Effects of distal and proximal arm muscles fatigue on multi-joint movement organization

To investigate the strategies developed by the central nervous system to compensate for fatigue in muscles, we studied the changes in the relative mechanical contribution of the joint torques in a multi-joint movement following an isometric exhaustion test. Eighteen male subjects performed throws, moving the arm in the horizontal plane, before and after two fatigue protocols. Muscular fatigue was induced either in the distal (extensor digitorum communis) or in the proximal (triceps brachii) agonist muscle of the arm. The kinematic, kinetic and electromyographic parameters of the movement were analysed. The subjects produced two different coordinations following the fatigue protocols. In the distal fatigue condition, the wrist angular velocity was maintained by decreasing elbow active torque. In the proximal fatigue condition, the compensatory strategy involved increasing the contribution of the wrist. In fact, the control of elbow and wrist was modified in order to compensate for the different mechanical effects.     

Stimulated and voluntary fatiguing contractions of quadriceps femoris differently disturb postural control

Muscle fatigue affects muscle strength and postural control. However, it is not known whether impaired postural control after fatiguing muscular exercise depends on the nature of the muscle contraction. To answer this question, the present study analyzes changes in postural control after two fatiguing exercises of equal duration and intensity but that induced different magnitudes of strength loss. The effects of fatiguing contractions of the femoris quadriceps were compared for voluntary muscular contraction (VOL) and neuromuscular electrical stimulation (ES) on muscle strength and postural control. Seventeen subjects completed these two fatiguing exercises. Maximal voluntary contraction (MVC) and postural control were recorded using an isokinetic dynamometer and a force platform that recorded the center of foot pressure. Recordings were performed before and after the completion of both fatiguing tasks. Results indicate that, after a fatiguing exercise, the ES exercise affected MVC more than the VOL exercise. Inversely, postural control was disturbed more after VOL exercise than after ES exercise. In conclusion, postural control disturbance is influenced by the nature of the muscular contraction (voluntary vs. non-voluntary) and the type of the motor unit solicited (tonic vs. phasic) rather than by the magnitude of strength loss.     

The pressor response to voluntary and electrically evoked isometric contractions in man

Summary Blood pressure and heart rate changes during sustained isometric exercise were studied in 11 healthy male volunteers. The responses were measured during voluntary and involuntary contractions of the biceps brachii at 30% of maximal voluntary contraction (MVC), and the triceps surae at 30% and 50% MVC. Involuntary contractions were evoked by percutaneous electrical stimulation of the muscle.Measurements of the time to peak tension of maximal twitch showed the biceps brachii (67.0±7.9 ms) muscle to be rapidly contracting, and the triceps surae (118.0±10.5 ms) to be slow contracting. The systolic and diastolic blood pressures increased linearly throughout the contractions, and systolic blood pressure increased more rapidly than diastolic. There was no significant difference in response to stimulated or voluntary contractions, nor was there any significant difference between the responses to contractions of the calf or arm muscles at the same relative tension.In contrast the heart rate rose to a higher level (P<0.01) in the biceps brachii than the triceps surae at given % MVC, and during voluntary compared with the electrically evoked contractions in the two muscle groups.It was concluded that the arterial blood pressure response to isometric contractions, unlike heart rate, is primarily due to a reflex arising within the active muscles (cf. Hultman and Sjöholm 1982) which is associated with relative tension but independent of contraction time and muscle mass.     

Electrical stimulation superimposed onto voluntary muscular contraction reduces deterioration of both postural control and quadriceps femoris muscle strength

Fatiguing exercise of the quadriceps femoris muscle degrades postural control in human subjects. The aim of this work was to compare the effects of the fatigue of the quadriceps femoris induced by voluntary muscular contraction (VC), and by electrical stimulation (ES) superimposed onto voluntary muscular contraction (VC+ES), on postural control and muscle strength. Fourteen healthy young adults participated in the study. Postural control and muscle strength were evaluated using a stable force platform and an isokinetic dynamometer, respectively, before (PRE condition) and after the completion of each fatiguing exercise (immediately: POST condition; after a 5 min recovery time: POST 5 condition). In POST, both postural control and muscle strength were impaired by both fatiguing exercises. However, the impairment was higher for VC than for VC+ES. In POST 5, for both fatiguing exercises, postural control recovered its initial level while muscle strength did not. These results suggest that superimposing ES onto voluntary muscular contractions (VCs) impaired muscle strength and postural control less than did VCs alone. However the duration of recovery of these two neurophysiological functions did not differ for the two fatiguing exercises. For both exercises, postural control was restored faster than the ability to produce muscular strength.     

