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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/64029
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dc.creatorSara Quaglia de Campos Giampápt_BR
dc.creatorMarcos Mônico-Netopt_BR
dc.creatorMarco Tulio de Mellopt_BR
dc.creatorHelton de Sá Souzapt_BR
dc.creatorSergio Tufikpt_BR
dc.creatorKil Sun Leept_BR
dc.creatorMarcia Kiyomi Koikept_BR
dc.creatorAlexandra Alberta Dos Santospt_BR
dc.creatorEdnei Luiz Antoniopt_BR
dc.creatorAndrey Jorge Serrapt_BR
dc.creatorPaulo José Ferreira Tuccipt_BR
dc.creatorHanna Karen Moreira Antunespt_BR
dc.date.accessioned2024-02-16T16:24:40Z-
dc.date.available2024-02-16T16:24:40Z-
dc.date.issued2016-
dc.citation.volume11pt_BR
dc.citation.issue11pt_BR
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0167029pt_BR
dc.identifier.issn1932-6203pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/64029-
dc.description.resumoBackground: Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation. Methods: Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated. Results: Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway. Conclusions: Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.pt_BR
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentEEF - DEPARTAMENTO DE ESPORTESpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofPLoS ONEpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectSleep deprivationpt_BR
dc.subjectCardiac dysfunctionpt_BR
dc.subjectResistance trainingpt_BR
dc.subject.otherPrivação do sonopt_BR
dc.subject.otherInsuficiência cardíacapt_BR
dc.subject.otherTreino aeróbicopt_BR
dc.titleParadoxical sleep deprivation causes cardiac dysfunction and the impairment is attenuated by resistance trainingpt_BR
dc.title.alternativeA privação paradoxal do sono causa disfunção cardíaca e o prejuízo é atenuado pelo treinamento de resistênciapt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0167029pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9983-8812pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9515-1260pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3896-2208pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0525-5371pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-2390-2774pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5556-8061pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5407-8183pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9793-670Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-6648-0957pt_BR
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