Arq. Bras. Cardiol. 2022; 119(4): 574-584
Resistance Exercise Training Mitigates Left Ventricular Dysfunctions in Pulmonary Artery Hypertension Model
Leôncio Lopes Soares
, Luciano Bernardes Leite
, Luiz Otávio Guimarães Ervilha
, Bruna Aparecida Fonseca da Silva
, Maíra Oliveira de Freitas
, Alexandre Martins Oliveira Portes
, Leonardo Mateus Teixeira Rezende
, Filipe Rios Drummond
, Miguel Araújo Carneiro Junior
, Mariana Machado Neves
, Emily Correna Carlo Reis
, Antônio José Natali
This Original Article is referred by the Short Editorial "Cardioprotective Effect of Resistance Exercise on Left Ventricular Remodeling Associated with Monocrotaline-Induced Pulmonary Arterial Hypertension".
Abstract
Background
The right ventricular hypertrophy and dilation observed in pulmonary artery hypertension (PAH) damages the left ventricle (LV) dynamics by flattening the interventricular septum.
Objective
To investigate whether low- to moderate-intensity resistance exercise training (RT) is beneficial to LV and cardiomyocyte contractile functions in rats during the development of monocrotaline (MCT)-induced PAH.
Methods
Male Wistar rats (Body weight: ~ 200 g) were used. To assess the time to potential heart failure onset (i.e., end point), rats were divided into sedentary hypertension until failure (SHF, n=6) and exercise hypertension until failure (EHF, n=6) groups. To test RT effects, rats were divided into sedentary control (SC, n = 7), sedentary hypertension (SH, n=7), and exercise hypertension (EH, n=7) groups. PAH was induced by two MCT injections (20 mg/kg, with 7 days interval). Exercise groups were submitted to an RT protocol (Ladder climbing; 55-65% of carrying maximal load), 5 times/week. Statistical significance was assumed at P < 0.05.
Results
RT prolonged the end point (~25 %), enhanced the physical effort tolerance (~ 55%), and mitigated the LV and cardiomyocyte contractility dysfunctions promoted by MCT by preserving the ejection fraction and fractional shortening, the amplitude of shortening, and the velocities of contraction and relaxation in cardiomyocytes. RT also prevented increases in left ventricle fibrosis and type I collagen caused by MCT, and maintained the type III collagen and myocyte dimensions reduced by MCT.
Conclusion
Low- to moderate-intensity RT benefits LV and cardiomyocyte contractile functions in rats during the development of MCT-induced PAH.
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