Exercise training counteracts the cardiac metabolic remodelling induced by experimental pulmonary arterial hypertension

• Tipo: Artigo em Revista Científica Internacional
• Data: 2022

Autores

Filipe Morais (Autor) Outra; Rita Nogueira-Ferreira (Autor) Outra; Hugo Rocha (Autor) Outra; José A. Duarte (Autor) FADEUP; Laura Vilarinho (Autor) Outra; Ana F. Silva (Autor) Outra; Adelino Leite-Moreira (Autor) FMUP; Mário Santos (Autor) Outra; Rita Ferreira (Autor) Outra; Daniel Moreira-Gonçalves (Autor) FADEUP

Revista

Título: Archives of Biochemistry and Biophysics

Vol. 730

Páginas: 109419/1- 109419/10

ISSN: 0003-9861

Editora: Elsevier

Indexação

ISI Web of Knowledge - 0 Citações

Scopus - 1 Citação

Classificação Científica

FOS: Ciências sociais

Outras Informações

ID Authenticus: P-00X-9Q7

DOI: 10.1016/j.abb.2022.109419

Abstract (EN): 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-1 alpha) and peroxisome proliferator-activated receptor gamma (PPAR-gamma). 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.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 10