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POINT-COUNTERPOINT
Aliverti and Macklem (1, 3) speculate on the role of expiratory muscle recruitment in their schematic representation of the development of exercise intolerance in COPD. The phenotype they referred to as recruiter would be characterized by a high respiratory muscle oxygen consumption resulting in low blood and oxygen availability to the contracting peripheral muscles and little or no dynamic hyperinflation. Our clinical experience and a review of the literature suggest, however, that such a phenotype would be rather unusual. For instance, most patients with COPD exhibit dynamic hyperinflation during exercise (6). Moreover, dynamic hyperinflation occurs as early as in GOLD stage I patients (7), suggesting that it would be unlikely for expiratory muscle recruitment to precede dynamic hyperinflation in the progression of COPD. The low estimate of oxygen availability to the contracting muscles proposed by Aliverti and Macklem is also inconsistent with the notion that O2 delivery to the lower limb is typically preserved in COPD (4, 9). Finally, skeletal muscle dysfunction characterized by low oxidative capacity and muscle endurance as well as by an impaired contractile protein metabolism (2, 5, 8), has been reported early in the disease, even before detectable reduction in expiratory flows. Because of these considerations, we doubt that expiratory muscle recruitment is central in the development of exercise intolerance in COPD.
O'Donnell and Webb make a compelling case about the key role of dynamic hyperinflation and impaired respiratory mechanics in exercise intolerance in COPD. However, this does not preclude a role for limb muscle dysfunction in limiting exercise in COPD. For example, inspiratory capacity and tidal volume at peak exercise contribute to <50% of the variability in peak 
O2 (6). Furthermore, the experience gain in lung transplantation confirms that altered pulmonary mechanics is insufficient to explain the pathophysiology of exercise intolerance in COPD (10).
Intolerance to daily activities is a frequent complaint in COPD. As emphasized in this debate, there is an agreement on the complexity of the determinants of exercise tolerance in COPD. Failure to acknowledge the multifactorial nature of this problem in general, and the importance of deficient peripheral muscles in specific, will lead to suboptimal clinical interventions.
REFERENCES
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