Reduced exercise capacity has been reported previously in patients with OSA hypopnea syndrome (OSAHS), although the underlying mechanisms are unclear. What are the underlying mechanisms of reduced exercise capacity in untreated patients with OSAHS? Is there a role for systemic or pulmonary vascular abnormalities? This was a cross-sectional observational study in which 14 patients with moderate to severe OSAHS and 10 control participants (matched for age, BMI, smoking history, and FEV ) underwent spirometry, incremental cycle cardiopulmonary exercise test (CPET) with arterial line, resting echocardiography, and assessment of arterial stiffness (pulse wave velocity PWV and augmentation index AIx). Patients (age, 50 ± 11 years; BMI, 30.5 ± 2.7 kg/m ; smoking history, 2.4 ± 4.0 pack-years; FEV to FVC ratio, 0.78 ± 0.04; FEV , 85 ± 14% predicted, mean ± SD for all) had mean ± SD apnea hypopnea index of 43 ± 19/h. At rest, PWV, AIx, and mean pulmonary artery pressure (PAP) were higher in patients vs control participants (P < .05). During CPET, patients showed lower peak work rate (WR) and oxygen uptake and greater dyspnea ratings compared with control participants (P < .05 for all). Minute ventilation (V· ), ventilatory equivalent for CO output (V· /V·CO ), and dead space volume (V ) to tidal volume (V ) ratio were greater in patients vs control participants during exercise (P < .05 for all). Reduction in V to V ratio from rest to peak exercise was greater in control participants compared with patients (0.24 ± 0.08 vs 0.04 ± 0.14, respectively; P = .001). Dyspnea intensity at the highest equivalent WR correlated with corresponding values of V· /V·CO (r = 0.65; P = .002), and dead space ventilation (r = 0.70; P = .001). Age, PWV, and mean PAP explained approximately 70% of the variance in peak WR, whereas predictors of dyspnea during CPET were rest-to-peak change in V to V ratio and PWV (R  = 0.50; P < .001). Patients with OSAHS showed evidence of pulmonary gas exchange abnormalities during exercise (in the form of increased dead space) and resting systemic vascular dysfunction that may explain reduced exercise capacity and increased exertional dyspnea intensity.