Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10400.18/8562 |
Resumo: | Exercise training provides several cardiovascular benefits in both physiological and pathological conditions; however, its use as a therapeutic tool for pulmonary arterial hypertension (PAH) has been poorly explored. This study aimed to extend the comprehension of the cardioprotective effects of exercise training in the set of PAH focusing on the metabolic changes promoted by exercise in the right ventricle (RV). The monocrotaline animal model of PAH was used and male Wistar rats were submitted to two weeks of treadmill exercise training (5 days/week, 60 min/day, 25 m/min) following disease establishment. Trained rats showed an improved diastolic function (lower end-diastolic pressure and tau) despite the presence of cardiac overload (increased peak systolic pressure, end-diastolic pressure and arterial elastance). This enhanced hemodynamic response was paralleled by an increased uptake of glucose to cardiomyocytes through glucose transporter type 4 (GLUT4) followed by increased lactate dehydrogenase (LDH) activity. Exercise did not reverse the decrease of fatty acid oxidation related to PAH but increased the content of the transcription factors peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and peroxisome proliferator-activated receptor gamma (PPAR-γ). Two weeks of exercise did not modulate the changes in amino acid metabolism secondary to PAH. Our work suggests that continuous aerobic exercise of moderate intensity, despite its short-term duration and application in a late stage of the disease, supports the RV response to PAH by promoting a shift in the cardiac metabolic phenotype. |
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Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertensionAcylcarnitine ProfileGlucose MetabolismPulmonary Arterial HypertensionRight VentricleTreadmill ExerciseDoenças GenéticasExercise training provides several cardiovascular benefits in both physiological and pathological conditions; however, its use as a therapeutic tool for pulmonary arterial hypertension (PAH) has been poorly explored. This study aimed to extend the comprehension of the cardioprotective effects of exercise training in the set of PAH focusing on the metabolic changes promoted by exercise in the right ventricle (RV). The monocrotaline animal model of PAH was used and male Wistar rats were submitted to two weeks of treadmill exercise training (5 days/week, 60 min/day, 25 m/min) following disease establishment. Trained rats showed an improved diastolic function (lower end-diastolic pressure and tau) despite the presence of cardiac overload (increased peak systolic pressure, end-diastolic pressure and arterial elastance). This enhanced hemodynamic response was paralleled by an increased uptake of glucose to cardiomyocytes through glucose transporter type 4 (GLUT4) followed by increased lactate dehydrogenase (LDH) activity. Exercise did not reverse the decrease of fatty acid oxidation related to PAH but increased the content of the transcription factors peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and peroxisome proliferator-activated receptor gamma (PPAR-γ). Two weeks of exercise did not modulate the changes in amino acid metabolism secondary to PAH. Our work suggests that continuous aerobic exercise of moderate intensity, despite its short-term duration and application in a late stage of the disease, supports the RV response to PAH by promoting a shift in the cardiac metabolic phenotype.Highlights: Two weeks of exercise training improved right ventricle diastolic function in MCT rats; Exercise increased glucose uptake through GLUT4 and its oxidation to lactate; Exercise did not reverse MCT-induced decrease reliance of RV on fatty acid oxidation; Exercise moderately impacted amino acid metabolism in the RV of MCT rats; Metabolic adaptations of trained RV are regulated by PGC-1α and PPAR-γ.This work was supported by “Fundação para a Ciência e a Tecnologia” – FCT, European Union, QREN, FEDER and COMPETE for funding the LAQV-REQUIMTE (UIDB/50006/2020), UnIC (UIDB/IC/00051/2020 and UIDP/00051/2020), CIAFEL (UIDB/00617/2020) and UMIB (UIDB/00215/2020 and UIDP/00215/2020) research units, RISE - Health Research Network-From the Lab to the Community (LA/P/0053/ 2020), ITR - Laboratory for Integrative and Translational Research in Population Health (LA/P/0064/2020) and the research projects DOCnet (NORTE-01-0145-FEDER-000003) and NETDIAMOND (SAICT-PAC/ 0047/2015). Rita Nogueira-Ferreira acknowledges FCT for the research contract CEECIND/03935/2021 under the CEEC Individual 2021.ElsevierRepositório Científico do Instituto Nacional de SaúdeMorais, FilipeNogueira-Ferreira, RitaRocha, HugoDuarte, José A.Vilarinho, LauraSilva, Ana F.Leite-Moreira, AdelinoSantos, MárioFerreira, RitaMoreira-Gonçalves, Daniel2023-03-20T10:45:59Z2022-11-152022-11-15T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10400.18/8562engArch Biochem Biophys. 2022 Nov 15;730:109419. doi: 10.1016/j.abb.2022.109419. Epub 2022 Sep 29.0003-986110.1016/j.abb.2022.109419info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-07-20T15:42:38Zoai:repositorio.insa.pt:10400.18/8562Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T18:43:12.278131Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
