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Acta Physiol Scand Suppl. 1986;556:137-48.

Fatigue of submaximal static contractions.


Experiments are described which suggest that the loss of force generating capacity seen during fatigue from intermittent, submaximal voluntary contractions of the quadriceps muscle cannot be explained by any of the usual factors thought to be responsible for fatigue. During the first 30 min of intermittent contractions at 30% MVC the force generated periodically by a brief test train of 50 Hz stimulation and by brief maximal voluntary contractions both declined by 50%. Yet no significant changes were seen in the muscle lactate, ATP or phosphocreatine. Glycogen depletion was confined only to the type I and type IIA fibres, with less than 10% totally depleted. The depletion patterns indicated that the type IIAB and type IIB motor units were not recruited during the first 30 min. The central nervous system appeared to remain capable of generating full muscle activation since the force from maximal voluntary efforts declined in parallel with that from 50 Hz stimulation. We suggest that, in this type of fatigue, the loss of force may be largely due to impaired excitation/contraction coupling. This possibility is supported by the disproportionate depression of the twitches recorded between contractions compared with that from 50 Hz stimulation (low frequency fatigue). The single unit EMG recordings suggest that, in sustained and repeated submaximal contractions, muscle contractile failure is compensated by recruitment of additional motor units rather than by rate coding of those already active. During intermittent contractions large increases in the surface EMG were associated with only modest increases in firing rates. In sustained contractions when the EMG was held constant the discharge rates declined in parallel with the force. In constant force contractions involving about 35% muscle contractile failure no changes in discharge rates were seen despite substantial increases in EMG.

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