The Effect of Pulmonary Rehabilitation on Carotid Chemoreceptor Activity and Sensitivity in COPD
Authors: Byers Bradley W , Fuhr Desi P , Moore Linn E , Bhutani Mohit , Wong Eric , Stickland Michael K 
Published: November 2023

Chronic Obstructive Pulmonary Disease (COPD) is a respiratory disease characterized by progressive, partially reversible airway obstruction. While considered a disease of the lungs, COPD is associated with increased cardiovascular (CV) mortality; this increased CV risk may result from heightened sympathetic nervous activity secondary to elevated carotid chemoreceptor (CC) activity/sensitivity. Our recent work suggests that COPD patients have an exaggerated resting CC activity/sensitivity which appears to contribute to increased tonic vasoconstriction.

Experimental chronic heart failure is characterized by heightened CC activity/sensitivity, and exercise training has been shown to normalize CC activity/sensitivity in this population. COPD patients are commonly referred to pulmonary rehabilitation (PR), an exercise‐based intervention shown to be effective in improving dyspnea, exercise tolerance, and quality of life. However, the physiological mechanisms underlying these improvements are unclear. The purpose of this study was to examine the effects of PR on CC activity/sensitivity in COPD.

A case control study design was used; COPD patients either attended PR (experimental) or no PR (control) for 6–8 weeks. CC activity and sensitivity, exercise tolerance, and resting dyspnea were assessed before and after the respective 6–8 week period. Resting CC activity was determined by the reduction in minute ventilation (V̇E) while breathing transient hyperoxia (FIO2=1.0). CC sensitivity was evaluated by the increase in V̇E relative to the drop in arterial saturation while breathing hypoxic gas (ΔV̇E/ΔSpO2). Exercise tolerance was assessed by six minute walk distance (6MWD), and the 0–4 modified Medical Research Council questionnaire (MMRC) was used to determine resting dyspnea.

To date, data (mean±SD) have been collected on 45 patients completing PR (FEV1 57±21% predicted; age 67±7 years) and 6 controls (FEV1 68±19% predicted; age 71±6 years). Patients completing PR improved exercise tolerance (pre 6MWD: 441±80 m, post: 478±110 m, p<0.001) and reduced resting dyspnea (pre MMRC: 2.41±0.82, post: 2.15±0.84, p=0.04). Resting CC activity was unchanged following PR (pre: −1.07±1.55 L/min, post: −0.93±1.46 L/min, p=0.60), and similarly no change was observed in the control group (pre: −0.73±0.65 L/min, post: −0.96±1.36 L/min, p=0.53). CC sensitivity also remained unchanged in both the experimental (pre: 0.08±0.07 L/min/%SpO2, post: 0.11±0.15 L/min/%SpO2, p=0.561) and control (pre: 0.26±0.17 L/min/%SpO2, post: 0.31±0.11 L/min/%SpO2, p=0.363) groups.

Current data suggest that PR does not influence CC activity/sensitivity in COPD. While previous studies have shown that exercise training normalizes CC activity/sensitivity in other diseases, it is possible that the intensity or length of PR is insufficient to elicit reductions in CC activity/sensitivity. Alternately, despite improving exercise tolerance and resting dyspnea, exercise training may not affect CC activity/sensitivity in COPD.

Support or Funding Information

Funding for this work is provided by Alberta Innovates Health Solutions, Canadian Institutes of Health Research, and Heart & Stroke Foundation of Alberta, NWT & Nunavut. (PI: M. Stickland).