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Journal ArticleDOI

Spinal and Supraspinal Factors in Human Muscle Fatigue

Simon C. Gandevia
- 10 Jan 2001 - 
- Vol. 81, Iss: 4, pp 1725-1789
TLDR
Evidence for "central" fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it.
Abstract
Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal cha...

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Citations
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Journal ArticleDOI

Skeletal Muscle Fatigue: Cellular Mechanisms

TL;DR: Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.
Journal ArticleDOI

Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production

TL;DR: O Ongoing research continues to probe the mechanisms by which oxidants influence skeletal muscle contractile properties and to explore interventions capable of protecting muscle from oxidant-mediated dysfunction.
Journal ArticleDOI

The Proprioceptive Senses: Their Roles in Signaling Body Shape, Body Position and Movement, and Muscle Force

TL;DR: Proprioceptive senses, particularly of limb position and movement, deteriorate with age and are associated with an increased risk of falls in the elderly and the more recent information available on proprioception has given a better understanding of the mechanisms underlying these senses.
Journal ArticleDOI

Muscle damage from eccentric exercise: mechanism, mechanical signs, adaptation and clinical applications

TL;DR: The ability of muscle to rapidly adapt following the damage from eccentric exercise raises the possibility of clinical applications of mild eccentric exercise, such as for protecting a muscle against more major injuries.
Journal ArticleDOI

The adaptations to strength training : morphological and neurological contributions to increased strength.

TL;DR: The gains in strength with HRST are undoubtedly due to a wide combination of neurological and morphological factors, although there is contrary evidence suggesting no change in cortical or corticospinal excitability.
References
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Journal ArticleDOI

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Fred Plum
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TL;DR: This is the first volume of the proposed many-sectioned "Handbook" in which the American Physiological Society intends to present comprehensively the entire field of physiology.
Journal ArticleDOI

Handbook of Sensory Physiology

Journal Article

Muscle and tendon: properties, models, scaling, and application to biomechanics and motor control

TL;DR: Their integrated ability to generate force statically and dynamically is studied by formulating a generic model of the "musculotendon actuator", which has only one parameter, the ratio of tendon length at rest to muscle fiberlength at rest.
Journal ArticleDOI

Corticocortical inhibition in human motor cortex.

TL;DR: In ten normal volunteers, a transcranial magnetic or electric stimulus that was subthreshold for evoking an EMG response in relaxed muscles was used to condition responses evoked by a later, suprathreshold magnetic orElectric test shock to suggest that the suppression was produced by an action on cortical, rather than spinal excitability.
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