We have previously shown an attenuation of hypoxic pulmonary hypertension by exercise training ET (15), although the mechanism was not determined. The present study examined the effect of ET on the pulmonary arterial pressure (Pap) response of rats to short and long term hypoxia. After 3 weeks of treadmill training, male rats were divided into two groups: one (HT) was placed in hypobaric hypoxia (380 Torr); the second remained in normoxia (NT). Both groups continued to train in normoxia for 10 days, after which they were studied at rest and during hypoxic and normoxic exercise. Sedentary normoxic (NS) and hypoxic (HS) littermates were exposed to the same environments as their trained counterparts. Resting and exercise hypoxic PaO₂ were higher in NT and HT than in NS and HS, respectively, although alveolar ventilation of trained rats was not higher. Lower A-a PO₂ and higher effective lung diffusing capacity for O₂ (DLO₂) in NT vs NS and in HT vs HS suggest ET improved efficacy of gas exchange. Pulmonary arterial pressure (Pap) and Pap/cardiac output (Pap/Q) were lower in NT than NS in hypoxia, indicating ET attenuates the initial vasoconstriction of hypoxia. However, ET had no effect on chronic hypoxic pulmonary hypertension: Pap and Pap/Q in hypoxia were similar in HS vs HT. However, right ventricular weight was lower in HT than in HS, although Pap was not different. Since ET attenuates the initial pulmonary vasoconstriction of hypoxia, development of pulmonary hypertension may be delayed in HT rats, and the time during which right ventricular afterload is elevated may be shorter in this group. ET effects may improve the response to acute hypoxia by increasing efficacy of gas exchange and lowering right ventricular work.