Literature DB >> 27605530

Maximal intermittent contractions of the first dorsal interosseous inhibits voluntary activation of the contralateral homologous muscle.

Justin J Kavanagh1, Matthew R Feldman2, Michael J Simmonds2.   

Abstract

The aim of this study was to investigate how maximal intermittent contractions for a hand muscle influence cortical and reflex activity, as well as the ability to voluntarily activate, the homologous muscle in the opposite limb. Twelve healthy subjects (age: 24 ± 3 years, all right hand dominant) performed maximal contractions of the dominant limb first dorsal interosseous (FDI), and activity of the contralateral FDI was examined in a series of experiments. Index finger abduction force, FDI EMG, motor evoked potentials and heteronomous reflexes were obtained from the contralateral limb during brief non-fatiguing contractions. The same measures, as well as the ability to voluntarily activate the contralateral FDI, were then assessed in an extended intermittent contraction protocol that elicited fatigue. Brief contractions under non-fatigued conditions increased index finger abduction force, FDI EMG, and motor evoked potential amplitude of the contralateral limb. However, when intermittent maximal contractions were continued until fatigue, there was an inability to produce maximal force with the contralateral limb (~30%) which was coupled to a decrease in the level of voluntary activation (~20%). These declines were present without changes in reflex activity, and regardless of whether cortical or motor point stimulation was used to assess voluntary activation. It is concluded that performing maximal intermittent contractions with a single limb causes an inability of the CNS to maximally drive the homologous muscle of the contralateral limb. This was, in part, mediated by mechanisms that involve the motor cortex ipsilateral to the contracting limb.
Copyright © 2016, Journal of Neurophysiology.

Entities:  

Keywords:  Fatigue; crossed-effects; ipsilateral motor cortex; motor control

Year:  2016        PMID: 27605530      PMCID: PMC5110640          DOI: 10.1152/jn.00367.2016

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  32 in total

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