resolved redundancy across both muscles and limbs and directly compared predictions to experimental measures across multiple perturbation directions that elicit different intra- and interlimb coordination patterns. Further, although some candidate task-level variables and cost functions generated indistinguishable predictions in a single biomechanical context, we identified a common optimization framework that could predict up to 48 experimental conditions per animal (n = 3) across both perturbation directions and different biomechanical contexts created by altering animals' postural configuration. Predictions were further improved by imposing experimentally-derived muscle synergy constraints, suggesting additional task variables or costs that may be relevant to the neural control of balance. These results suggested that reduced-dimension neural control mechanisms such as muscle synergies can achieve similar kinetics to the optimal solution, but with increased control effort (≈2×) compared to individual muscle control. Our results are consistent with the idea that hierarchical, task-level neural control mechanisms previously associated with voluntary tasks may also be used in automatic brainstem-mediated pathways for balance.     

Normal muscle strength and fatigability in patients with effort syndromes.

To examine fatigue mechanisms in an unselected series of patients with excess fatigue ("effort syndromes") their muscle function was compared with that of normal subjects. Voluntary performance was assessed with a cycle ergometer to exhaustion and by maximal isometric contractions of the quadriceps femoris. The mean maximal heart rate in patients during ergometry was 89% of the predicted rate, and quadriceps strength was either normal or was inappropriate for the available muscle, which suggested submaximal effort. Contractile performance was examined in the absence of volition with stimulated contractions of the adductor pollicis. During stimulated fatiguing activity patients were neither weaker nor more fatigable than controls; thus the excess fatigue experienced by the patients was not due to a defect of the contractile apparatus. The increased perception of effort must therefore be due to impairment of central rather than peripheral mechanisms. The optimal approach to treatment of effort syndromes combines physical and psychological techniques.     

A comparison of central aspects of fatigue in submaximal and maximal voluntary contractions.

Magnetic and electrical stimulation at different levels of the neuraxis show that supraspinal and spinal factors limit force production in maximal isometric efforts ("central fatigue"). In sustained maximal contractions, motoneurons become less responsive to synaptic input and descending drive becomes suboptimal. Exercise-induced activity in group III and IV muscle afferents acts supraspinally to limit motor cortical output but does not alter motor cortical responses to transcranial magnetic stimulation. "Central" and "peripheral" fatigue develop more slowly during submaximal exercise. In sustained submaximal contractions, central fatigue occurs in brief maximal efforts even with a weak ongoing contraction (<15% maximum). The presence of central fatigue when much of the available motor pathway is not engaged suggests that afferent inputs contribute to reduce voluntary activation. Small-diameter muscle afferents are likely to be activated by local activity even in sustained weak contractions. During such contractions, it is difficult to measure central fatigue, which is best demonstrated in maximal efforts. To show central fatigue in submaximal contractions, changes in motor unit firing and force output need to be characterized simultaneously. Increasing central drive recruits new motor units, but the way this occurs is likely to depend on properties of the motoneurons and the inputs they receive in the task. It is unclear whether such factors impair force production for a set level of descending drive and thus represent central fatigue. The best indication that central fatigue is important during submaximal tasks is the disproportionate increase in subjects' perceived effort when maintaining a low target force.     

Perceptions of effort and heaviness during fatigue and during the size-weight illusion

Previous work has shown that force perception and the sense of motor effort are different attributes of sensorimotor function. This study explores the hypothesis that one reason force and effort perceptions are distinct is to inform an individual of impaired motor function when muscular force lags effort. This hypothesis predicts that effort and force perceptions will dissociate when motor function is impaired by fatigue but not during the size-weight illusion. All subjects reported a distinct increase in effort when lifting a standard test weight as fatigue developed. When fatigue was sufficiently marked so that they could barely lift the test weight, they rated their effort as similar to that required to lift a maximal weight in the unfatigued state. The perceived heaviness of the test weight also increased as fatigue developed, but this fatigue-weight illusion was smaller than the increase in effort for all subjects and displayed greater variability. In contrast, both the perceived weight of a small object and the effort required to lift it increased in parallel when small and large objects were lifted sequentially. The size-weight and size-effort illusions appear to be examples of a common phenomenon in which perceptual experience is rescaled to maintain acuity under different working conditions. The fatigue-weight illusion also has the effect of increasing perceptual acuity as the subject's weight lifting range decreases due to fatigue.     

