Altered cardiorespiratory response to exercise in overweight and obese women with polycystic ovary syndrome

In polycystic ovary syndrome (PCOS), cardiovascular risk is increased. Peak O(2) uptake ([Formula: see text]) predicts the cardiovascular risk. We were the first to examine the contribution of systemic O(2) delivery and arteriovenous O(2) difference to [Formula: see text] in overweight and obese women with PCOS. Fifteen overweight or obese PCOS women and 15 age‐, anthropometry‐, and physical activity‐matched control women performed a maximal incremental cycling exercise test. Alveolar gas exchange (volume turbine and mass spectrometry), arterial O(2) saturation (pulse oximetry), and cardiac output (CO) (impedance cardiography) were monitored. Hb concentration was determined. Arterial O(2) content and arteriovenous O(2) difference (C(a‐v)O(2)) (Fick equation) were calculated. Insulin resistance was evaluated by homeostasis model assessment (HOMA‐IR). PCOS women had lower [Formula: see text] than controls (40 ± 6 vs. 46 ± 5 mL/min/kg fat‐free mass [FFM], P = 0.011). Arterial O(2) content was similarly maintained in the groups throughout the exercise test (P > 0.05). Linear regression analysis revealed a pronounced response of CO to increasing [Formula: see text] in PCOS women during the exercise test: A ∆CO/∆ [Formula: see text] slope was steeper in PCOS women than in controls (β = 5.84 vs. β = 5.21, P = 0.004). Eventually, the groups attained similar peak CO and peak CO scaled to FFM (P > 0.05). Instead, C(a‐v)O(2) at peak exercise was lower in PCOS women than in controls (13.2 ± 1.6 vs. 14.8 ± 2.4 mL O(2)/100 mL blood, P = 0.044). HOMA‐IR was similar in the groups (P > 0.05). The altered cardiorespiratory responses to exercise in overweight and obese PCOS women indicate that PCOS per se is associated with alterations in peripheral adjustments to exercise rather than with limitations of systemic O(2) delivery.