We used functional criteria to exclude asthmatic patients from the analysis. Furthermore, only a minority of the 15 asthmatic patients of Paré et al3 had the degree of hyperinflation seen in our COPD patients. Thus, the two study populations were quite different. Nevertheless, the mechanisms underlying the volume effects could be similar. Although the results of the study by Paré et al3 are consistent with a volume response due to peripheral airway recruitment, our data do not support this relationship. To the extent that maximal forced expiratory flows at the midexpiratory phase (FEF25–75) and at 75% of vital capacity (FEF75) reflect the contribution of the peripheral airways, we found no significant correlations between these flow parameters and the improvements in our volume indices (Table 3 of Newton et al,1). ΔFEV1/FVC also did not correlate with ΔFEF25–75 and ΔFEF75 (unpublished data). Alternatively, FEF25–75 and FEF75 may not reflect the effects on peripheral airways in COPD patients, and the mechanism proposed by Paré et al,3 does pertain. Further studies are required to elucidate this issue.