Effects of knee and ankle muscle fatigue on postural control in the unipedal stance

The aim of this study was to compare the effects of acute muscle fatigue of the ankle and knee musculature on postural control by immediate measures after performing fatiguing tasks (POST condition). One group of subjects (n = 8) performed a fatiguing task by voluntary contractions of the triceps surae (group TRI) and the other (n = 9) performed a fatiguing task by voluntary contractions of the quadriceps femoris (group QUA). Each muscle group was exercised until the loss of maximal voluntary contraction torque reached 50% (isokinetic dynamometer). Posture was assessed by measuring the centre of foot pressure (COP) with a force platform during a test of unipedal quiet standing posture with eyes closed. Initially (in PRE condition), the mean COP velocity was not significantly different between group TRI and group QUA. In POST condition, the mean COP velocity increased more in group QUA than in group TRI. The postural control was more impaired by knee muscle fatigue than by ankle muscle fatigue.     

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.     

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

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

Human tibialis anterior contractile responses following fatiguing exercise with and without beta-adrenoceptor blockade

The effects of oral propranolol (2 x 80 mg/day) on the contractile responses to twitch and tetanic electrical stimulation were examined in the tibialis anterior (TA) muscle of seven healthy young males. The TA muscle was fatigued by four forms of repeated isometric contractions: (1) maximal voluntary contractions (MVC), (2) MVC with circulation occluded, (3) electrically evoked contractions with 20 Hz supramaximal voltage stimulation and (4) electrically evoked contractions with circulation occluded. Each contraction was sustained for 10 s with 5 s recovery. Duration of exercise was 10 min for intact circulation and 4 min for circulatory occlusion. Pre-exercise, both the twitch contraction time and the 1/2 relaxation time were significantly (P less than 0.05) longer with beta-blockade than placebo. beta-blockade did not affect torque output during tetanic stimulation or MVC. Immediately post-exercise, the peak twitch torque was reduced in all beta-blocked and placebo conditions except electrically induced exercise with intact circulation. The 1/2 relaxation time was significantly lengthened by repeated MVC with circulation intact; beta-blockade caused a greater lengthening than placebo (P less than 0.05). The tetanic torque was reduced immediately post-exercise at each of 10, 20, 50 and 100 Hz for both beta-blockade and placebo for each form of exercise. There were no significant beta-blockade effects. Torque output at 10 Hz was still reduced up to 10 min post-exercise. In contrast, 100 Hz torque output recovered by 5 min post-exercise. The changes in tetanic responses were qualitatively similar with intact circulation and with circulatory occlusion. In the tibialis anterior muscle, the effects of fatiguing exercise are not accentuated by beta-blockade. These data in the TA are notably different from those in the triceps surae, where greater fatigue has been shown with beta-blockade.     

Role of limb movement in the modulation of motor unit discharge rate during fatiguing contractions

Motor unit firing rates of the triceps brachii muscle have been shown to decline during sustained isometric contractions, but not if the fatiguing contraction incorporates arm movements. The purpose of this study was to determine the impact of the actual physical displacement of the limb on the maintenance of motor unit discharge rate during dynamic muscle fatigue. An isometric force pulse paradigm was used to recreate the motor unit activity patterns that occur during a dynamic contraction. With this paradigm, the variable force output that would occur during a dynamic contraction remained intact, but the movement of the limb was eliminated. Motor unit firing rates declined in the isometric force pulse protocol. Thus, factors related to the actual movement of the limb appear to enable the maintenance of motor unit discharge rates during fatigue.     

