Background. Pulmonary hypertension (PH) is a hallmark of heart failure (HF), developing in ~60% of patients with left ventricular systolic dysfunction and ~70% of patients with isolated left ventricular diastolic dysfunction. The pathogenesis of PH in HF is complex, with two distinct subsets of PH due to HF identified: 1) isolated post-capillary PH (IpcPH) and 2) combined pre- and postcapillary PH (CpcPH) (Vachiery et al., 2019). Patients with HF universally complain of exertional intolerance, but the causes may differ between patients with different phenotypes. Exercise introduces a substantial stress to the lungs, where elevations in venous return and cardiac output (Q) increase pulmonary blood volume and blood flow by 50% and 300%, respectively (Flamm et al., 1990). The healthy, highly compliant and low resistance pulmonary vasculature can readily accommodate these marked increases in blood volume and flow with inevitable but relatively small increases in pulmonary vascular pressures. However, this reserve to accommodate increased pulmonary blood flow is likely compromised in HF patients, particularly those with PH, with a consequent impairment in right ventricular reserve and aerobic capacity (Gorter et al., 2018). Aim. To determine: 1) the impact of pulmonary hypertension on the pulmonary haemodynamic response to exercise in patients with HF; 2) whether the pulmonary haemodynamic response to exercise is different in patients with IpcPH vs. CpcPH; and 3) the relationship between the pulmonary haemodynamic response to exercise and exercise capacity in HF patients. Methods. Thirty-nine stable HF patients undergoing right-heart catheterisation performed exhaustive incremental exercise (10 W every 3 min starting from 10 W) on a recumbent cycle ergometer. Systolic, diastolic and mean pulmonary arterial pressure (sPAP, dPAP and mPAP), and pulmonary capillary wedge pressure (PCWP) were measured beat-by-beat at end expiration and averaged over 5-10 cardiac cycles. Q was determined via direct Fick. Transpulmonary pressure gradient (TPG; mPAP – PCWP), pulmonary vascular resistance (PVR; TPG/Q), and pulmonary arterial compliance [PAC; stroke volume/(sPAP – dPAP)] were calculated. Results. The effect if PH on the haemodynamic response to exercise in HF: At peak exercise, the ratio mPAP to Q (i.e. unit increase in pressure for a unit increase in blood flow) was greater in HF patients with PH vs. HF patients without PH (9.7 ± 3.4 vs. 5.2 ± 1.5 mmHg/L/min−1, P < 0.001). By contrast, PAC at peak exercise was lower in HF patients with PH compared to HF patients without PH (1.2 ± 0.3 vs. 1.9 ± 0.2 mL/mmHg, P = 0.004). Importantly, both a greater mPAP-Q ratio (r2 = −0.549, P < 0.001) and a lower absolute PAC (r2 = 0.632, P < 0.001) at peak exercise were significantly related to impaired exercise capacity (i.e. lower peak oxygen consumption, VO2peak) across all HF patients. Effect of PH subtype on the haemodynamic response to exercise in HF: Post catheterization, patients were classified as having no PH (n = 11), IpcPH (n = 11), or CpcPH (n = 17). At peak exercise, mPAP was greater in CpcPH vs. IpcPH and no PH (57 ± 8 vs. 46 ± 10 and 34 ± 11 mmHg, P ≤ 0.029). PCWP at peak exercise was greater in CpcPH compared to no PH (30 ± 7 vs. 19 ± 8 mmHg, P < 0.001), but similar between CpcPH and IpcPH (30 ± 7 vs. 28 ± 10 mmHg, P = 0.215). The absolute increase in mPAP, PWCP and TPG from rest to peak exercise was not different between no PH, IpcPH and CpcPH. By contrast, the slope of the mPAP-Q, PCWP-Q and TPG-Q relationship during exercise was greater in CpcPH vs. IpcPH vs. no PH (mPAP-Q: 7.2 ± 3.2 vs. 4.1 ± 3.9 vs. 2.6 ± 1.7 mmHg/L/min−1; PCWP-Q: 4.2 ± 1.4 vs. 3.3 ± 1.2 vs. 2.9 ± 1.5 mmHg/L/min−1; TPG-Q: 4.3 ± 2.1 vs. 3.2 ± 1.8 vs. 2.6 ± 1.4 mmHg/L/min−1); however, only the differences between no PH and CpcPH were statistically significant. The slope of the mPAP-Q and the TPG-Q relationship in response to exercise was inversely related to VO2peak across all HF patients (mPAP-Q: r = −0.603, P = 0.02; TPG-Q: r = −0.592, P < 0.01). Conclusion. The pulmonary haemodynamic response to exercise in HF with PH is characterized by an exaggerated rise in pulmonary vascular pressures and limited or no pulmonary vascular reserve, both of which appear to be key determinants of exercise limitation in these patients. This pulmonary vascular limitation to exercise is further worsened by the development of combined pre- and postcapillary PH (CpcPH). Mechanistically, PH likely contributes to exercise intolerance in HF through a substantial increase in right ventricular afterload that restricts right ventricular contractile reserve and forward-flow of blood from the right ventricle to the pulmonary vasculature and systemic circulation.