Document Detail

Impairment of neuromuscular propagation during human fatiguing contractions at submaximal forces.
MedLine Citation:
PMID:  8387589     Owner:  NLM     Status:  MEDLINE    
1. The purpose of the study was to examine the dependence of neuromuscular propagation impairment on the level of isometric force sustained to the endurance limit. The task involved human volunteers sustaining a submaximal abduction force with the index finger by activating the first dorsal interosseous muscle as long as possible. 2. The submaximal force was sustained at one of three levels (20, 35 or 65% of maximum) by increasing motor unit activity, as indicated by the electromyogram (EMG), during the fatiguing contraction. Although the EMG increased during the fatiguing contraction, the EMG was significantly less than maximum at the endurance limit for all subjects (deficit of 19-55% of maximum). This deficit was inversely related to the level of the sustained submaximal force. 3. The maximum voluntary contraction and twitch forces were significantly reduced following the fatiguing contraction. As with the EMG, the degree of force reduction was greatest for the subjects who sustained the low target forces. 4. The fatiguing contraction caused a 12-23% decline in M wave amplitude, a 33-51% increase in M wave duration, and no change in M wave area. The decline in M wave amplitude, which is an index of neuromuscular propagation impairment, was greatest among the subjects who sustained the low target forces. 5. The mean power frequency of the EMG decreased by a similar amount (50-57%) during the fatiguing contraction for all three groups of subjects. 6. A model representing the interaction of processes that enhance and impair force was developed to explain the recovery of twitch force following the sustained contractions at different target forces. 7. We conclude that the fatigue experienced by a subject when force is sustained at a submaximal value does involve an impairment of neuromuscular propagation. This impairment is one factor that limits muscle excitation during a submaximal, fatiguing contraction and contributes to the diminished force capability by the end of the fatigue task.
A J Fuglevand; K M Zackowski; K A Huey; R M Enoka
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  460     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  1993 Jan 
Date Detail:
Created Date:  1993-06-10     Completed Date:  1993-06-10     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  549-72     Citation Subset:  IM    
Department of Exercise and Sport Sciences, University of Arizona, Tucson 85721.
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MeSH Terms
Fatigue / physiopathology*
Muscle Contraction / physiology*
Neuromuscular Junction / physiology*
Physical Endurance / physiology
Synaptic Transmission / physiology*
Transcutaneous Electric Nerve Stimulation
Grant Support

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