Effect of low frequency fatigue on human muscle strength and fatigability during subsequent stimulated activity

Summary Fatiguing contractions of the adductor pollicis muscle were produced by intermittent supramaximal stimulation of the ulnar nerve in a set frequency pattern, in six normal subjects. At the end of an initial fatiguing contraction series, low frequency fatigue (LFF) had been induced and persisted at 15 min of recovery. Stimulated fatiguing activity was then repeated in an identical fashion to the initial series. At high frequencies, declines in force were similar for both series. At low frequencies, declines in force were greater during the second series despite similar changes in compound muscle action potential amplitude. This confirmation that LFF persists during subsequent stimulated activity, and reduces low but not high frequency fatigue resistance, suggests that the impaired endurance of fatigued muscle during voluntary activity primarily results from peripheral changes at low frequency. These findings also have implications for therapeutic electrical stimulation of muscle.     

Effects of contraction duration on low-frequency fatigue in voluntary and electrically induced exercise of quadriceps muscle in humans

The aims of this study were to investigate if low-frequency fatigue (LFF) dependent on the duration of repeated muscle contractions and to compare LFF in voluntary and electrically induced exercise. Male subjects performed three 9-min periods of repeated isometric knee extensions at 40% maximal voluntary contraction with contraction plus relaxation periods of 30 plus 60?s, 15 plus 30?s and 5 plus 10?s in protocols 1, 2 and 3, respectively. The same exercise protocols were repeated using feedback-controlled electrical stimulation at 40% maximal tetanic torque. Before and 15?min after each exercise period, knee extension torque at 1, 7, 10, 15, 20, 50 and 100?Hz was assessed. During voluntary exercise, electromyogram root mean square (EMG_rms) of the vastus lateralis muscle was evaluated. The 20-Hz torque:100-Hz torque (20:100?Hz torque) ratio was reduced more after electrically induced than after voluntary exercise (P?P?rms were greater in protocol 1 (P?相似文献   

Central fatigue during a long-lasting submaximal contraction of the triceps surae

Our purpose was to study central fatigue and its dependence on peripheral reflex inhibition during a sustained submaximal contraction of the triceps surae. In 11 healthy subjects, superimposed twitches, surface electromyograms (EMG) from the medial head of the gastrocnemius (MG) and soleus (SOL) muscles, maximal compound motor action potentials (M_max), tracking error and tremor were recorded during sustained fatiguing contractions at a torque level corresponding to 30% of maximal voluntary contraction (MVC). When the endurance limit (401±91 s) of the voluntary contraction (VC-I) was reached, the triceps surae could be electrically stimulated to the same torque level for an additional 1 min in 10 of the 11 subjects. These subjects were then able to continue the contraction voluntarily (voluntary contraction II, VC-II) for another 85±48 s. At the endurance limit of VC-I, the superimposed twitch was larger than during the unfatigued MVC, while there was no significant difference between the twitch at the endurance limit of VC-II and MVC. The EMG amplitude of both MG and SOL at the endurance limit of VC-I was significantly less than that during the MVC. While the EMG amplitude of MG increased further during VC-II, SOL EMG remained unchanged, neither muscle reaching their unfatigued MVC values. This difference was diminished for SOL by taking into account its decrease in M_max found during VC-II, and relative EMG levels approached their MVC values. These results clearly indicate that a higher voluntary muscle activation was achievable after 1 min of electrical muscle stimulation, which continued metabolic stress and contractile fatigue processes but allowed for supraspinal, muscle spindle and/or motoneuronal recovery. It is concluded that peripheral reflex inhibition of -motoneurons via small-diameter muscle afferents is of minor significance for the development of the central fatigue that was found to occur during the first voluntary contraction.     

