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New insights on contraction efficiency in patients with Duchenne muscular dystrophy

Identifieur interne : 001767 ( Pmc/Curation ); précédent : 001766; suivant : 001768

New insights on contraction efficiency in patients with Duchenne muscular dystrophy

Auteurs : Lilian Lacourpaille [France] ; François Hug [France, Australie] ; Arnaud Guével [France] ; Yann Péréon [France] ; Armelle Magot [France] ; Jean-Yves Hogrel [France] ; Antoine Nordez [France]

Source :

RBID : PMC:4157166

Abstract

The decrease in muscle strength in patients with Duchenne muscular dystrophy (DMD) is mainly explained by a decrease in the number of active contractile elements. Nevertheless, it is possible that other electrochemical and force transmission processes may contribute. The present study aimed to quantify the effect of DMD on the relative contribution of electrochemical and force transmission components of the electromechanical delay (i.e., time lag between the onset of muscle activation and force production) in humans using very high frame rate ultrasound. Fourteen patients with DMD and thirteen control subjects underwent two electrically evoked contractions of the biceps brachii with the ultrasound probe over the muscle belly. The electromechanical delay was significantly longer in DMD patients compared with controls (18.5 ± 3.9 vs. 12.5 ± 1.4 ms, P < 0.0001). More precisely, DMD patients exhibited a longer delay between the onset of muscle fascicles motion and force production (13.6 ± 3.1 vs. 7.9 ± 2.0 ms, P < 0.0001). This delay was correlated to the chronological age of the DMD patients (r = 0.66; P = 0.01), but not of the controls (r = −0.45; P = 0.10). No significant difference was found for the delay between the onset of muscle stimulation and the onset of muscle fascicle motion. These results highlight the role of the alteration of muscle force transmission (delay between the onset of fascicle motion and force production) in the impairments of the contraction efficiency in patients with DMD.


Url:
DOI: 10.1152/japplphysiol.00544.2014
PubMed: 25103971
PubMed Central: 4157166

