DOI: 10.3390/antiox15101232 ISSN: 2076-3921

Blueberry Extract and Resistance Training in Severe Pulmonary Arterial Hypertension: Effects on Lung and Right-Ventricle Function and Structure

Luciano Bernardes Leite, Leôncio Lopes Soares, Sebastião Felipe Ferreira Costa, Luiz Otávio Guimarães-Ervilha, Sara Caco dos Lúcio Generoso, Mirielly Alexia Miranda Xavier, Arthur Eduardo de Carvalho Quintão, Matheus Soares Faria, Thainá Iasbik-Lima, Flavio Gilberto Herter, Patrick Turck, Alex Sander da Rosa Araujo, Tiago Fernandes, Bruno Rocha de Avila Pelozin, Edilamar Menezes Oliveira, Pedro Forte, Mariana Machado-Neves, Emily Correna Carlo Reis, Antônio José Natali

This study evaluated the effects of blueberry extract and resistance training on lung and right ventricle (RV) function and structure in severe experimental pulmonary arterial hypertension (PAH). PAH was induced in male Wistar rats by a single intraperitoneal injection of monocrotaline (60 mg/kg). One day later, the animals started receiving blueberry extract (100 mg/kg daily by gavage) and underwent a three-week moderate-intensity resistance exercise protocol (ladder climbing—15 climbs, a 60 s interval, a 60% load, one session/day, 5 days/wk). After these treatments and echocardiographic assessment, the animals were euthanized, and lung and RV samples were collected for mechanical, morphological, biochemical, and molecular analyses. Both blueberry extract and resistance training attenuated RV dysfunction and pulmonary artery resistance observed over the development of severe PAH. In addition, single RV myocyte mechanical function was maintained in treated rats. Moreover, the applied treatments mitigated oxidative imbalance and adverse structural remodeling in both the lung and RV. Furthermore, the interventions promoted partial or complete preservation of calcium regulatory protein expression. In conclusion, blueberry extract and resistance training, either alone or in combination, alleviate cardiopulmonary oxidative imbalance and adverse structural remodeling, sustain RV myocyte contractility and the expression of calcium regulatory proteins, and thus conserve pulmonary and RV function in severe PAH induced by monocrotaline.