title: Chemosensitivity, Cardiovascular Risk, and the Ventilatory Response to Exercise in COPD.
abstract: COPD is associated with elevated cardiovascular risk and a potentiated ventilatory response to exercise. Enhanced carotid chemoreceptor (CC) activity/sensitivity is present in other clinical conditions, has been shown to contribute to sympathetic vasoconstrictor outflow, and is predictive of mortality. CC activity/sensitivity, and the resulting functional significance, has not been well examined in COPD. We hypothesized that CC activity/sensitivity would be elevated in COPD, and related to increased pulse wave velocity (a marker of CV risk) and the ventilatory response to exercise.
  
  
  METHODS
  30 COPD patients and 10 healthy age-matched controls were examined. Participants performed baseline cardiopulmonary exercise and pulmonary function testing. CC activity was later evaluated by the drop in ventilation with breathing 100% O2, and CC sensitivity was then assessed by the ventilatory response to hypoxia (ΔVE/ΔSpO2). Peripheral arterial stiffness was subsequently evaluated by measurement of pulse wave velocity (PWV) using applanation tonometry while the subjects were breathing room air, and then following chemoreceptor inhibition by breathing 100% O2 for 2 minutes.
  
  
  RESULTS
  CC activity, CC sensitivity, PWV and the ventilatory response to exercise were all increased in COPD relative to controls. CC sensitivity was related to PWV; however, neither CC activity nor CC sensitivity was related to the ventilatory response to exercise in COPD. CC inhibition by breathing 100% O2 normalized PWV in COPD, while no effect was observed in controls.
  
  
  CONCLUSIONS
  CC activity and sensitivity are elevated in COPD, and appear related to cardiovascular risk; however, CC activity/sensitivity does not contribute to the potentiated ventilatory response to exercise.
authors.affiliation: Pulmonary Division, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.|G.F. MacDonald Centre for Lung Health, Covenant Health, Edmonton, Alberta, Canada.
authors.forename: Michael K
authors.initials: MK
authors.lastname: Stickland
authors.affiliation: Pulmonary Division, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Desi P
authors.initials: DP
authors.lastname: Fuhr
authors.affiliation: Pulmonary Division, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Heather
authors.initials: H
authors.lastname: Edgell
authors.affiliation: Pulmonary Division, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Brad W
authors.initials: BW
authors.lastname: Byers
authors.affiliation: Pulmonary Division, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Mohit
authors.initials: M
authors.lastname: Bhutani
authors.affiliation: Pulmonary Division, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Eric Y L
authors.initials: EY
authors.lastname: Wong
authors.affiliation: Faculty of Physical Education and Recreation, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Craig D
authors.initials: CD
authors.lastname: Steinback
mesh_terms: D000368:Aged; D002318:Cardiovascular Diseases / Q000150:complications* / Q000503:physiopathology; D002319:Cardiovascular System / Q000503:physiopathology; D016022:Case-Control Studies; D015444:Exercise; D005080:Exercise Test; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010100:Oxygen; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D063177:Pulse Wave Analysis; D012119:Respiration; D012129:Respiratory Function Tests; D012306:Risk; D059289:Vascular Stiffness / Q000502:physiology
chemical_list: D010100:Oxygen