Rationale: OSA has been associated with reduced exercise capacity. Endothelial dysfunction and exercise-induced pulmonary hypertension (ePH) may be mediators of this impairment. We hypothesized that OSA severity would be associated with impaired exercise performance, endothelial dysfunction, and ePH. Methods: Subjects with untreated OSA were recruited. Subjects underwent endothelial function, and cardiopul-monary exercise testing with an echocardiogram immediately before and following exercise. Results: 22 subjects were recruited with mean age 56 +/- 8 years, 74 % male, BMI 29 +/- 3 kg/m(2), and AHI 22 +/- 12 events/hr. Peak VO2 did not differ from normal (99.7 +/- 17.3 % predicted; p = 0.93). There was no significant association between OSA severity (as AHI, ODI) and exercise capacity, endothelial function, or pulmonary artery pressure. However, ODI, marker of RV diastolic dysfunction, and BMI together explained 59.3 % of the variability of exercise performance (p < 0.001) via our exploratory analyses. Conclusions: Exercise capacity was not impaired in this OSA cohort. Further work is needed to elucidate mechanisms linking sleep apnea, obesity, endothelial dysfunction and exercise impairment.