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The effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled hearts

dc.contributor.authorKemi, Ole J.en_US
dc.contributor.authorHoydal, Morten A.en_US
dc.contributor.authorMacQuaide, Niallen_US
dc.contributor.authorHaram, Per M.en_US
dc.contributor.authorKoch, Lauren G.en_US
dc.contributor.authorBritton, Steven L.en_US
dc.contributor.authorEllingsen, Oyvinden_US
dc.contributor.authorSmith, Godfrey L.en_US
dc.contributor.authorWisloff, Ulriken_US
dc.date.accessioned2011-11-10T15:36:44Z
dc.date.available2012-11-02T18:56:47Zen_US
dc.date.issued2011-09en_US
dc.identifier.citationKemi, Ole J.; Hoydal, Morten A.; MacQuaide, Niall; Haram, Per M.; Koch, Lauren G.; Britton, Steven L.; Ellingsen, Oyvind; Smith, Godfrey L.; Wisloff, Ulrik (2011). "The effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled hearts." Journal of Cellular Physiology 226(9): 2235-2243. <http://hdl.handle.net/2027.42/87039>en_US
dc.identifier.issn0021-9541en_US
dc.identifier.issn1097-4652en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/87039
dc.description.abstractThe response of transverse (T)‐tubules to exercise training in health and disease remains unclear. Therefore, we studied the effect of exercise training on the density and spacing of left ventricle cardiomyocyte T‐tubules in normal and remodeled hearts that associate with detubulation, by confocal laser scanning microscopy. First, exercise training in normal rats increased cardiomyocyte volume by 16% ( P  < 0.01), with preserved T‐tubule density. Thus, the T‐tubules adapted to the physiologic hypertrophy. Next, we studied T‐tubules in a rat model of metabolic syndrome with pressure overload‐induced concentric left ventricle hypertrophy, evidenced by 15% ( P  < 0.01) increased cardiomyocyte size. These rats had only 85% ( P  < 0.01) of the T‐tubule density of control rats. Exercise training further increased cardiomyocyte volume by 8% ( P  < 0.01); half to that in control rats, but the T‐tubule density remained unchanged. Finally, post‐myocardial infarction heart failure induced severe cardiac pathology, with a 70% ( P  < 0.01) increased cardiomyocyte volume that included both eccentric and concentric hypertrophy and 55% ( P  < 0.01) reduced T‐tubule density. Exercise training reversed 50% ( P  < 0.01) of the pathologic hypertrophy, whereas the T‐tubule density increased by 40% ( P  < 0.05) compared to sedentary heart failure, but remained at 60% of normal hearts ( P  < 0.01). Physiologic hypertrophy associated with conserved T‐tubule spacing (∼1.8–1.9 µm), whereas in pathologic hypertrophy, T‐tubules appeared disorganized without regular spacing. In conclusion, cardiomyocytes maintain the relative T‐tubule density during physiologic hypertrophy and after mild concentric pathologic hypertrophy, whereas after severe pathologic remodeling with a substantial loss of T‐tubules; exercise training reverses the remodeling and partly corrects the T‐tubule density. J. Cell. Physiol. 226: 2235–2243, 2011. © 2010 Wiley‐Liss, Inc.en_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.titleThe effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled heartsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelKinesiology and Sportsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Anesthesiology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationotherInstitute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UKen_US
dc.contributor.affiliationotherDepartment of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norwayen_US
dc.contributor.affiliationotherLaboratory of Experimental Cardiology, Catholic University of Leuven, Leuven, Belgiumen_US
dc.contributor.affiliationotherDepartment of Cardiothoracic Surgery, St. Olavs Hospital, Trondheim, Norwayen_US
dc.contributor.affiliationotherDepartment of Cardiology, St. Olavs Hospital, Trondheim, Norwayen_US
dc.contributor.affiliationotherInstitute of Cardiovascular and Medical Sciences, University of Glasgow, West Medical Building, Glasgow G12 8QQ, UK.en_US
dc.identifier.pmid21660947en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/87039/1/22559_ftp.pdf
dc.identifier.doi10.1002/jcp.22559en_US
dc.identifier.sourceJournal of Cellular Physiologyen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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