Exercise training delays cardiac dysfunction and prevents calcium handling abnormalities in sympathetic hyperactivity-induced heart failure mice

Página do item simplificado
dc.contributor.authorMedeiros, Alessandra
dc.contributor.authorRolim, Natale Pinheiro Lage
dc.contributor.authorOliveira, Rodrigo da Silva Fermino de
dc.contributor.authorRosa, Kaleizu Teodoro
dc.contributor.authorMattos, Katt Coelho
dc.contributor.authorCasarini, Dulce Elena [UNIFESP]
dc.contributor.authorIrigoyen, Maria Claudia
dc.contributor.authorKrieger, Eduardo Moacyr
dc.contributor.authorKrieger, Jose Eduardo
dc.contributor.authorNegrao, Carlos Eduardo
dc.contributor.authorBrum, Patricia Chakur
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:49:19Z
dc.date.available2016-01-24T13:49:19Z
dc.date.issued2008-01-01
dc.description.abstractExercise training (ET) is a coadjuvant therapy in preventive cardiology. It delays cardiac dysfunction and exercise intolerance in heart failure (HF); however, the molecular mechanisms underlying its cardioprotection are poorly understood. We tested the hypothesis that ET would prevent Ca2+ handling abnormalities and ventricular dysfunction in sympathetic hyperactivity-induced HF mice. A cohort of male wildtype (WT) and congenic (alpha 2A/alpha 2C)-adrenoceptor knockout ((alpha 2A/alpha 2C)ARKO) mice with C57BL6/J genetic background (3-5 mo of age) were randomly assigned into untrained and exercise-trained groups. ET consisted of 8-wk swimming session, 60 min, 5 days/wk. Fractional shortening (FS) was assessed by two-dimensional guided M-mode echocardiography. the protein expression of ryanodine receptor (RyR), phospho-Ser(2809)-RyR, sarcoplasmic reticulum Ca2+ ATPase (SERCA2), Na+/Ca2+ exchanger (NCX), phospholamban (PLN), phospho-Ser(16)-PLN, and phospho-Thr(17)-PLN were analyzed by Western blotting. At 3 mo of age, no significant difference in FS and exercise tolerance was observed between WT and (alpha 2A/alpha 2C)ARKO mice. At 5 mo, when cardiac dysfunction is associated with lung edema and increased plasma norepinephrine levels, (alpha 2A/alpha 2C)ARKO mice presented reduced FS paralleled by decreased SERCA2 (26%) and NCX (34%). Conversely, (alpha 2A/alpha 2C)ARKO mice displayed increased phospho-Ser(16)-PLN (76%) and phospho-Ser(2809)-RyR (49%). ET in (alpha 2A/alpha 2C)ARKO mice prevented exercise intolerance, ventricular dysfunction, and decreased plasma norepinephrine. ET significantly increased the expression of SERCA2 (58%) and phospho-Ser(16)-PLN (30%) while it restored the expression of phospho-Ser(2809)-RyR to WT levels. Collectively, we provide evidence that improved net balance of Ca2+ handling proteins paralleled by a decreased sympathetic activity on ET are, at least in part, compensatory mechanisms against deteriorating ventricular function in HF.en
dc.description.affiliationUniv São Paulo, Sch Phys Educ & Sport, Dept Biodinam Movimento Corpo Humano, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Heart Inst InCor, Sch Med, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Div Nephrol, Dept Med, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Nephrol, Dept Med, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt
dc.description.sponsorshipIDFAPESP: 2002/04588 – 8pt
dc.description.sponsorshipIDFAPESP: 2004/00745–7pt
dc.format.extent103-109
dc.identifierhttps://dx.doi.org/10.1152/japplphysiol.00493.2007
dc.identifier.citationJournal of Applied Physiology. Bethesda: Amer Physiological Soc, v. 104, n. 1, p. 103-109, 2008.
dc.identifier.doi10.1152/japplphysiol.00493.2007
dc.identifier.issn8750-7587
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/30239
dc.identifier.wosWOS:000252398700014
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofJournal of Applied Physiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCalcium handling proteinsen
dc.subjectVentricular functionen
dc.subjectPlasma norepinephrine levelsen
dc.subjectCardiomyopathyen
dc.subjectExercise conditioningen
dc.titleExercise training delays cardiac dysfunction and prevents calcium handling abnormalities in sympathetic hyperactivity-induced heart failure miceen
dc.typeinfo:eu-repo/semantics/article
Arquivos
Coleções
EPM - Artigos