When obesity and COPD collide: Physiological and clinical consequences

University of Oxford (2011) Proc Physiol Soc 23, SA97

Research Symposium: When obesity and COPD collide: Physiological and clinical consequences

D. O'Donnell1

1. Queen's University, Kingston, Ontario, Canada.

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The prevalence of both chronic obstructive pulmonary disease (COPD) and obesity is increasing steadily throughout the western world. Several recent studies demonstrate that the prevalence of obesity is greater among patients with COPD than in the general population. A recent population study found that in Canada, the prevalence of obesity in COPD was as high as 25% and greater than the non-COPD population (17%) (1). Unlike the general population where obesity prevalence is escalating, it has remained stable over a 13 year observation period in COPD. Increased activity limitation and healthcare utilization were found much more commonly in obese COPD patients compared with non-obese COPD. The presence of obesity has paradoxically been shown to convey a survival advantage in patients with more severe COPD but extreme obesity in COPD has been associated with increased respiratory-related mortality (2). Obese subjects with COPD demonstrate reduced exercise capacity as measured by six-minute walk distance but not as measured by cycle endurance tests (3-6). To begin to reconcile these apparent contradictions, a better understanding is needed of the interactions between COPD, obesity, activity limitation and respiratory symptoms. A recent study has shown that increasing BMI has profound effects on resting pulmonary function measurements in patients with airway obstruction (7). Thus, residual volume and functional residual capacity decreased exponentially as BMI increased in COPD. The volume reducing effects of increased BMI are seen even in the overweight range and it is noteworthy that existing predictive equations for lung volume do not account for this important effect. Given the known restrictive ventilatory deficit associated with obesity and the propensity for increased airway closure and expiratory flow limitation at the lower operating volumes, one would anticipate that the combination of obesity and COPD would have added deleterious effects with respect to dyspnea and exercise intolerance. However, when one compares ventilatory constraints during cycle exercise (which unloads the excess body mass) in obese and lean COPD patients, matched for FEV1, there is no clear disadvantage seen in the former (3-6). Exercise endurance time, measured during constant work rate cycle exercise testing, has been shown to be similar in obese and normal weight COPD patients despite increased metabolic and ventilatory requirements associated with excessive weight (3-6). We have postulated that the volume reduction effects of obesity in COPD and the recruitment of a higher resting inspiratory capacity convey a mechanical advantage that counter-balances the known restrictive effects and increased elastic loading of obesity (4-6). Obesity causes lung deflation of similar magnitude to that achieved during pharmacological or surgical volume lung volume reduction. A recent mechanical study has shown that in patients with moderate COPD who have mild obesity, static elastic recoil pressure of the lungs and intra-abdominal pressures are significantly increased compared with lean COPD patients with similar airway obstruction (6). Mean expiratory flow rates during exercise were not diminished despite lower operating lung volumes in the obese COPD group, possibly because of the increased driving pressure for flow. However, we were unable to show any significant advantage with respect to diaphragmatic function in the obese COPD patient compared to the normal weight control. Respiratory muscle performance and recruitment patterns throughout exercise were similar in obese and lean COPD groups (6). These studies collectively indicate that abnormalities in dynamic ventilatory mechanics and the associated respiratory discomfort are not appreciably greater in obese COPD patients than in lean controls, at least during cycle exercise. During weight-bearing exercise (treadmill walking), we anticipate that the higher metabolic and ventilatory requirements of this task will force an earlier onset of critical respiratory mechanical constraints in obese COPD patients than during weight-supported cycle exercise at comparable power outputs. However, it remains to be seen whether the long held belief that “respiratory factors are the proximate cause of activity limitation during daily activities in patients with combined COPD and obesity” is actually true.



Where applicable, experiments conform with Society ethical requirements.

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