The activity of 50 single motor units was recorded in the biceps brachii muscle of human subjects while they performed submaximal isometric elbow flexion contractions that were sustained to induce fatigue. The purposes of this study were to examine the influence of fatigue on motor unit threshold force and to determine the relationship between the threshold force of recruitment and the initial interimpulse interval on the discharge rates of single motor units during a fatiguing contraction. The discharge rate of most motor units that were active from the beginning of the contraction declined during the fatiguing contraction, whereas the discharge rates of most newly recruited units were either constant or increased slightly. The absolute threshold forces of recruitment and derecruitment decreased, and the variability of interimpulse intervals increased after the fatigue task. The change in motor unit discharge rate during the fatigue task was related to the initial rate, but the direction of the change in discharge rate could not be predicted from the threshold force of recruitment or the variability in the interimpulse intervals. The discharge rate of most motor units declined despite an increase in the excitatory drive to the motoneuron pool during the fatigue task.

SUMMARY1. Previous work has shown that the H reflex excitability of the human soleus motoneurones is reduced during fatigue and is accompanied by a corresponding decrease in electromyographic (EMG) activity during maximal voluntary contractions. These findings were consistent with the existence of a reflex whereby xmotoneurones are inhibited by sensory input from the fatigued muscle.2. To elucidate the contribution of different-sized afferents in such reflex inhibition, compression of the sciatic nerve was used in an attempt to block large myelinated afferents prior to fatigue. 3. Fatigue of the soleus muscle was induced under ischaemic conditions by intermittent electrical stimulation at 15 Hz in ten healthy subjects. These subjects also participated in a control test in which the compression block was followed by ischaemia without fatigue.4. Following nerve compression alone, both the mean maximal plantarflexion torque and the associated EMG for all ten subjects declined by 18-8+ 162% (S.D.) and 13 4 + 17 2 %, respectively. 5. Following fatigue, there were five subjects in whom the large afferents remained blocked and the experimental findings were consistent with the existence of reflex inhibition during fatigue. The mean maximal plantarflexion torque decreased further by 36 2 + 7 6 % from the value following the compression block compared to a decrease of 5-0 + 9-9 % in the ischaemia control. The mean EMG associated with these contractions also decreased from post-block values by 56 8 + 19-6 % following fatigue and by only 6-4 + 8-0 % following ischaemia alone.6. The peripheral excitability of the neuromuscular junction and muscle fibre membrane was adequate following fatigue as evidenced by only modest changes in the M wave (muscle compound action potential). The descending motor drive was deemed sufficient because of the absence of any large interpolated twitches superimposed upon the maximal voluntary contraction in all but two subjects.7. The declines in maximal plantarflexion torque and the associated EMG activity were very similar to those found in a previous study in which the sensory input was unaltered. The findings demonstrated that any reflex inhibition of the o-motoneurone

SUMMARY1. Human soleus muscles were fatigued under ischaemic conditions by intermittent stimulation at 15 Hz. When maximal voluntary plantarflexion was then attempted, the loss of torque was found to be associated with a reduction in voluntary EMG activity.2. The decrease in EMG activity could not have been due to 'exhaustion' of descending motor drive in the central nervous system since fatigue had been induced by electrical stimulation of peripheral nerve fibres. Similarly, the decrease could not be explained by changes at the neuromuscular junction or muscle fibre membrane, since changes in the M wave (evoked muscle compound action potential) were relatively modest.3. When the excitability of the soleus motoneurones was tested during fatigue, using the H (Hoffmann) reflex, it was found to be significantly reduced. Control experiments with ischaemia or electrical stimulation, but without fatigue, failed to demonstrate any significant effects on reflex excitability.4. The findings in this study favour the concept of reflex inhibition of oz-motoneurones during fatigue.

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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.

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