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Pulmonary arterial hypertension (PAH) is a chronic disease characterized by increased pulmonary vascular resistance, right ventricular overload and systemic repercussions, including disorders in non-target organs. This study aimed to investigate the effects of PAH on the ventral prostate of adult Wistar rats, as well as the role of resistance training (RT) in modulating potential changes caused by the disease. Male rats (n = 32, 60 days old) were divided into four groups: sedentary control, sedentary PAH, RT control and PAH + RT. PAH was induced using two injections of monocrotaline, while rats were submitted to the RT protocol for a month. Afterward, the ventral prostate was collected and analysed for biometric, histopathological and oxidative parameters (CEUA 38/2021). The results showed that PAH significantly reduced the body and prostate weights and increased glandular epithelium and stroma proportions, besides causing epithelium atrophy and inflammatory infiltrates (p < .05). The activity of superoxide dismutase and catalase was lower, culminating in high levels of malondialdehyde and carbonyl proteins (p < .05). The exercise mainly influenced biometric and stereological parameters. The RT protocol minimized the negative effect of PAH regarding catalase activity, epithelium/lumen proportion and inflammatory infiltrate incidence. However, it was ineffective in restoring prostate weight and completely normalizing markers of oxidative stress. In conclusion, PAH induces significant morphofunctional changes in the ventral prostate, including oxidative damage and tissue remodelling. Although RT exerts protective effects, its benefits are limited, highlighting the need for complementary therapies to counteract PAH-induced prostate alterations fully.