Associations between force and fatigue in fast-twitch motor units of a cat hindlimb muscle

Associations were quantified between the control force and fatigue-induced force decline in 22 single fast-twitch-fatigable motor units of 5 deeply anesthetized adult cats. The units were subjected to intermittent stimulation at 1 train/s for 360 s. Two stimulation patterns were delivered in a pseudo-random manner. The first was a 500-ms train with constant interpulse intervals. The second pattern had the same number of stimuli, mean stimulus rate, and stimulus duration, but the stimulus pulses were rearranged to increase the force produced by the units in the control (prefatigue) state. The associations among the control peak tetanic force of these units, 3 indices of fatigue, and total cumulative force during fatiguing contractions were dependent, in part, on the stimulation pattern used to produce fatigue. The associations were also dependent, albeit to a lesser extent, on the force measure (peak vs. integrated) and the fatigue index used to quantify fatigue. It is proposed that during high-force fatiguing contractions, neural mechanisms are potentially available to delay and reduce the fatigue of fast-twitch-fatigable units for brief, but functionally relevant, periods. In contrast, the fatigue of slow-twitch fatigue-resistant units seems more likely to be controlled largely, if not exclusively, by metabolic processes within their muscle cells.     

等长伸膝动作的运动单元放电特征分析

本研究基于表面肌电分解技术,分析伸膝动作中不同发力状态下大腿肌肉运动单元的解码准确性,并对比神经特征和肌电特征在肌肉激活程度估计中的效果. 12名大学生分别以2种发力速度和4种发力等级完成伸膝动作的等长收缩.实验同步采集受试者股内侧肌和股外侧肌处的高密度表面肌电信号和伸膝动作收缩力.基于卷积核补偿算法解码肌电信号得到运动单元动作电位,提取神经特征用于收缩力的互相关分析.结果发现,对于股内侧肌,2种任务及4种收缩力等级下平均解码得到(7±4)个运动单元,股外侧肌平均解码得到(9±5)个运动单元.它们的平均脉冲信噪比(pulse-to-noise ratio,PNR)为30.1 d B,对应解码准确率大于90%.股内侧肌的两种神经特征与力之间的平均相关性分别为(0.79±0.08)和(0.80±0.08),股外侧肌的两种神经特征与力之间的平均相关性分别为(0.85±0.05)和(0.85±0.06).综上可见,基于肌电分解技术可以准确识别不同发力状态下大腿肌肉的运动单元放电活动,并且运动单元放电频率与伸膝动作力高度相关,研究结果可用于运动康复、运动训练及人机接口等领域.     

Neuromuscular adjustments that constrain submaximal EMG amplitude at task failure of sustained isometric contractions

The amplitude of the surface EMG does not reach the level achieved during a maximal voluntary contraction force at the end of a sustained, submaximal contraction, despite near-maximal levels of voluntary effort. The depression of EMG amplitude may be explained by several neural and muscular adjustments during fatiguing contractions, including decreased net neural drive to the muscle, changes in the shape of the motor unit action potentials, and EMG amplitude cancellation. The changes in these parameters for the entire motor unit pool, however, cannot be measured experimentally. The present study used a computational model to simulate the adjustments during sustained isometric contractions and thereby determine the relative importance of these factors in explaining the submaximal levels of EMG amplitude at task failure. The simulation results indicated that the amount of amplitude cancellation in the simulated EMG (～ 40%) exhibited a negligible change during the fatiguing contractions. Instead, the main determinant of the submaximal EMG amplitude at task failure was a decrease in muscle activation (number of muscle fiber action potentials), due to a reduction in the net synaptic input to motor neurons, with a lesser contribution from changes in the shape of the motor unit action potentials. Despite the association between the submaximal EMG amplitude and reduced muscle activation, the deficit in EMG amplitude at task failure was not consistently associated with the decrease in neural drive (number of motor unit action potentials) to the muscle. This indicates that the EMG amplitude cannot be used as an index of neural drive.     

Evidence of Significant Central Fatigue in Patients with Cancer-Related Fatigue during Repetitive Elbow Flexions till Perceived Exhaustion

Objective

To investigate whether fatigue induced by an intermittent motor task in patients with cancer-related fatigue (CRF) is more central or peripheral.