Cortical and spinal modulation of antagonist coactivation during a submaximal fatiguing contraction in humans

This study investigates the control mechanisms at the cortical and spinal levels of antagonist coactivation during a submaximal fatiguing contraction of the elbow flexors at 50% of maximal voluntary contraction (MVC). We recorded motor-evoked potentials in the biceps brachii and triceps brachii muscles in response to magnetic stimulation of the motor cortex (MEP) and corticospinal tract (cervicomedullary motor-evoked potentials--CMEPs), as well as the Hoffmann reflex (H-reflex) and maximal M-wave (Mmax) elicited by electrical stimulation of the brachial plexus, before, during, and after the fatigue task. The results showed that although the coactivation ratio did not change at task failure, the MVC torque produced by the elbow flexors declined by 48% (P < 0.01) with no change in MVC torque for the elbow extensors. While the MEP and CMEP areas (normalized to Mmax) of the biceps brachii increased ( approximately 50%) over the first 40% of the time to task failure and then plateaued, both responses in the triceps brachii increased ( approximately 150-180%) gradually throughout the fatigue task. In contrast to the monotonic increase in the MEP and CMEP of the antagonist muscles, the H-reflex of the triceps brachii exhibited a biphasic modulation, increasing during the first part of the contraction before declining subsequently to 65% of its initial value. Collectively, these results suggest that the level of coactivation during a fatiguing contraction is mediated by supraspinal rather than spinal mechanisms and involves differential control of agonist and antagonist muscles.     

Comparison of brain activation after sustained non-fatiguing and fatiguing muscle contraction: a positron emission tomography study

The concept of fatigue refers to a class of acute effects that can impair motor performance, and not to a single mechanism. A great deal is known about the peripheral mechanisms underlying the process of fatigue, but our knowledge of the roles of the central structures in that process is still very limited. During fatigue, it has been shown that peripheral apparatus is capable of generating adequate force while central structures become insufficient/sub-optimal in driving them. This is known as central fatigue, and it can vary between muscles and different tasks. Fatigue induced by submaximal isometric contraction may have a greater central component than fatigue induced by prolonged maximal efforts. We studied the changes in regional cerebral blood flow (rCBF) of brain structures after sustained isometric muscle contractions of different submaximal force levels and of different durations, and compared them with the conditions observed when the sustained muscle contraction becomes fatiguing. Changes in cortical activity, as indicated by changes in rCBF, were measured using positron emission tomography (PET). Twelve subjects were studied under four conditions: (1) rest condition; (2) contraction of the m. biceps brachii at 30% of MVC, sustained for 60 s; (3) contraction at 30% of MVC, sustained for 120 s, and; (4) contraction at 50% of MVC, sustained for 120 s. The level of rCBF in the activated cortical areas gradually increased with the level and duration of muscle contraction. The fatiguing condition was associated with predominantly contralateral activation of the primary motor (MI) and the primary and secondary somatosensory areas (SI and SII), the somatosensory association area (SAA), and the temporal areas AA and AI. The supplementary motor area (SMA) and the cingula were activated bilaterally. The results show increased cortical activation, confirming that increased effort aimed at maintaining force in muscle fatigue is associated with increased activation of cortical neurons. At the same time, the activation spread to several cortical areas and probably reflects changes in both excitatory and inhibitory cortical circuits. It is suggested that further studies aimed at controlling afferent input from the muscle during fatigue may allow a more precise examination of the roles of each particular region involved in the processing of muscle fatigue.     

Neuromuscular fatigue during repeated exhaustive submaximal static contractions of knee extensor muscles in endurance-trained,power-trained and untrained men

The neural and muscular changes during fatigue produced in repeated submaximal static contractions of knee extensors were measured. Three groups of differently adapted male subjects (power-trained, endurance-trained and untrained, 15 in each) performed the exercise that consisted of 10 trials of submaximal static contractions at the level of 40% of maximal voluntary contraction (MVC) force till exhaustion with the inter-trial rest intervals of 1 min. MVC force, reaction time and patellar reflex time components before and after the fatiguing exercise and following 5, 10 and 15 min of recovery were recorded. Endurance-trained athletes had a significantly longer holding times for all the 10 trials compared with power-trained athletes and untrained subjects. However, no significant differences in static endurance between power-trained athletes and untrained subjects were noted. The fatigue test significantly prolonged the time between onset of electrical and mechanical activity (electromechanical delay) in voluntary and reflex contractions. The electromechanical delay in voluntary contraction condition for power-trained and untrained subjects and in reflex condition for endurance-trained subjects had not recovered 15 min after cessation of exercise. No significant changes in the central component of visual reaction time (premotor time of MVC) and latency of patellar reflex were noted after fatiguing static exercise. It is concluded, that in this type of exercise the fatigue development may be largely owing to muscle contractile failure.     