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<p>The decrease in muscle strength in patients with Duchenne muscular dystrophy (DMD) is mainly explained by a decrease in the number of active contractile elements. Nevertheless, it is possible that other electrochemical and force transmission processes may contribute. The present study aimed to quantify the effect of DMD on the relative contribution of electrochemical and force transmission components of the electromechanical delay (i.e., time lag between the onset of muscle activation and force production) in humans using very high frame rate ultrasound. Fourteen patients with DMD and thirteen control subjects underwent two electrically evoked contractions of the biceps brachii with the ultrasound probe over the muscle belly. The electromechanical delay was significantly longer in DMD patients compared with controls (18.5 ± 3.9 vs. 12.5 ± 1.4 ms,
<italic>P</italic>
< 0.0001). More precisely, DMD patients exhibited a longer delay between the onset of muscle fascicles motion and force production (13.6 ± 3.1 vs. 7.9 ± 2.0 ms,
<italic>P</italic>
< 0.0001). This delay was correlated to the chronological age of the DMD patients (
<italic>r</italic>
= 0.66;
<italic>P</italic>
= 0.01), but not of the controls (
<italic>r</italic>
= −0.45;
<italic>P</italic>
= 0.10). No significant difference was found for the delay between the onset of muscle stimulation and the onset of muscle fascicle motion. These results highlight the role of the alteration of muscle force transmission (delay between the onset of fascicle motion and force production) in the impairments of the contraction efficiency in patients with DMD.</p>
</div>
</front>
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<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">J Appl Physiol (1985)</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Appl. Physiol</journal-id>
<journal-id journal-id-type="hwp">jap</journal-id>
<journal-id journal-id-type="pmc">jap</journal-id>
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<title-group>
<article-title>New insights on contraction efficiency in patients with Duchenne muscular dystrophy</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Lacourpaille</surname>
<given-names>Lilian</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Hug</surname>
<given-names>François</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Guével</surname>
<given-names>Arnaud</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Péréon</surname>
<given-names>Yann</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Magot</surname>
<given-names>Armelle</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Hogrel</surname>
<given-names>Jean-Yves</given-names>
</name>
<xref ref-type="aff" rid="aff5">
<sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Nordez</surname>
<given-names>Antoine</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<aff id="aff1">
<sup>1</sup>
Laboratory Motricité, Interactions, Performance (EA 4334), Unite de Formation et de Recherche Sciences et Techniques des Activités Physiques et Sportives, University of Nantes, Nantes, France;</aff>
<aff id="aff2">
<sup>2</sup>
National Health and Medical Research Council, Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, University of Queensland, Brisbane, Queensland, Australia;</aff>
<aff id="aff3">
<sup>3</sup>
Centre de Référence Maladies Neuromusculaires Nantes-Angers, University of Nantes, Centre Hospitalier Universitaire, Nantes, France;</aff>
<aff id="aff4">
<sup>4</sup>
Atlantic Gene Therapies, Nantes, France; and</aff>
<aff id="aff5">
<sup>5</sup>
Institut de Myologie, GH Pitié-Salpêtrière, Paris, France</aff>
</contrib-group>
<author-notes>
<corresp id="cor1">Address for reprint requests and other correspondence: F. Hug,
<addr-line>Univ. of Nantes, Laboratory Motricité, Interactions, Performance (EA 4334), 25 bis boulevard Guy Mollet, BP 72206, 44322 Nantes cedex 3, France</addr-line>
(e-mail:
<email>francois.hug@univ-nantes.fr</email>
).</corresp>
</author-notes>
<pub-date pub-type="epub">
<day>7</day>
<month>8</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="ppub">
<day>15</day>
<month>9</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>15</day>
<month>9</month>
<year>2015</year>
</pub-date>
<pmc-comment> PMC Release delay is 12 months and 0 days and was based on the . </pmc-comment>
<volume>117</volume>
<issue>6</issue>
<fpage>658</fpage>
<lpage>662</lpage>
<history>
<date date-type="received">
<day>23</day>
<month>6</month>
<year>2014</year>
</date>
<date date-type="accepted">
<day>29</day>
<month>7</month>
<year>2014</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright © 2014 the American Physiological Society</copyright-statement>
<copyright-year>2014</copyright-year>
<copyright-holder>American Physiological Society</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zdg01814000658.pdf"></self-uri>
<abstract>
<p>The decrease in muscle strength in patients with Duchenne muscular dystrophy (DMD) is mainly explained by a decrease in the number of active contractile elements. Nevertheless, it is possible that other electrochemical and force transmission processes may contribute. The present study aimed to quantify the effect of DMD on the relative contribution of electrochemical and force transmission components of the electromechanical delay (i.e., time lag between the onset of muscle activation and force production) in humans using very high frame rate ultrasound. Fourteen patients with DMD and thirteen control subjects underwent two electrically evoked contractions of the biceps brachii with the ultrasound probe over the muscle belly. The electromechanical delay was significantly longer in DMD patients compared with controls (18.5 ± 3.9 vs. 12.5 ± 1.4 ms,
<italic>P</italic>
< 0.0001). More precisely, DMD patients exhibited a longer delay between the onset of muscle fascicles motion and force production (13.6 ± 3.1 vs. 7.9 ± 2.0 ms,
<italic>P</italic>
< 0.0001). This delay was correlated to the chronological age of the DMD patients (
<italic>r</italic>
= 0.66;
<italic>P</italic>
= 0.01), but not of the controls (
<italic>r</italic>
= −0.45;
<italic>P</italic>
= 0.10). No significant difference was found for the delay between the onset of muscle stimulation and the onset of muscle fascicle motion. These results highlight the role of the alteration of muscle force transmission (delay between the onset of fascicle motion and force production) in the impairments of the contraction efficiency in patients with DMD.</p>
</abstract>
<kwd-group>
<kwd>myopathy</kwd>
<kwd>force</kwd>
<kwd>ultrasound</kwd>
<kwd>electromechanical delay</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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