The main hemodynamic abnormality in COPD is raised pulmonary vascular resistance and pulmonary hypertension. This is particularly evident when the vascular bed is stressed as in exercise; the absence of reserve collateral vessels prevents the normal reduction in pulmonary vascular resistance, and hence, pressure increases with flow. The increased afterload reduces right ventricular ejection fraction and stroke volume, but cardiac output is maintained by a relative tachycardia. Although most patients have a ventilatory limitation to exercise, in the later stages of the disease, hemodynamic factors may contribute. Studies of the effects of physical training on pulmonary hemodynamics have been few but none has shown any significant improvement. Occasionally there may be an increase in arteriovenous oxygen difference, accounting for the increase in symptom-limited oxygen consumption seen in some patients. The absence of hemodynamic effects of training may be due to insufficient training intensity. The often impressive increases in work tolerance after training may be due in part to an increase in muscular coordination and technique, as well as to metabolic training effects and psychologic factors.