We thank Young and Hopkins for their interesting comments on our article (September 2009).1 They suggest that low-grade systemic inflammation mediated by interleukin-6 (IL-6) may act concomitantly on the skeletal muscles and pulmonary vasculature to impair exercise capacity in patients with COPD. It has been shown that IL-6 is increased in the plasma of patients with COPD2 and induces the release of acute-phase proteins; furthermore, IL-6 probably has other systemic effects that have not yet been fully elucidated. The hypothesis put forward by Young and Hopkins is partly supported by our results. Our study1 did not establish a link between systemic inflammation and exercise capacity, because it focused on the mechanism of pulmonary hypertension in patients with COPD. However, we found a weak but significant correlation between the 6-min walk distance and plasma IL-6 level (r = −0.329, P =.04). However, as stated in our article, the 6-min walk distance did not correlate with mean pulmonary artery pressure. Only very few studies found that mean pulmonary artery pressure determined the severity of exercise limitation in COPD.3 We fully agree with Young and Hopkins that any drugs designed to improve exercise capacity in COPD must have several targets, as shown in their Figure 1. Indeed, in our opinion, a drug that only lowers mean pulmonary artery pressure is likely to improve neither the dyspnea nor the exercise capacity and is probably not worth pursuing. It is also important to emphasize that smoke exposure in genetically susceptible individuals promotes the development of COPD4 and may also promote the development of comorbidities through systemic inflammation.