Reduced Maximal Force during Acute Anterior Knee Pain Is Associated with Deficits in Voluntary Muscle Activation.
Identifieur interne : 001989 ( PubMed/Curation ); précédent : 001988; suivant : 001990Reduced 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] ; 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.
DOI: 10.1371/journal.pone.0161487
PubMed: 27559737
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Voluntary Muscle Activation.</title><author><name sortKey="Salomoni, Sauro" sort="Salomoni, Sauro" uniqKey="Salomoni S" first="Sauro" last="Salomoni">Sauro Salomoni</name><affiliation wicri:level="1"><nlm:affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane</wicri:regionArea></affiliation></author><author><name sortKey="Tucker, Kylie" sort="Tucker, Kylie" uniqKey="Tucker K" first="Kylie" last="Tucker">Kylie Tucker</name><affiliation wicri:level="1"><nlm:affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane</wicri:regionArea></affiliation></author><author><name sortKey="Hug, Francois" sort="Hug, Francois" uniqKey="Hug F" first="François" last="Hug">François Hug</name><affiliation wicri:level="1"><nlm:affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane</wicri:regionArea></affiliation></author><author><name sortKey="Mcphee, Megan" sort="Mcphee, Megan" uniqKey="Mcphee M" first="Megan" last="Mcphee">Megan Mcphee</name><affiliation wicri:level="1"><nlm:affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane</wicri:regionArea></affiliation></author><author><name sortKey="Hodges, Paul" sort="Hodges, Paul" uniqKey="Hodges P" first="Paul" last="Hodges">Paul Hodges</name><affiliation wicri:level="1"><nlm:affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane</wicri:regionArea></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Pain (physiopathology)</term><term>Adult</term><term>Anxiety</term><term>Cross-Over Studies</term><term>Electromyography</term><term>Fear</term><term>Female</term><term>Healthy Volunteers</term><term>Humans</term><term>Isometric Contraction</term><term>Knee (physiopathology)</term><term>Male</term><term>Muscle Strength</term><term>Muscle, Skeletal (physiopathology)</term><term>Stress, Mechanical</term><term>Young Adult</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Anxiété</term><term>Contraction isométrique</term><term>Contrainte mécanique</term><term>Douleur aigüe (physiopathologie)</term><term>Femelle</term><term>Force musculaire</term><term>Genou (physiopathologie)</term><term>Humains</term><term>Jeune adulte</term><term>Muscles squelettiques (physiopathologie)</term><term>Mâle</term><term>Peur</term><term>Volontaires sains</term><term>Électromyographie</term><term>Études croisées</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Douleur aigüe</term><term>Genou</term><term>Muscles squelettiques</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Acute Pain</term><term>Knee</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Anxiety</term><term>Cross-Over Studies</term><term>Electromyography</term><term>Fear</term><term>Female</term><term>Healthy Volunteers</term><term>Humans</term><term>Isometric Contraction</term><term>Male</term><term>Muscle Strength</term><term>Stress, Mechanical</term><term>Young Adult</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Anxiété</term><term>Contraction isométrique</term><term>Contrainte mécanique</term><term>Femelle</term><term>Force musculaire</term><term>Humains</term><term>Jeune adulte</term><term>Mâle</term><term>Peur</term><term>Volontaires sains</term><term>Électromyographie</term><term>Études croisées</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27559737</PMID><DateCreated><Year>2016</Year><Month>08</Month><Day>26</Day></DateCreated><DateCompleted><Year>2017</Year><Month>08</Month><Day>07</Day></DateCompleted><DateRevised><Year>2017</Year><Month>08</Month><Day>07</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>8</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Reduced Maximal Force during Acute Anterior Knee Pain Is Associated with Deficits in Voluntary Muscle Activation.</ArticleTitle><Pagination><MedlinePgn>e0161487</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0161487</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Salomoni</LastName><ForeName>Sauro</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tucker</LastName><ForeName>Kylie</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The University of Queensland, School of Biomedical Sciences, Brisbane, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hug</LastName><ForeName>François</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University of Nantes, Laboratory "Motricité, Interactions, Performance" (EA 4334), Nantes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McPhee</LastName><ForeName>Megan</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hodges</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>The University of Queensland, Centre for Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>08</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Appl Physiol (1985). 2004 Jul;97(1):236-42</RefSource><PMID Version="1">15033969</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>BMC Musculoskelet Disord. 2011 Oct 12;12:230</RefSource><PMID 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MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001007" MajorTopicYN="N">Anxiety</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018592" MajorTopicYN="N">Cross-Over Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004576" MajorTopicYN="N">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005239" MajorTopicYN="N">Fear</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064368" MajorTopicYN="N">Healthy Volunteers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007537" MajorTopicYN="Y">Isometric Contraction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007717" MajorTopicYN="N">Knee</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053580" MajorTopicYN="N">Muscle Strength</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="N">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4999173</OtherID><CoiStatement>The authors have declared that no competing interests 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|clé= pubmed:27559737
|texte= Reduced Maximal Force during Acute Anterior Knee Pain Is Associated with Deficits in Voluntary Muscle Activation.
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