The high-intensity interval training mitigates the cardiac remodeling in spontaneously hypertensive rats

• Autor(a) principal: Engel, Letícia Estevam
• Data de Publicação: 2022
• Outros Autores: de Souza, Francilene Lima Agostinho, Giometti, Ines Cristina, Okoshi, Katashi [UNESP], Mariano, Thaoan Bruno, Ferreira, Natalia Zamberlan, Pinheiro, Dyovana Gomes, Floriano, Rafael Stuani, Aguiar, Andreo Fernando, Cicogna, Antônio Carlos [UNESP], Vechetti, Ivan José, Pacagnelli, Francis Lopes
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1016/j.lfs.2022.120959; http://hdl.handle.net/11449/249155
• topic: Hypertension; MAP kinase signaling system; Papillary muscles; Physical exercise

Aim: To evaluate the influence of high-intensity interval training (HIIT) on cardiac structural and functional characteristics and myocardial mitogen-activated protein kinase (MAPK) signaling in hypertensive rats. Methods: Male rats (12 months old) were divided into three groups: Wistar Kyoto rats (WKY, n = 8); sedentary spontaneously hypertensive rats (SED-SHR, n = 10), and trained spontaneously hypertensive rats (HIIT-SHR, n = 10). Systolic blood pressure (SBP), functional capacity, echocardiography, isolated papillary muscle, and gene expression of MAPK gene-encoding proteins associated with Elk1, cJun, ATF2, MEF2 were analyzed. Key findings: HIIT decreased SBP and increased functional capacity, left ventricular diastolic diameter, posterior wall thickness-left ventricle, relative wall thickness-left ventricle, and resting tension of the papillary muscle. In hypertensive rats, we observed a decrease in the gene-encoding ATF2 protein; this decrease was reversed by HIIT. Significance: The influence of HIIT in the SHR model in the compensated hypertension phase generated an increase in cardiac hypertrophy, attenuated myocardial diastolic dysfunction, lowered blood pressure, improved functional capacity, and reversed the alteration in gene-encoding ATF2 protein.