RESPONSE

Dear Editor-in-Chief Babb et al. (1) are “…concerned that the calculation of dysanapsis using predicted lung recoil will not accurately reflect true dysanapsis in all individuals.” In our study (2), we divided forced expired flow at 50% of forced vital capacity by the corresponding recoil pressure (Pst(l)50) for each subject. This was done to account for the fact that flow is sensitive to lung recoil as well as airway size. We used previously published regression estimates of Pst(l)50 (3,4). We are, of course, cognizant of the inherent limitations of predictive equations. However, in this case, the usage of predictive values does not appreciably alter the calculation of dysanapsis nor our overall conclusion and interpretation. First, we have measured Pst(l)50 directly using esophageal pressure measures in an identical fashion to that of Mead (3) in 17 young subjects free of any history of smoking. When compared with Mead’s predicted values, our measured values of Pst(l)50 deviated on average by only approximately 1 cm H2O. Furthermore, we found excellent agreement between our measured ratio and the predicted dysanapsis ratio (intraclass correlation (ICC) > 0.8). Second, it would require a large and most likely nonphysiologic difference in Pst(l)50 to have any effect on the subject groupings in our study (2). In order for the non–expiratory flow–limited subjects in our study to have a dysanapsis ratio similar to that of the flow-limited group, their Pst(l)50 would need to be 5 cm H2O higher. Applying a small source of variation (1.39 cm H2O) as suggested by Babb et al. to our values does not affect our classification of subjects. Babb et al. further suggest that it would be worthwhile to probe into the medical history of either lung infections or childhood asthma in these groups. This is, in our view, highly speculative and is an approach that would likely be fraught with methodological problems that would make interpretation difficult if not impossible. For example, most people have had a cold, the flu, or other types of transient pulmonary complication during their life. How would these self-report data be classified and stratified? Moreover, how would the considerable between-subject variation during periods of growth and childhood susceptibility to infections and asthma affect the interrelationship between the airways, the lungs, and the integrated pulmonary response to exercise? We wish to emphasize that Mead’s (3) and our (2) “measures” of airway size are indirect and are, admittedly, not true anatomic measures. Rather, they reflect a functional measure/index of airway size. A promising approach to studying possible male–female differences is to have quantitative anatomic measures of different airway generations using modern imaging methods such as computed tomography or magnetic resonance imaging in subjects for whom detailed lung mechanics data during exercise are also available. Paolo B. Dominelli, MSc Jordan A. Guenette, PhD Sabrina S. Wilkie, MSc Glen E. Foster, PhD A. William Sheel, PhD School of Kinesiology University of British Columbia Vancouver, British Columbia, Canada The authors declare no conflicts of interest.

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