Methods

Ten patients with CRF who were off chemo and radiation therapies and 14 age-matched healthy controls were enrolled. Participants completed a Brief Fatigue Inventory (BFI) and performed a fatigue task consisting of intermittent elbow-flexion contractions at submaximal (40% maximal voluntary contraction) intensity till self-perceived exhaustion. Twitch force was elicited by an electrical stimulation applied to the biceps brachii muscle. The relative degree of peripheral (muscle) vs. central contribution to fatigue induced by the intermittent motor task (IMT) was assessed using twitch force ratio (TF_ratio) defined as post IMT twitch force to pre IMT twitch force. The total number of trials (intermittent contractions) and total duration of all trials performed by each subject were also quantified.

Results

BFI scores were higher (p<0.001) in CRF than controls, indicating greater feeling of fatigue in CRF patients than controls. A significantly smaller number of trials and shorter total duration of the trials (p<0.05) were observed in CRF than control participants. The TF_ratio (0.81±0.05) in CRF was higher (p<0.05) compared with that of controls (0.62±0.05), suggesting CRF patients experienced a significantly lower degree of muscle (peripheral) fatigue at the time of perceived exhaustion.

Conclusion

Consistent with prior findings for fatigue under submaximal sustained contraction, our results indicate that motor fatigue in CRF is more of central than peripheral origin during IMT. Significant central fatigue in CRF patients limits their ability to prolong motor performance.     

Effect of selective fatiguing of the shank muscles on single-leg-standing sway.

Control of standing requires the continuous activity of the leg muscles. In single leg standing the system is less redundant and muscular activity is more intensive. The objective of this study was to examine the effect of force imbalance of the shank muscles, evoked by their selective fatiguing, on postural control in single-leg standing. Five healthy subjects performed two single-leg standing trials, lasting as long as the subject could maintain steady balance, and separated by a 240s quasi-isotonic sustained effort to induce fatigue of the Tibialis Anterior and Peroneus muscles. The following were on-line monitored: sway-related parameters, e.g., ground reaction force and center of pressure in the standing trials; and electromyogram of the Tibialis Anterior, Peroneus and Gastrocnemius muscles in all experiments. Simple and multiple linear regressions served to study the fatigue effects on the relationship between muscle activity and postural sway. The results indicate that the evoked muscle imbalance leads to (a) increased postural sway; (b) increased correlation between muscle activity, and sway-related parameters. Thus, with the reduction of the level of redundancy the system becomes more synchronized. These results have potential relevance for cases of muscle impairment, in which electrical stimulation is required to augment muscle activity.     

Force variability is mostly not motor noise: Theoretical implications for motor control

Variability in muscle force is a hallmark of healthy and pathological human behavior. Predominant theories of sensorimotor control assume ‘motor noise’ leads to force variability and its ‘signal dependence’ (variability in muscle force whose amplitude increases with intensity of neural drive). Here, we demonstrate that the two proposed mechanisms for motor noise (i.e. the stochastic nature of motor unit discharge and unfused tetanic contraction) cannot account for the majority of force variability nor for its signal dependence. We do so by considering three previously underappreciated but physiologically important features of a population of motor units: 1) fusion of motor unit twitches, 2) coupling among motoneuron discharge rate, cross-bridge dynamics, and muscle mechanics, and 3) a series-elastic element to account for the aponeurosis and tendon. These results argue strongly against the idea that force variability and the resulting kinematic variability are generated primarily by ‘motor noise.’ Rather, they underscore the importance of variability arising from properties of control strategies embodied through distributed sensorimotor systems. As such, our study provides a critical path toward developing theories and models of sensorimotor control that provide a physiologically valid and clinically useful understanding of healthy and pathologic force variability.     

Fatigue and recovery of dynamic and steady-state performance in frog skeletal muscle

Muscle fatigue reflects alterations of both activation and cross-bridge function, which will have markedly different affects on steady-state vs. dynamic performance. Such differences offer insight into the specific origins of fatigue, its mechanical manifestation, and its consequences for animal movement. These were inferred using dynamic contractions (twitches and cyclic work as might occur during locomotion) and steady-state performance with maximal, sustained activation (tetani, stiffness, and isokinetic force) during fatigue and then recovery of frog (Rana pipiens) anterior tibialis muscle. Stiffness remained unaltered during early fatigue of force and then declined only 25% as force dropped 50%, suggesting a decline with fatigue in first the force-generating ability and then the number of cross bridges. The relationship between stiffness and force was different during fatigue and recovery; thus the number of cross bridges and force per cross bridge are not intimately linked. Twitch duration increased with fatigue and then recovered, with trajectories that were remarkably similar to and linear with changes in tetanic force, perhaps belying a common mechanism. Twitch force increased and then returned to resting levels during fatigue, reflecting a slowing of activation kinetics and a decline in cross-bridge number and force. Net cyclic work fatigued to the degree of becoming negative when tetanic force had declined only 15%. Steady-state isokinetic force (i.e., shortening work) declined by 75%, while cyclic shortening work declined only 30%. Slowed activation kinetics were again responsible, augmenting cyclic shortening work but greatly augmenting lengthening work (reducing net work). Steady-state measures can thus seriously mislead regarding muscle performance in an animal during fatigue.     

