In this regard, our team has recently confirmed that small airway dysfunction at spirometry exists in the majority of PAH patients (60%) despite preserved FEV1/VC, and that this promotes the development of DH under the increased ventilatory demand in response to physical task: in fact, during the accelerated ventilatory response to exercise, 60% of PAH patients did increase their EELV (i.e., DH) by an average of 0.50L from rest to peak exercise, whereas age- and sex-matched healthy subjects did decrease it by an average of 0.45L. Similar levels of DH have been reported in healthy subjects between 40 and 80 years of age, patients with mild-to-severe COPD, CHF, and recently also in a heterogeneous group of patients with precapillary pulmonary hypertension, but at much lower V'E and work-rate than in our more homogeneous group of PAH patients. Our team did also show that DH had serious sensory consequences for PAH patients. DH imposed severe mechanical constraints on VT expansion during exercise on a background of progressively increasing central neural drive: VT was truncated from below by the increasing EELV and constrained from above by the TLC envelope and the relatively reduced IRV. It is generally accepted that in this setting dyspnoea results from the conscious awareness of the increasing disparity between respiratory effort (or neural drive to breathe) and simultaneous thoracic volume displacement. The notion that DH and the subsequent constraint of VT expansion contributed to exertional dyspnoea was bolstered by the strong inverse correlation between dyspnoea intensity and both the increase dynamic EELV/TLC(%) (R=0.70, p<0.05) and the reduced IRV/TLC(%) (R=-0.78, p<0.05) at a standardized exercise stimulus.