Reflex inhibition during muscle fatigue in endurance-trained and sedentary individuals

Reflex inhibition of the motoneuron pool following fatiguing contractions may be mediated by the build-up of byproducts of fatigue. Endurance training is accompanied by neuromuscular adaptations that would alter the production and/or clearance of metabolic substrates. The purpose of the study was to determine the extent of reflex inhibition during and after fatigue in endurance-trained individuals compared to sedentary controls. Subjects produced isometric ankle plantarflexion contractions at 30% of maximal voluntary contraction (MVC) until their MVC torque declined by 30%. H-reflexes were measured during a brief rest period every 3 min as well as superimposed upon the contraction every minute. Both groups of subjects experienced a similar amount of reflex inhibition by the end of the fatiguing protocol, although the endurance time was twice as long for the endurance-trained subjects. The endurance-trained subjects showed a greater reduction in H-reflex amplitude early in the fatiguing protocol compared to the sedentary subjects. These experiments have demonstrated that the neuromuscular processes associated with fatigue-related reflex inhibition must be multi-faceted and cannot be explained solely by small-diameter afferents responding to the byproducts of muscle contraction. Electronic Publication     

Influence of fatigue on hand muscle coordination and EMG-EMG coherence during three-digit grasping

Fingertip force control requires fine coordination of multiple hand muscles within and across the digits. While the modulation of neural drive to hand muscles as a function of force has been extensively studied, much less is known about the effects of fatigue on the coordination of simultaneously active hand muscles. We asked eight subjects to perform a fatiguing contraction by gripping a manipulandum with thumb, index, and middle fingers while matching an isometric target force (40% maximal voluntary force) for as long as possible. The coordination of 12 hand muscles was quantified as electromyographic (EMG) muscle activation pattern (MAP) vector and EMG-EMG coherence. We hypothesized that muscle fatigue would cause uniform changes in EMG amplitude across all muscles and an increase in EMG-EMG coherence in the higher frequency bands but with an invariant heterogeneous distribution across muscles. Muscle fatigue caused a 12.5% drop in the maximum voluntary contraction force (P < 0.05) at task failure and an increase in the SD of force (P < 0.01). Although EMG amplitude of all muscles increased during the fatiguing contraction (P < 0.001), the MAP vector orientation did not change, indicating that a similar muscle coordination pattern was used throughout the fatiguing contraction. Last, EMG-EMG coherence (0-35 Hz) was significantly greater at the end than at the beginning of the fatiguing contraction (P < 0.01) but was heterogeneously distributed across hand muscles. These findings suggest that similar mechanisms are involved for modulating and sustaining digit forces in nonfatiguing and fatiguing contractions, respectively.     

Dynamic stability control in forward falls: postural corrections after muscle fatigue in young and older adults

Many studies report that muscle strength loss may alter the human system’s capacity to generate rapid force for balance corrections after perturbations, leading to deficient recovery behaviours. Yet little is known regarding the effect of modifications in the neuromuscular system induced by fatigue on dynamic stability control during postural perturbations. This study investigates the effect of muscle strength decline induced by fatiguing contractions on the dynamic stability control of young and older adults during forward falls. Eleven young and eleven older male adults had to regain balance after sudden falls before and after submaximal fatiguing knee extension–flexion contractions. Young subjects had a higher margin of stability than older ones before and after the fatiguing task. This reflects their enhanced ability in using mechanisms for maintaining dynamic stability (i.e. a greater base of support). The margin of stability, the boundary of the base of support and the position of the extrapolated centre of mass, remained unaffected by the reduction in muscle strength induced by the fatiguing contractions, indicating an appropriate adjustment of the motor commands to compensate the deficit in muscle strength. Both young and older adults were able to counteract the decreased horizontal ground reaction forces after the fatiguing task by flexing their knee to a greater extent, leading to similar decreases in the horizontal velocity of centre of mass as in the pre fatigue condition. The results demonstrate the ability of the central nervous system to rapidly modify the execution of postural corrections including mechanisms for maintaining dynamic stability.     

