Unraveling the role of high-intensity resistance training on left ventricle proteome: Is there a shift towards maladaptation?

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dc.citation.volume152
dc.contributor.authorDantas, Patricia Sousa [UNIFESP]
dc.contributor.authorSakata, Maisa Mayumi [UNIFESP]
dc.contributor.authorPerez, Juliana Dineia [UNIFESP]
dc.contributor.authorWatanabe, Regina Lucia Harumi [UNIFESP]
dc.contributor.authorBizerra, Fernando Cesar [UNIFESP]
dc.contributor.authorNeves, Vander Jose das
dc.contributor.authorGuzzoni, Vinicius
dc.contributor.authorMarcondes, Fernanda Klein
dc.contributor.authorCasarini, Dulce Elena [UNIFESP]
dc.contributor.authorCunha, Tatiana Sousa [UNIFESP]
dc.coverageOxford
dc.date.accessioned2020-07-22T13:23:00Z
dc.date.available2020-07-22T13:23:00Z
dc.date.issued2016
dc.description.abstractHigh-intensity resistance training (RT) induces adaptations that improve physiological function. However, high intensity, volume and/or frequency may lead to injury and other health issues such as adverse cardiac effects. The aim of this study was to evaluate the effect of RT on left ventricle proteome, and to identify the pathways involved on the harmful adaptations induced by this protocol. Male Wistar rats were randomized into 2 groups: Trained (T) and Sedentary (S). Animals from T group were trained for 6 weeks, and then all the animals were sacrificed and left ventricle was isolated for analysis. We identified 955 proteins, and 93 proteins were considereden
dc.description.abstract36 were expressed exclusively in T group, and 4 in S group. Based on quantitative analysis, 42 proteins were found overexpressed and 11 underexpressed in T group compared with S group. Using the Gene Ontology to relate the biological processes in which these proteins are involved, we conclude that RT protocol promotes changes similar to those found in the initial phase of heart failure, but we also observed a concomitant increased expression of protective proteins, suggesting the activation of pathways to avoid major damages on left ventricle and delay the onset of pathological hypertrophy. Statement of significance of the study: Our study shows that high-intensity RT protocol changes left ventricle proteome, modifying metabolic profile of heart tissue and inducing the expression of proteins that acts against cardiac injury. We hypothesize that these adaptations occur to prevent the onset of cardiac dysfunction. Despite highly significant, it remains to be determined whether these adaptations are sufficient to further keep left ventricle function and exert cardioprotection, and whether this panel will be shifted towards maladaptation, and heart failure. (c) 2016 Elsevier Inc. All rights reserved.en
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Dept Med, Discipline Nephrol, Sao Paulo, SP, Brazil
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Dept Physiol, Discipline Nutr Physiol, Sao Paulo, SP, Brazil
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Dept Med, Discipline Infect Dis, Special Mycol Lab LEMI, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Estadual Campinas, Fac Dent Piracicaba FOP UNICAMP, Dept Physiol Sci, Piracicaba, SP, Brazil
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Inst Sci & Technol, Dept Sci & Technol, BR-12231280 Sao Jose Dos Campos, SP, Brazil
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Dept Med, Discipline Nephrol, Sao Paulo, SP, Brazil
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Dept Physiol, Discipline Nutr Physiol, Sao Paulo, SP, Brazil
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Dept Med, Discipline Infect Dis, Special Mycol Lab LEMI, Sao Paulo, SP, Brazil
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Inst Sci & Technol, Dept Sci & Technol, BR-12231280 Sao Jose Dos Campos, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo-FAPESP
dc.description.sponsorshipFAEP/UNICAMP
dc.description.sponsorshipCAPES, Brazil
dc.description.sponsorshipIDFAPESP: 02/05427-8
dc.description.sponsorshipIDFAEP/UNICAMP: 398/03
dc.description.sponsorshipIDFAEP/UNICAMP: 680/03
dc.format.extent156-164
dc.identifierhttp://dx.doi.org/10.1016/j.lfs.2016.03.040
dc.identifier.citationLife Sciences. Oxford, v. 152, p. 156-164, 2016.
dc.identifier.doi10.1016/j.lfs.2016.03.040
dc.identifier.issn0024-3205
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/55979
dc.identifier.wosWOS:000375728500019
dc.language.isoeng
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofLife Sciences
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectProteomics shotgunen
dc.subjectRat proteomicsen
dc.subjectHigh-intensity resistance trainingen
dc.subjectCardiac hypertrophyen
dc.subjectPathological hypertrophyen
dc.titleUnraveling the role of high-intensity resistance training on left ventricle proteome: Is there a shift towards maladaptation?en
dc.typeinfo:eu-repo/semantics/article
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