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Cited by 1,050

The DOI matches its Crossref record.

Changes in muscle contractile properties and neural control during human muscular fatigue

Bigland‐Ritchie, B., Woods, J. J.·1984·Muscle & Nerve
DOI 10.1002/mus.880070902
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Abstract

The factors limiting force production and exercise endurance time have been briefly described, together with some of the changes occurring at various sites within the muscle and central nervous system. Evidence is presented that, in fatigue of sustained maximal voluntary contractions (MVC) executed by well‐motivated subjects, the reduction in force generating capacity need not be due to a decline in central nervous system (CNS) motor drive or to failing neuromuscular transmission, but can be attributed solely to contractile failure of the muscles involved. However, despite this conclusion, both the integrated electromyogram (EMG) and the mean firing rate of individual motor units do decline progressively during sustained MVC. This, however, does not necessarily result in loss of force since the parallel slowing of muscle contractile speed reduces tetanic fusion frequency. It is suggested that the range of motoneuron firing rates elicited by voluntary effort is regulated and limited for each muscle to the minimum required for maximum force generation, thus preventing neuromuscular transmission failure and optimizing motor control. Such a CNS regulating mechanism would probably require some reflex feedback from the muscle.

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Metadata

Authors
Bigland‐Ritchie, B., & Woods, J. J.
Venue
Muscle & Nerve
Publisher
Wiley
Published
1984-12
Volume
7
Issue
9
Pages
691-699
ISSN
  • 0148-639X (ISSN-L)
  • 1097-4598
DOI
10.1002/mus.880070902
OpenAlex
W2112718015
Cited by
1,050
References
0
FWCI
6.81
Type
journal article
Language
en
Open access
closed

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.