Impaired central hemodynamics in chronic obstructive pulmonary disease during submaximal exercise

It is unknown whether central hemodynamics are impaired during exercise in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that, at a similar absolute (V)over dotO(2) during exercise, COPD patients would have a lower stroke volume and cardiac output compared with healthy controls. Furthermore, we hypothesized that greater static hyperinflation [ratio of inspiratory capacity to total lung capacity (IC/TLC)] and expiratory intrathoracic pressure would be significantly related to the lower cardiac output and stroke volume responses in COPD patients. Clinically stable COPD (n = 13; FEV1/FVC: 52 +/- 13%) and controls (n = 10) performed constant workload submaximal exercise at an absolute (V)over dotO(2) of similar to 1.3 L/min. During exercise, inspiratory capacity maneuvers were performed to determine operating lung volumes and cardiac output (via open-circuit acetylene rebreathe technique) and esophageal pressure were measured. At similar absolute (V)over dotO(2) during exercise (P = 0.81), COPD had lower cardiac output than controls (COPD: 11.0 +/- 1.6 vs. control: 12.2 +/- 1.2 L/min, P = 0.03) due to a lower stroke volume (COPD: 107 +/- 13 vs. control: 119 +/- 19 mL, P = 0.04). The heart rate response during exercise was not different between groups (P = 0.66). FEV1 (% predicted) and IC/TLC were positively related to stroke volume (r = 0.68, P = 0.01 and r = 0.77, P < 0.01). Last, esophageal pressure-time integral during inspiration was positively related to cardiac output (r = 0.56, P = 0.047). These data demonstrate that COPD patients have attenuated cardiac output and stroke volume responses during exercise compared with control. Furthermore, these data suggest that the COPD patients with the most severe hyperinflation and more negative inspiratory intrathoracic pressures have the most impaired central hemodynamic responses. NEW & NOTEWORTHY Chronic obstructive pulmonary disease leads to cardiac structural changes and pulmonary derangements that impact the integrative response to exercise. However, it is unknown whether these pathophysiological alterations influence the cardiac response during exercise. Herein, we demonstrate that COPD patients exhibit impaired central hemodynamics during exercise that are worsened with greater hyperinflation.