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Clin Exp Pharmacol Physiol. 2006 Apr;33(4):400-5.

Evidence for a supraspinal contribution to human muscle fatigue.

Author information

1
Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, New South Wales, Australia. jl.taylor@unsw.edu.au

Abstract

1. Muscle fatigue can be defined as any exercise-induced loss of ability to produce force with a muscle or muscle group. It involves processes at all levels of the motor pathway between the brain and the muscle. Central fatigue represents the failure of the nervous system to drive the muscle maximally. It is defined as a progressive exercise-induced reduction in voluntary activation or neural drive to the muscle. Supraspinal fatigue is a component of central fatigue. It can be defined as an exercise-induced decline in force caused by suboptimal output from the motor cortex. 2. When stimulus intensity is set appropriately, transcranial magnetic stimulation (TMS) over the motor cortex during an isometric maximal voluntary contraction (MVC) of the elbow flexors commonly evokes a small twitch-like increment in flexion force. This increment indicates that, despite the subject's maximal effort, motor cortical output at the moment of stimulation was not maximal and was not sufficient to drive the motoneurons to produce maximal force from the muscle. An exercise-induced increase in this increment demonstrates supraspinal fatigue. 3. Supraspinal fatigue has been demonstrated during fatiguing sustained and intermittent maximal and submaximal contractions of the elbow flexors where it accounts for about one-quarter of the loss of force of fatigue. It is linked to activity and the development of fatigue in the tested muscles and is little influenced by exercise performed by other muscles. 4. The mechanisms of supraspinal fatigue are unclear. Although changes in the behaviour of cortical neurons and spinal motoneurons occur during fatigue, they can be dissociated from supraspinal fatigue. One factor that may contribute to supraspinal fatigue is the firing of fatigue-sensitive muscle afferents that may act to impair voluntary descending drive.

[Indexed for MEDLINE]

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