title |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
spellingShingle |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension Morais, Filipe Acylcarnitine Profile Glucose Metabolism Pulmonary Arterial Hypertension Right Ventricle Treadmill Exercise Doenças Genéticas |
title_short |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
title_full |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
title_fullStr |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
title_full_unstemmed |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
title_sort |
Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension |
author |
Morais, Filipe |
author_facet |
Morais, Filipe Nogueira-Ferreira, Rita Rocha, Hugo Duarte, José A. Vilarinho, Laura Silva, Ana F. Leite-Moreira, Adelino Santos, Mário Ferreira, Rita Moreira-Gonçalves, Daniel |
author_role |
author |
author2 |
Nogueira-Ferreira, Rita Rocha, Hugo Duarte, José A. Vilarinho, Laura Silva, Ana F. Leite-Moreira, Adelino Santos, Mário Ferreira, Rita Moreira-Gonçalves, Daniel |
author2_role |
author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Repositório Científico do Instituto Nacional de Saúde |
dc.contributor.author.fl_str_mv |
Morais, Filipe Nogueira-Ferreira, Rita Rocha, Hugo Duarte, José A. Vilarinho, Laura Silva, Ana F. Leite-Moreira, Adelino Santos, Mário Ferreira, Rita Moreira-Gonçalves, Daniel |
dc.subject.por.fl_str_mv |
Acylcarnitine Profile Glucose Metabolism Pulmonary Arterial Hypertension Right Ventricle Treadmill Exercise Doenças Genéticas |
topic |
Acylcarnitine Profile Glucose Metabolism Pulmonary Arterial Hypertension Right Ventricle Treadmill Exercise Doenças Genéticas |
description |
Exercise training provides several cardiovascular benefits in both physiological and pathological conditions; however, its use as a therapeutic tool for pulmonary arterial hypertension (PAH) has been poorly explored. This study aimed to extend the comprehension of the cardioprotective effects of exercise training in the set of PAH focusing on the metabolic changes promoted by exercise in the right ventricle (RV). The monocrotaline animal model of PAH was used and male Wistar rats were submitted to two weeks of treadmill exercise training (5 days/week, 60 min/day, 25 m/min) following disease establishment. Trained rats showed an improved diastolic function (lower end-diastolic pressure and tau) despite the presence of cardiac overload (increased peak systolic pressure, end-diastolic pressure and arterial elastance). This enhanced hemodynamic response was paralleled by an increased uptake of glucose to cardiomyocytes through glucose transporter type 4 (GLUT4) followed by increased lactate dehydrogenase (LDH) activity. Exercise did not reverse the decrease of fatty acid oxidation related to PAH but increased the content of the transcription factors peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and peroxisome proliferator-activated receptor gamma (PPAR-γ). Two weeks of exercise did not modulate the changes in amino acid metabolism secondary to PAH. Our work suggests that continuous aerobic exercise of moderate intensity, despite its short-term duration and application in a late stage of the disease, supports the RV response to PAH by promoting a shift in the cardiac metabolic phenotype. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-11-15 2022-11-15T00:00:00Z 2023-03-20T10:45:59Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10400.18/8562 |
url |
http://hdl.handle.net/10400.18/8562 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Arch Biochem Biophys. 2022 Nov 15;730:109419. doi: 10.1016/j.abb.2022.109419. Epub 2022 Sep 29. 0003-9861 10.1016/j.abb.2022.109419 |
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info:eu-repo/semantics/openAccess |
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openAccess |
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application/pdf |
dc.publisher.none.fl_str_mv |
Elsevier |
publisher.none.fl_str_mv |
Elsevier |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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