Low anaerobic threshold and increased skeletal muscle lactate production in subjects with Huntington's disease
Identifieur interne : 001574 ( Main/Exploration ); précédent : 001573; suivant : 001575Low anaerobic threshold and increased skeletal muscle lactate production in subjects with Huntington's disease
Auteurs : Andrea Ciammola [Italie] ; Jenny Sassone [Italie] ; Monica Sciacco [Italie] ; Niccol E. Mencacci [Italie] ; Michela Ripolone [Italie] ; Caterina Bizzi [Italie] ; Clarissa Colciago [Italie] ; Maurizio Moggio [Italie] ; Gianfranco Parati [Italie] ; Vincenzo Silani [Italie] ; Gabriella Malfatto [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-01.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Aged, Anaerobic Threshold (physiology), Anaerobic threshold, Analysis of Variance, Cells, Cultured, Female, Heart (physiology), Human, Humans, Huntington Disease (pathology), Huntington Disease (physiopathology), Huntington disease, Huntington's disease, Lactates, Lactic Acid (blood), Lactic Acid (metabolism), Lactic acid, Male, Microscopy, Electron, Transmission (methods), Middle Aged, Mitochondria, Mitochondria, Muscle (pathology), Mitochondria, Muscle (ultrastructure), Muscle, Skeletal (cytology), Muscle, Skeletal (metabolism), Muscle, Skeletal (pathology), Muscle, Skeletal (ultrastructure), Nervous system diseases, Respiration, Striated muscle, Young Adult, anaerobic threshold, mitochondria, skeletal muscle.
- MESH :
- chemical , blood : Lactic Acid.
- chemical , metabolism : Lactic Acid.
- cytology : Muscle, Skeletal.
- metabolism : Muscle, Skeletal.
- methods : Microscopy, Electron, Transmission.
- pathology : Huntington Disease, Mitochondria, Muscle, Muscle, Skeletal.
- physiology : Anaerobic Threshold, Heart.
- physiopathology : Huntington Disease.
- ultrastructure : Mitochondria, Muscle, Muscle, Skeletal.
- Adult, Aged, Analysis of Variance, Cells, Cultured, Female, Humans, Male, Middle Aged, Respiration, Young Adult.
Abstract
Mitochondrial defects that affect cellular energy metabolism have long been implicated in the etiology of Huntington's disease (HD). Indeed, several studies have found defects in the mitochondrial functions of the central nervous system and peripheral tissues of HD patients. In this study, we investigated the in vivo oxidative metabolism of exercising muscle in HD patients. Ventilatory and cardiometabolic parameters and plasma lactate concentrations were monitored during incremental cardiopulmonary exercise in twenty‐five HD subjects and twenty‐five healthy subjects. The total exercise capacity was normal in HD subjects but notably the HD patients and presymptomatic mutation carriers had a lower anaerobic threshold than the control subjects. The low anaerobic threshold of HD patients was associated with an increase in the concentration of plasma lactate. We also analyzed in vitro muscular cell cultures and found that HD cells produce more lactate than the cells of healthy subjects. Finally, we analyzed skeletal muscle samples by electron microscopy and we observed striking mitochondrial structural abnormalities in two out of seven HD subjects. Our findings confirm mitochondrial abnormalities in HD patients' skeletal muscle and suggest that the mitochondrial dysfunction is reflected functionally in a low anaerobic threshold and an increased lactate synthesis during intense physical exercise. © 2010 Movement Disorder Society
Url:
- https://api.istex.fr/document/CEA9BE03E3EE1DE9544159D3B59E82A19843CD96/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081141
DOI: 10.1002/mds.23258
Affiliations:
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Luca Hospital, IRCCS Istituto Auxologico Italiano, Milan</wicri:regionArea><placeName><settlement type="city">Milan</settlement><region nuts="2">Lombardie</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Clinical Medicine and Prevention, Università di Milano‐Bicocca, Milan</wicri:regionArea><placeName><settlement type="city">Milan</settlement><region nuts="2">Lombardie</region></placeName></affiliation></author><author><name sortKey="Silani, Vincenzo" sort="Silani, Vincenzo" uniqKey="Silani V" first="Vincenzo" last="Silani">Vincenzo Silani</name><affiliation wicri:level="3"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Neurology and Laboratory of Neuroscience, Centro “Dino Ferrari” Università degli Studi di Milano ‐ IRCCS Istituto Auxologico Italiano, Milan</wicri:regionArea><placeName><settlement type="city">Milan</settlement><region nuts="2">Lombardie</region></placeName></affiliation></author><author><name sortKey="Malfatto, Gabriella" sort="Malfatto, Gabriella" uniqKey="Malfatto G" first="Gabriella" last="Malfatto">Gabriella Malfatto</name><affiliation wicri:level="3"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Cardiology, S. Luca Hospital, IRCCS Istituto Auxologico Italiano, Milan</wicri:regionArea><placeName><settlement type="city">Milan</settlement><region nuts="2">Lombardie</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-01">2011-01</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="130">130</biblScope><biblScope unit="page" to="137">137</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CEA9BE03E3EE1DE9544159D3B59E82A19843CD96</idno><idno type="DOI">10.1002/mds.23258</idno><idno type="ArticleID">MDS23258</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Anaerobic