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This study investigated whether previous resistance exercise training (RT) affects the progression of right ventricular dysfunction and remodeling in rats with severe pulmonary artery hypertension (PAH). Male Wistar rats were submitted to a RT protocol (i.e., ladder-climbing) for 8 weeks, while controls remained in cages without exercising. Then, exercised rats were randomly divided into trained monocrotaline discontinued (TMD), and trained monocrotaline continued (TMC) groups. Subsequently, they received a single monocrotaline injection (i.e., 60 mg/kg) and the TMD group stopped RT, while the TMC group exercised for an additional 6-week period. After euthanasia, right ventricle (RV) was dissected and processed for histological and single RV myocyte analyses. Previous RT increased physical effort tolerance, prevented pulmonary artery resistance augment (i.e., AT/ET) and mitigated the reduction in RV systolic function (i.e., TAPSE). RT also lessened impairments in single RV myocyte contractility and intracellular calcium transient (i.e., amplitude, and times to peak and relaxation) in the TMC group only. Moreover, RT inhibited adverse RV remodeling (i.e., hypertrophy and collagen deposition) in both trained groups. In conclusion, previous RT attenuates the progression of RV dysfunction and remodeling in rats with severe monocrotaline-induced PAH, being the extension of protective effects dependent on the exercise training continuity.