Queen's University - Utility Bar

QSpace at Queen's University >
Theses, Dissertations & Graduate Projects >
Queen's Theses & Dissertations >

Please use this identifier to cite or link to this item: http://hdl.handle.net/1974/7551

Title: EXERCISE LIMITATION IN MILD COPD: THE ROLE OF RESPIRATORY MECHANICAL FACTORS
Authors: Chin, Roberto Carlos

Files in This Item:

File Description SizeFormat
Chin_Roberto_C_201209_MSc.pdf5.52 MBAdobe PDFView/Open
Keywords: Mild COPD
Dead Space Loading
Dyspnea
Exercise Limitation
Issue Date: 28-Sep-2012
Series/Report no.: Canadian theses
Abstract: The majority of patients with chronic obstructive pulmonary disease (COPD) have milder airway obstruction and are not diagnosed in a timely fashion. Nevertheless, these patients are largely under-studied; this, despite new evidence of increased morbidity and mortality in this sub-population. Recent studies have highlighted the increased ventilatory requirements and abnormalities in respiratory mechanics as important features to explain the relatively reduced exercise tolerance and greater exertional dyspnea in these patients. However, it remains uncertain whether such abnormal mechanical factors actually limit exercise capacity in mild COPD. Accordingly, the objective of this study was to determine whether ventilatory constraints represent a primary factor in exercise limitation and increased dyspnea in this patient group. To determine the role of mechanical factors in exercise limitation in mild COPD, we selectively loaded the respiratory system by adding dead space (DS) to the breathing circuit. We compared ventilation, breathing pattern, operating lung volumes, and dyspnea intensity during incremental cycle exercise in 20 patients with GOLD stage I COPD (post-bronchodilator FEV1/FVC=61±5%, and FEV1=95±11% predicted; mean±SD) and 20 healthy age-, sex- and BMI-matched subjects under two conditions, in randomized order: unloaded control (CTRL) or ventilatory stimulation by 600mL of an added DS. Compared to the CTRL condition, both healthy and COPD participants had small decreases in peak work rate and no significant increase in peak ventilation with the added DS. At the highest equivalent work rate of 60 watts, DS caused a smaller increase in tidal volume (VT) in COPD compared with healthy subjects (+0.26±0.29 vs. +0.56±0.22 L respectively, p<0.01) with a correspondingly greater increase in dyspnea intensity (+1.8±1.8 vs. +0.2±0.6 Borg units, respectively, p<0.0001). At peak exercise, COPD patients failed to significantly increase VT, reflecting the fact that end-inspiratory lung volume (EILV) could not increase with DS vs. CTRL (5.25±0.91 vs. 5.16±0.84 L, respectively, p=0.41). This contrasts the results in health where EILV increased with DS vs. CTRL (5.40±1.01 vs. 5.13±0.90 L, respectively, p<0.05). We conclude that the lower exercise performance in mild COPD, compared with health, is explained by critical respiratory mechanical constraints which limit further increases in ventilation to support a higher metabolic load.
Description: Thesis (Master, Physiology) -- Queen's University, 2012-09-28 12:04:50.507
URI: http://hdl.handle.net/1974/7551
Appears in Collections:Physiology Graduate Theses
Queen's Theses & Dissertations

Items in QSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

 

  DSpace Software Copyright © 2002-2008  The DSpace Foundation - TOP