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Continuous aerobic exercise prevents detrimental remodeling and right heart myocyte contraction and calcium cycling dysfunction in pulmonary artery hypertension.

Research paper by Franciany F de Jesus Silva, Filipe Rios FR Drummond, Meilene Ribeiro MR Fidelis, Maíra Oliveira MO Freitas, Tiago Ferreira TF Leal, Leonardo Mateus LM Teixeira de Rezende, Anselmo A Gomes de Moura, Emily Correna EC Carlo Reis, Antônio José AJ Natali

Indexed on: 22 Oct '20Published on: 17 Oct '20Published in: Journal of cardiovascular pharmacology



Abstract

Pulmonary artery hypertension (PAH) imposes right heart and lung detrimental remodeling which impairs cardiac contractility, physical effort tolerance and survival. The effects of an early moderate-intensity continuous aerobic exercise training on the right ventricle and lung structure, and on contractility and the calcium (Ca) transient in isolated myocytes from rats with severe PAH induced by monocrotaline were analyzed. Rats were divided into control sedentary (CS); control exercise (CE); monocrotaline sedentary (MS); and monocrotaline exercise (ME) groups. Animals from CE and ME groups underwent a moderate-intensity aerobic exercise on a treadmill (60 min/day; 60% intensity) for 32 days, after a monocrotaline (60 mg/kg body weight i.p.) or saline injection. The pulmonary artery resistance was higher in MS than in CS (1.36-fold) and was reduced by 39.39 % in ME compared with MS. Compared with MS, the ME group presented reduced alveolus (17 %) and blood vessel (46 %) wall, fibrosis (25.37 %) and type I collagen content (55.78 %); and increased alveolus (52.96 %) and blood vessel (146.97 %) lumen. In the right ventricle, ME group exhibited diminished hypertrophy index (25.53 %) and type I collagen content (40.42 %) and improved myocyte contraction [i.e. reduced times to peak (29.27 %) and to 50% relax (13.79 %)] and intracellular Ca transient [i.e. decreased times to peak (16.06 %) and to 50% decay (7.41 %)] compared with MS. Thus, early moderate-intensity continuous aerobic exercise prevents detrimental remodeling in the right heart and lung, increases in the pulmonary artery resistance and dysfunction in single myocyte contraction and Ca cycling in this model.

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