Introduction: In individuals with dyspnea on exertion (DOE) and suspected exercise pulmonary hypertension (exPH), oxygen uptake (VO 2 ), cardiac output (CO), peripheral oxygen extraction (Ca-vO 2 ), and mean pulmonary artery pressure (mPAP) have been well characterized during incremental exercise but less is known about the kinetics of post-exercise recovery patterns. Hypothesis: Exercise recovery cardiac output kinetics are slowed in patients with exPH. Methods: Upright maximum incremental ramp cycle ergometry cardiopulmonary exercise testing with invasive hemodynamic monitoring and serial blood gas measurements during exercise and recovery was performed in 50 consecutive patients referred for evaluation of DOE of unclear etiology. VO 2 , arterial and venous oxygen content (Ca-vO 2 ), Fick cardiac output, and mPAP were analyzed from rest, peak exercise, and 2 minutes post-exercise. ExPH was defined in a consistent manner with recent consensus statements (ΔmPAP/ΔCO >3.0 mmHg/L/min) from rest to peak exercise. Results: Among 50 patients with DOE, [62% female, Age 61.7±11.8, BMI 30.7±8.2] 2-min post-exercise VO 2 was -56±11%, CO: -22±19%, Ca-vO 2 :-42±15% compared to peak exercise values. The % fall in CO at 2min was significantly lower in the 26 patients with exPH compared to the 24 patients without exPH (Table). The average mPAP remained elevated at 2 min post-exercise (>20mmHg) in exPH despite normal average resting values. Conclusions: Patients with exPH demonstrate slowed CO recovery kinetics in conjunction with persistent PAP elevation 2-min post-exercise. Persistent elevation in blood flow through the pulmonary circuit at a time conducive to non-invasive assessment of PAP (i.e. by echocardiography) may lend itself to non-invasive detection of exercise-PH in patients undergoing evaluation of dyspnea on exertion.