Threshold (physiology)</term><term>Anaerobic threshold</term><term>Analysis of Variance</term><term>Cells, Cultured</term><term>Female</term><term>Heart (physiology)</term><term>Human</term><term>Humans</term><term>Huntington Disease (pathology)</term><term>Huntington Disease (physiopathology)</term><term>Huntington disease</term><term>Huntington's disease</term><term>Lactates</term><term>Lactic Acid (blood)</term><term>Lactic Acid (metabolism)</term><term>Lactic acid</term><term>Male</term><term>Microscopy, Electron, Transmission (methods)</term><term>Middle Aged</term><term>Mitochondria</term><term>Mitochondria, Muscle (pathology)</term><term>Mitochondria, Muscle (ultrastructure)</term><term>Muscle, Skeletal (cytology)</term><term>Muscle, Skeletal (metabolism)</term><term>Muscle, Skeletal (pathology)</term><term>Muscle, Skeletal (ultrastructure)</term><term>Nervous system diseases</term><term>Respiration</term><term>Striated muscle</term><term>Young Adult</term><term>anaerobic threshold</term><term>mitochondria</term><term>skeletal muscle</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Lactic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Lactic Acid</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Microscopy, Electron, Transmission</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Huntington Disease</term><term>Mitochondria, Muscle</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Anaerobic Threshold</term><term>Heart</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Mitochondria, Muscle</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Analysis of Variance</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Respiration</term><term>Young Adult</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Acide lactique</term><term>Chorée de Huntington</term><term>Homme</term><term>Lactate</term><term>Mitochondrie</term><term>Muscle strié</term><term>Pathologie du système nerveux</term><term>Seuil anaérobie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mitochondrial defects that affect cellular energy metabolism have long been implicated in the etiology of Huntington's disease (HD). Indeed, several studies have found defects in the mitochondrial functions of the central nervous system and peripheral tissues of HD patients. In this study, we investigated the in vivo oxidative metabolism of exercising muscle in HD patients. Ventilatory and cardiometabolic parameters and plasma lactate concentrations were monitored during incremental cardiopulmonary exercise in twenty‐five HD subjects and twenty‐five healthy subjects. The total exercise capacity was normal in HD subjects but notably the HD patients and presymptomatic mutation carriers had a lower anaerobic threshold than the control subjects. The low anaerobic threshold of HD patients was associated with an increase in the concentration of plasma lactate. We also analyzed in vitro muscular cell cultures and found that HD cells produce more lactate than the cells of healthy subjects. Finally, we analyzed skeletal muscle samples by electron microscopy and we observed striking mitochondrial structural abnormalities in two out of seven HD subjects. Our findings confirm mitochondrial abnormalities in HD patients' skeletal muscle and suggest that the mitochondrial dysfunction is reflected functionally in a low anaerobic threshold and an increased lactate synthesis during intense physical exercise. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Italie</li></country><region><li>Lombardie</li></region><settlement><li>Milan</li></settlement></list><tree><country name="Italie"><region name="Lombardie"><name sortKey="Ciammola, Andrea" sort="Ciammola, Andrea" uniqKey="Ciammola A" first="Andrea" last="Ciammola">Andrea Ciammola</name></region><name sortKey="Bizzi, Caterina" sort="Bizzi, Caterina" uniqKey="Bizzi C" first="Caterina" last="Bizzi">Caterina Bizzi</name><name sortKey="Colciago, Clarissa" sort="Colciago, Clarissa" uniqKey="Colciago C" first="Clarissa" last="Colciago">Clarissa Colciago</name><name sortKey="Malfatto, Gabriella" sort="Malfatto, Gabriella" uniqKey="Malfatto G" first="Gabriella" last="Malfatto">Gabriella Malfatto</name><name sortKey="Mencacci, Niccol E" sort="Mencacci, Niccol E" uniqKey="Mencacci N" first="Niccol E." last="Mencacci">Niccol E. Mencacci</name><name sortKey="Moggio, Maurizio" sort="Moggio, Maurizio" uniqKey="Moggio M" first="Maurizio" last="Moggio">Maurizio Moggio</name><name sortKey="Parati, Gianfranco" sort="Parati, Gianfranco" uniqKey="Parati G" first="Gianfranco" last="Parati">Gianfranco Parati</name><name sortKey="Parati, Gianfranco" sort="Parati, Gianfranco" uniqKey="Parati G" first="Gianfranco" last="Parati">Gianfranco Parati</name><name sortKey="Ripolone, Michela" sort="Ripolone, Michela" uniqKey="Ripolone M" first="Michela" last="Ripolone">Michela Ripolone</name><name sortKey="Sassone, Jenny" sort="Sassone, Jenny" uniqKey="Sassone J" first="Jenny" last="Sassone">Jenny Sassone</name><name sortKey="Sciacco, Monica" sort="Sciacco, Monica" uniqKey="Sciacco M" first="Monica" last="Sciacco">Monica Sciacco</name><name sortKey="Silani, Vincenzo" sort="Silani, Vincenzo" uniqKey="Silani V" first="Vincenzo" last="Silani">Vincenzo Silani</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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