Until its end stages, PAH in reality represents a dynamic limitation (ie, of exercise) rather than a static one (ie, at rest). Recognizing that many patients are symptomatic with effort, it seems intuitive that patients should be evaluated in a dynamic fashion. Moreover, in early disease, resting hemodynamics may be normal, whereas hemodynamic evaluation during exercise may reveal clinically silent loss of pulmonary microvasculature. The use of stress echocardiography to noninvasively assess hemodynamics has been practiced for > 30 years, and reference values for exercise sPAP have been established.6 Fifteen years ago, it was shown that very large stroke volumes in varsity athletes may result in a large rise in sPAP, challenging conventional thinking.7 Bidart et al8 have demonstrated differences in the relationship between flow and pressure (pulmonary vascular resistance) in normal subjects vs subjects with pulmonary disease. Recent studies have begun to clarify the clinical correlates of exercise-induced pulmonary hypertension (PH). Invasive and noninvasive studies show that the slope of linearized mean pulmonary artery pressure-cardiac output (mPAP/Q) relationships in normal subjects should not exceed 3 mmHg/L/min.9 Estimation of PAP with treadmill exercise, or even supine bike, is technically challenging due to time constraints or motion related to exercise or tachypnea. In addition, patients may be deconditioned and, therefore, unable to exercise sufficiently. Thus, novel approaches are needed that can increase pulmonary blood flow in a titratable fashion, while echocardiography is performed. To address these challenges, in this issue of CHEST (see page 959), Lau et al10 present data that dobutamine stress echocardiography can serve well as a means to solve the issues.