Devin B Phillips1, Sophie É Collins2, Tracey L Bryan3, Eric Y L Wong3, M Sean McMurtry4, Mohit Bhutani3, Michael K Stickland5. 1. Division of Pulmonary Medicine, Faculty of Medicine and Dentistry, University of Alberta, Canada; Faculty of Kinesiology, Sport, and Recreation, University of Alberta, Canada. 2. Division of Pulmonary Medicine, Faculty of Medicine and Dentistry, University of Alberta, Canada; Faculty of Rehabilitation Medicine, University of Alberta, Canada. 3. Division of Pulmonary Medicine, Faculty of Medicine and Dentistry, University of Alberta, Canada. 4. Division of Cardiology, Faculty of Medicine and Dentistry, University of Alberta, Canada. 5. Division of Pulmonary Medicine, Faculty of Medicine and Dentistry, University of Alberta, Canada; G.F. MacDonald Centre for Lung Health, Covenant Health, Edmonton, Alberta, Canada. Electronic address: michael.stickland@ualberta.ca.
Abstract
BACKGROUND:Patients with chronic obstructive pulmonary disease (COPD) have an exaggerated ventilatory response to exercise, contributing to exertional dyspnea and exercise intolerance. We recently demonstrated enhanced activity and sensitivity of the carotid chemoreceptor (CC) in COPD which may alter ventilatory and cardiovascular regulation and negatively affect exercise tolerance. We sought to determine whether CC inhibition improves ventilatory and cardiovascular regulation, dyspnea and exercise tolerance in COPD. METHODS:Twelve mild-moderate COPD patients (FEV1 83 ± 15 %predicted) and twelve age- and sex-matched healthy controls completed twotime-to-symptom limitation (TLIM) constant load exercise tests at 75% peak power output with either intravenous saline or low-dose dopamine (2 μg·kg-1·min-1, order randomized) to inhibit the CC. Ventilatory responses were evaluated using expired gas data and dyspnea was evaluated using a modified Borg scale. Inspiratory capacity maneuvers were performed to determine operating lung volumes. Cardiac output was estimated using impedance cardiography and vascular conductance was calculated as cardiac output/mean arterial pressure (MAP). RESULTS: At a standardized exercise time of 4-min and at TLIM; ventilation, operating volumes and dyspnea were unaffected by dopamine in COPD patients and controls. In COPD, dopamine decreased MAP and increased vascular conductance at all time points. In controls, dopamine increased vascular conductance at TLIM, while MAP was unaffected. CONCLUSION: There was no change in time to exhaustion in either group with dopamine. These data suggest that the CC plays a role in cardiovascular regulation during exercise in COPD; however, ventilation, dyspnea and exercise tolerance were unaffected by CC inhibition in COPD patients.
RCT Entities:
BACKGROUND:Patients with chronic obstructive pulmonary disease (COPD) have an exaggerated ventilatory response to exercise, contributing to exertional dyspnea and exercise intolerance. We recently demonstrated enhanced activity and sensitivity of the carotid chemoreceptor (CC) in COPD which may alter ventilatory and cardiovascular regulation and negatively affect exercise tolerance. We sought to determine whether CC inhibition improves ventilatory and cardiovascular regulation, dyspnea and exercise tolerance in COPD. METHODS: Twelve mild-moderate COPDpatients (FEV1 83 ± 15 %predicted) and twelve age- and sex-matched healthy controls completed two time-to-symptom limitation (TLIM) constant load exercise tests at 75% peak power output with either intravenous saline or low-dose dopamine (2 μg·kg-1·min-1, order randomized) to inhibit the CC. Ventilatory responses were evaluated using expired gas data and dyspnea was evaluated using a modified Borg scale. Inspiratory capacity maneuvers were performed to determine operating lung volumes. Cardiac output was estimated using impedance cardiography and vascular conductance was calculated as cardiac output/mean arterial pressure (MAP). RESULTS: At a standardized exercise time of 4-min and at TLIM; ventilation, operating volumes and dyspnea were unaffected by dopamine in COPDpatients and controls. In COPD, dopamine decreased MAP and increased vascular conductance at all time points. In controls, dopamine increased vascular conductance at TLIM, while MAP was unaffected. CONCLUSION: There was no change in time to exhaustion in either group with dopamine. These data suggest that the CC plays a role in cardiovascular regulation during exercise in COPD; however, ventilation, dyspnea and exercise tolerance were unaffected by CC inhibition in COPDpatients.
Authors: Sophie É Collins; Devin B Phillips; M Sean McMurtry; Tracey L Bryan; D Ian Paterson; Eric Wong; Justin A Ezekowitz; Mary A Forhan; Michael K Stickland Journal: Front Physiol Date: 2020-03-12 Impact factor: 4.566