Ventilatory constraints and dyspnea during exercise in chronic obstructive pulmonary disease

2007 ◽  
Vol 32 (6) ◽  
pp. 1225-1238 ◽  
Author(s):  
Pierantonio Laveneziana ◽  
Chris M. Parker ◽  
Denis E. O’Donnell

Dyspnea (respiratory difficulty) and activity limitation are the primary symptoms of chronic obstructive pulmonary disease (COPD) and progress relentlessly as the disease advances, contributing to reduced quality of life. In COPD, the mechanisms of dyspnea are multifactorial, but abnormal dynamic ventilatory mechanics are believed to play a central role. In flow-limited patients with COPD, dynamic lung hyperinflation (DH) occurs during exercise and has serious sensory and mechanical consequences. In several studies, indices of DH strongly correlate with ratings of dyspnea intensity during exercise, and strategies that reduce resting hyperinflation (either pharmacological or surgical) consistently result in reduced exertional dyspnea. The mechanisms by which DH gives rise to exertional dyspnea and exercise intolerance are complex, but recent mechanistic studies suggest that DH-induced inspiratory muscle loading, restriction of tidal volume expansion during exercise, and consequent neuromechanical uncoupling of the respiratory system are key components. This review examines the specific derangements of ventilatory mechanics that occur in COPD during exercise and attempts to provide a mechanistic rationale for the attendant respiratory discomfort and activity limitation.

Author(s):  
Bojana Butorac Petanjek ◽  
Sanja Popovic-Grle ◽  
Marina Abramovic ◽  
Suzana Kukulj ◽  
Nataša Karamarkovic Lazarušic

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Denis E. O'Donnell ◽  
Conor D. J. O'Donnell ◽  
Katherine A. Webb ◽  
Jordan A. Guenette

In many parts of the world, the prevalence of obesity is increasing at an alarming rate. The association between obesity, multiple comorbidities, and increased mortality is now firmly established in many epidemiological studies. However, the link between obesity and exercise intolerance is less well studied and is the focus of this paper. Although exercise limitation is likely to be multifactorial in obesity, it is widely believed that the respiratory mechanical constraints and the attendant dyspnea are important contributors. In this paper, we examined the evidence that critical ventilatory constraint is a proximate source of exercise limitation in individuals with mild-to-moderate obesity. We first reviewed existing information on exercise performance, including ventilatory and perceptual response patterns, in obese individuals who are otherwise healthy. We then considered the impact of obesity in patients with preexisting respiratory mechanical abnormalities due to chronic obstructive pulmonary disease (COPD), with particular reference to the effect on dyspnea and exercise performance. Our main conclusion, based on the existing and rather sparse literature on the subject, is that abnormalities of dynamic respiratory mechanics are not likely to be the dominant source of dyspnea and exercise intolerance in otherwise healthy individuals or in patients with COPD with mild-to-moderate obesity.


2015 ◽  
Vol 119 (8) ◽  
pp. 882-888 ◽  
Author(s):  
Jayson R. Gifford ◽  
Joel D. Trinity ◽  
Gwenael Layec ◽  
Ryan S. Garten ◽  
Song-Young Park ◽  
...  

This study sought to determine if qualitative alterations in skeletal muscle mitochondrial respiration, associated with decreased mitochondrial efficiency, contribute to exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). Using permeabilized muscle fibers from the vastus lateralis of 13 patients with COPD and 12 healthy controls, complex I (CI) and complex II (CII)-driven State 3 mitochondrial respiration were measured separately (State 3:CI and State 3:CII) and in combination (State 3:CI+CII). State 2 respiration was also measured. Exercise tolerance was assessed by knee extensor exercise (KE) time to fatigue. Per milligram of muscle, State 3:CI+CII and State 3:CI were reduced in COPD ( P < 0.05), while State 3:CII and State 2 were not different between groups. To determine if this altered pattern of respiration represented qualitative changes in mitochondrial function, respiration states were examined as percentages of peak respiration (State 3:CI+CII), which revealed altered contributions from State 3:CI (Con 83.7 ± 3.4, COPD 72.1 ± 2.4%Peak, P < 0.05) and State 3:CII (Con 64.9 ± 3.2, COPD 79.5 ± 3.0%Peak, P < 0.05) respiration, but not State 2 respiration in COPD. Importantly, a diminished contribution of CI-driven respiration relative to the metabolically less-efficient CII-driven respiration (CI/CII) was also observed in COPD (Con 1.28 ± 0.09, COPD 0.81 ± 0.05, P < 0.05), which was related to exercise tolerance of the patients ( r = 0.64, P < 0.05). Overall, this study indicates that COPD is associated with qualitative alterations in skeletal muscle mitochondria that affect the contribution of CI and CII-driven respiration, which potentially contributes to the exercise intolerance associated with this disease.


Respiration ◽  
2011 ◽  
Vol 82 (6) ◽  
pp. 492-500 ◽  
Author(s):  
Yuji Higashimoto ◽  
Noritsugu Honda ◽  
Toshiyuki Yamagata ◽  
Toshiki Matsuoka ◽  
Kazushige Maeda ◽  
...  

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