Pulmonary arterial hypertension (PAH), defined as a mean pulmonary arterial pressure (mPAP) of ≥25 mmHg at rest and pulmonary arterial wedge pressure ≤15 mmHg, is consistently associated with reduced exercise capacity and intolerable dyspnoea (respiratory difficulty) on exertion. Dyspnoea is a complex multifaceted and highly personalized sensory experience, the source and mechanisms of which are incompletely understood. Activity-related dyspnoea appears to be the earliest and the most frequent complaint for which patients with PAH seek medical attention. This symptom progresses relentlessly with time leading invariably to avoidance of activity with consequent skeletal muscle deconditioning and an impoverished quality of life. Unfortunately, effective management of this disabling symptom awaits a better understanding of its underlying physiology. Previous studies on mechanisms of exertional dyspnoea in PAH have largely and mostly focused on the cardiovascular determinants of respiratory discomfort. However, respiratory mechanics abnormalities could contribute to exertional dyspnoea in these patients. For instance, PAH patients may exhibit reduced expiratory flows at low lung volumes at spirometry (namely instantaneous forced expiratory flows measured after 50% and 75% of the FVC has been exhaled [FEF50% and FEF75%] lower than predicted), despite a preserved forced expiratory volume in 1 second/forced vital capacity ratio (FEV1/FVC). Several studies have shown that such a finding ("small airway disease") could be common in certain PAH cohorts, have either related it to incidental descriptions of airway wall thickening with lymphocytic infiltration in PAH or proposed several other speculative explanatory mechanisms, either biological or mechanical. Whatever its cause, reduced expiratory flows at low lung volumes imply that the operating tidal volume (VT) range becomes closer than normally to residual volume (RV) mostly through an increase in RV (elevated residual volume/total lung capacity ratio, RV/TLC). The reduced difference between forced and tidal expiratory flows promotes dynamic lung hyperinflation [i.e., a progressive increase in end-expiratory lung volume (EELV)] under conditions of increased ventilatory demand. Dynamic lung hyperinflation (DH) increases the mechanical inspiratory load that the respiratory muscles must overcome to produce ventilation (V'E), places the diaphragm at mechanical disadvantage, and reduces the ability of VT to expand appropriately during exercise, thus imposing "restrictive" mechanics: VT is therefore truncated from below by the increasing EELV and constrained from above by the total lung capacity (TLC) envelope and the relatively reduced inspiratory reserve volume (IRV). Dynamic hyperinflation-induced critical mechanical constraint of VT expansion has serious sensory consequences, i.e., increase in dyspnoea intensity, as clearly shown in patients with chronic obstructive pulmonary disease and chronic heart failure.