Human motor unit recruitment and derecruitment during long lasting intermittent contractions.

Seven healthy subjects were investigated in cyclic ramp-and-hold long lasting isometric contractions. Wire branched electrodes were used for selective recording of single motor unit (MU) potentials from m. biceps brachii. MU behaviour was defined in terms of recruitment/derecruitment thresholds (RT and DT) and the duration of interspike intervals (ISI). A total of 63 MUs was investigated: 40 units were active from the beginning of the task performance and another 23 were recruited later. There were no changes in the recruitment pattern of MUs with fatigue development - a short first ISI followed by a very long second one and an almost constant firing rate after this transient phase. The tendency of RT to gradually decrease dominates the results. Thus, the required constant rate of force increase with fatigue development was maintained mostly by the mechanisms of space coding (i.e., decrease of RT and recruitment of additional MUs). Oppositely, the time behaviour of the DT changes was not uniform and rate coding was an essential mechanism in the adaptation of MU activity to muscle fatigue during relaxation phases. The recruitment pattern and fatigue related behaviour of the additionally recruited MUs were similar to those of MUs active from the first cycle of the motor task performance.     

The neural control of coactivation during fatiguing contractions revisited

In addition to the role of muscle coactivation, a major question in the field is how antagonist activation is controlled to minimize its opposing effect on agonist muscle performance. Muscle fatigue is an interesting condition to analyze the neural adjustments in antagonist muscle activity and to gain more insights into the control mechanisms of coactivation. In that context, previous studies have reported that although the EMG activity of agonists and antagonists increase in parallel, the ratio between EMG activities in the two sets of muscles during a fatiguing submaximal contraction decreased progressively and contributed to a reduction in the time to task failure. In contrast, more recent studies using a novel normalization procedure indicated that the agonist/antagonist ratio remained relatively constant, suggesting that the fatigue-related increase in coactivation does not impede performance. Current knowledge also indicates that peripheral mechanisms cannot by themselves mediate the intensity of antagonist coactivation during fatiguing contractions, implying that supraspinal mechanisms are involved. The unique modulation of the synaptic input from Ia afferents to the antagonist motor neurones during a fatiguing contraction of the agonist muscles further suggests a separate control of the two sets of muscles.     

Selective Effect of Physical Fatigue on Motor Imagery Accuracy

While the use of motor imagery (the mental representation of an action without overt execution) during actual training sessions is usually recommended, experimental studies examining the effect of physical fatigue on subsequent motor imagery performance are sparse and yielded divergent findings. Here, we investigated whether physical fatigue occurring during an intense sport training session affected motor imagery ability. Twelve swimmers (nine males, mean age 15.5 years) conducted a 45 min physically-fatiguing protocol where they swam from 70% to 100% of their maximal aerobic speed. We tested motor imagery ability immediately before and after fatigue state. Participants randomly imagined performing a swim turn using internal and external visual imagery. Self-reports ratings, imagery times and electrodermal responses, an index of alertness from the autonomic nervous system, were the dependent variables. Self-reports ratings indicated that participants did not encounter difficulty when performing motor imagery after fatigue. However, motor imagery times were significantly shortened during posttest compared to both pretest and actual turn times, thus indicating reduced timing accuracy. Looking at the selective effect of physical fatigue on external visual imagery did not reveal any difference before and after fatigue, whereas significantly shorter imagined times and electrodermal responses (respectively 15% and 48% decrease, p<0.001) were observed during the posttest for internal visual imagery. A significant correlation (r = 0.64; p<0.05) was observed between motor imagery vividness (estimated through imagery questionnaire) and autonomic responses during motor imagery after fatigue. These data support that unlike local muscle fatigue, physical fatigue occurring during intense sport training sessions is likely to affect motor imagery accuracy. These results might be explained by the updating of the internal representation of the motor sequence, due to temporary feedback originating from actual motor practice under fatigue. These findings provide insights to the co-dependent relationship between mental and motor processes.