Neck muscle fatigue affects postural control in man

We hypothesised that, since anomalous neck proprioceptive input can produce perturbing effects on posture, neck muscle fatigue could alter body balance control through a mechanism connected to fatigue-induced afferent inflow. Eighteen normal subjects underwent fatiguing contractions of head extensor muscles. Sway during quiet stance was recorded by a dynamometric platform, both prior to and after fatigue and recovery, with eyes open and eyes closed. After each trial, subjects were asked to rate their postural control. Fatigue was induced by having subjects stand upright and exert a force corresponding to about 35% of maximal voluntary effort against a device exerting a head-flexor torque. The first fatiguing period lasted 5 min (F1). After a 5-min recovery period (R1), a second period of fatiguing contraction (F2) and a second period of recovery (R2) followed. Surface EMG activity from dorsal neck muscles was recorded during the contractions and quiet stance trials. EMG median frequency progressively decreased and EMG amplitude progressively increased during fatiguing contractions, demonstrating that muscle fatigue occurred. After F1, subjects swayed to a larger extent compared with control conditions, recovering after R1. Similar findings were obtained after F2 and after R2. Although such behaviour was detectable under both visual conditions, the effects of fatigue reached significance only without vision. Subjective scores of postural control diminished when sway increased, but diminished more, for equal body sway, after fatigue and recovery. Contractions of the same duration, but not inducing EMG signs of fatigue, had much less influence on body sway or subjective scoring. We argue that neck muscle fatigue affects mechanisms of postural control by producing abnormal sensory input to the CNS and a lasting sense of instability. Vision is able to overcome the disturbing effects connected with neck muscle fatigue.     

Pattern of descending excitation of presumed propriospinal neurones at the onset of voluntary movement in humans

Mazevet , D. & Pierrot -Deseilligny , E. 1994. Pattern of descending excitation of presumed propriospinal neurones at the onset of voluntary movement in humans. Acta Physiol Scand 150, 27–38. Received 2 April 1993, accepted 30 July 1993. ISSN 0001–6772. Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de ? Hôpital, 75651 Paris cedex 13, France. The pattern of activation of presumed ‘propriospinal’ neurones was investigated in human subjects during phasic voluntary contractions of one of the following muscles: biceps, triceps, flexor carpi radialis (FCR), flexor carpi ulnaris (FCU) and extensor carpi radialis (ECR). Changes in the amplitude of the H reflex (FCR, ECR), or the tendon jerk (biceps, triceps) were used to assess the excitability of the corresponding motorneurone pools after conditioning stimulation. Conditioning stimuli were applied to the musculo-cutaneous, triceps and ulnar nerves. In most cases reflex facilitation was not observed at rest and was only disclosed at the onset of contraction. The characteristics of this facilitation (3–4 ms central delay, short duration, low threshold, depression when the afferent input was increased) are consistent with those previously attributed to ‘propriospinal’ excitation. It is argued that the contraction-associated facilitation was descending in origin. The descending facilitation of the ‘propriospinal’ system had a characteristic pattern in that the pathways selected by higher centres were those receiving the afferent feedback from the contracting muscle. These results provide further insight into the organization of human ‘propriospinal’ pathways: (1) it is confirmed that afferents from each muscle activate a specific subset of neurones; and (2) it is suggested that the projections of each subset are divergent, implying that individual neurones project onto diverse motor nuclei, an organization that would favour the coordination of multi-joint movements. Such an organization is discussed in relation to the possible role of the propriospinal system in the control of normal human upper limb movements.