Key points During fatiguing contractions, the output of the motoneurone pool decreases despite maximal voluntary drive. The precise mechanism for this reduction is unknown. To assess whether changes in the intrinsic behaviour of motoneurones due to their repetitive activity during maximal voluntary contractions are responsible for the reduction of motoneurone output, we measured the recurrent motoneurone discharge produced antidromically by supramaximal stimulation of peripheral nerve. These recurrent responses are known as F-waves when measured in the EMG. Maximal voluntary contractions strongly depressed the probability of occurrence of F-waves and their area when measured at rest after the contractions. The strength and time course of the depression increased with the duration of the contraction for the abductor digiti minimi muscle. Moreover, the observed depression of F-waves could not be explained by altered excitability of the peripheral motor axons. Hence, we propose that the depression in F-waves is caused by activity-dependent changes at the soma or the initial segment and that this may contribute to central fatigue. Abstract Despite maximal voluntary effort, the output of human motoneurone pools diminishes during fatigue. To assess motoneurone behaviour, we measured recurrent discharges evoked antidromically by supramaximal nerve stimulation after isometric maximal voluntary contractions (MVCs). They were measured as F-waves in the electromyographic activity (EMG). Supramaximal stimuli to the common peroneal and ulnar nerves evoked F-waves at rest before and after MVCs in tibialis anterior (TA) and abductor digit minimi (ADM), respectively. F-waves were depressed immediately after a sustained MVC. For TA, the size and time course of depression of the F-wave area (26 +/- 13%; mean +/- SD; P= 0.007) and persistence (similar to 20%) were similar after a 10-s or 1-min MVC. For ADM, the decline in F-wave area (39.8 +/- 19.6%; P < 0.01) was similar after the two contractions but the decline in persistence (probability of occurrence) of the F-wave differed (14.6 +/- 10.5% and 32.5 +/- 17.1% after 10-s and 1-min MVCs respectively). Comparison of a very long (2-min) with a very short (2-s) MVC in ADM showed that the depression of F-wave area, as well as persistence, was greater after the longer contraction. This suggests, at least for ADM, that the depression is related to the duration of voluntary activity and that the decrease in F-waves could contribute to central fatigue. To examine whether changes in motor axon excitability caused the depression, we measured compound muscle action potentials (M-waves) to submaximal stimulation of the ulnar nerve after a 2-s and 2-min MVC. Submaximal M-waves were not depressed after a 2-s MVC. They were depressed by a 2-min MVC, but the time course of depression of the F- and M-waves differed. Thus, depression of F-waves does not simply reflect reduced excitability of peripheral motor axons. Hence, we propose that activity-dependent changes at the soma or the initial segment depress the recurrent discharge of human motoneurones and that this may contribute to central fatigue.
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