Reduced Maximal Force during Acute Anterior Knee Pain Is Associated with Deficits in Voluntary Muscle Activation
Identifieur interne : 001834 ( Main/Exploration ); précédent : 001833; suivant : 001835Reduced Maximal Force during Acute Anterior Knee Pain Is Associated with Deficits in Voluntary Muscle Activation
Auteurs : Sauro Salomoni [Australie] ; Kylie Tucker [Australie] ; François Hug [Australie, France] ; Megan Mcphee [Australie] ; Paul Hodges [Australie]Source :
- PLoS ONE [ 1932-6203 ] ; 2016.
Descripteurs français
- KwdFr :
- MESH :
- physiopathologie : Douleur aigüe, Genou, Muscles squelettiques.
- Adulte, Anxiété, Contraction isométrique, Contrainte mécanique, Femelle, Force musculaire, Humains, Jeune adulte, Mâle, Peur, Volontaires sains, Électromyographie, Études croisées.
English descriptors
- KwdEn :
- MESH :
- physiopathology : Acute Pain, Knee, Muscle, Skeletal.
- Adult, Anxiety, Cross-Over Studies, Electromyography, Fear, Female, Healthy Volunteers, Humans, Isometric Contraction, Male, Muscle Strength, Stress, Mechanical, Young Adult.
Abstract
Although maximal voluntary contraction (MVC) force is reduced during pain, studies using interpolated twitch show no consistent reduction of voluntary muscle drive. The present study aimed to test if the reduction in MVC force during acute experimental pain could be explained by increased activation of antagonist muscles, weak voluntary activation at baseline, or changes in force direction. Twenty-two healthy volunteers performed maximal voluntary isometric knee extensions before, during, and after the effects of hypertonic (pain) and isotonic (control) saline injections into the infrapatellar fat pad. The MVC force, voluntary activation, electromyographic (EMG) activity of agonist, antagonist, and auxiliary (hip) muscles, and pain cognition and anxiety scores were recorded. MVC force was 9.3% lower during pain than baseline (p < 0.001), but there was no systematic change in voluntary activation. Reduced MVC force during pain was variable between participants (SD: 14%), and was correlated with reduced voluntary activation (r = 0.90), baseline voluntary activation (r = − 0.62), and reduced EMG amplitude of agonist and antagonist muscles (all r > 0.52), but not with changes in force direction, pain or anxiety scores. Hence, reduced MVC force during acute pain was mainly explained by deficits in maximal voluntary drive.
Url:
DOI: 10.1371/journal.pone.0161487
PubMed: 27559737
PubMed Central: 4999173
Affiliations:
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Le document en format XML
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<term>Electromyography</term>
<term>Fear</term>
<term>Female</term>
<term>Healthy Volunteers</term>
<term>Humans</term>
<term>Isometric Contraction</term>
<term>Knee (physiopathology)</term>
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<term>Femelle</term>
<term>Force musculaire</term>
<term>Genou (physiopathologie)</term>
<term>Humains</term>
<term>Jeune adulte</term>
<term>Muscles squelettiques (physiopathologie)</term>
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<term>Peur</term>
<term>Volontaires sains</term>
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<term>Cross-Over Studies</term>
<term>Electromyography</term>
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<front><div type="abstract" xml:lang="en"><p>Although maximal voluntary contraction (MVC) force is reduced during pain, studies using interpolated twitch show no consistent reduction of voluntary muscle drive. The present study aimed to test if the reduction in MVC force during acute experimental pain could be explained by increased activation of antagonist muscles, weak voluntary activation at baseline, or changes in force direction. Twenty-two healthy volunteers performed maximal voluntary isometric knee extensions before, during, and after the effects of hypertonic (pain) and isotonic (control) saline injections into the infrapatellar fat pad. The MVC force, voluntary activation, electromyographic (EMG) activity of agonist, antagonist, and auxiliary (hip) muscles, and pain cognition and anxiety scores were recorded. MVC force was 9.3% lower during pain than baseline (p < 0.001), but there was no systematic change in voluntary activation. Reduced MVC force during pain was variable between participants (SD: 14%), and was correlated with reduced voluntary activation (r = 0.90), baseline voluntary activation (r = − 0.62), and reduced EMG amplitude of agonist and antagonist muscles (all r > 0.52), but not with changes in force direction, pain or anxiety scores. Hence, reduced MVC force during acute pain was mainly explained by deficits in maximal voluntary drive.</p>
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</div1>
</back>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
<region><li>Pays de la Loire</li>
</region>
<settlement><li>Nantes</li>
</settlement>
</list>
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<name sortKey="Hug, Francois" sort="Hug, Francois" uniqKey="Hug F" first="François" last="Hug">François Hug</name>
<name sortKey="Mcphee, Megan" sort="Mcphee, Megan" uniqKey="Mcphee M" first="Megan" last="Mcphee">Megan Mcphee</name>
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<country name="France"><region name="Pays de la Loire"><name sortKey="Hug, Francois" sort="Hug, Francois" uniqKey="Hug F" first="François" last="Hug">François Hug</name>
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</record>
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