When humans exercise, cardiac output (CO) increases, but there are only minor increases in pulmonary artery pressure (PAP). Whether the CO is accommodated via recruitment of unused pulmonary capillaries resulting in increased functional capillary surface area (FCSA), or via distention of already perfused capillaries, is unknown. We measured FCSA pre and during exercise, and we identify the physiologic mode of accommodation of increased blood flow during supine exercise in humans.
Ten subjects (9 female) with resting mean PAP (PAPm) < 25 mm Hg performed supine symptom-limited exercise. Hemodynamics were measured. The first-pass pulmonary circulatory metabolism of injected 3H-benzoyl-Phe-Ala-Pro (BPAP), which is proportional to FCSA, was measured at rest and at peak exercise. Data are mean±SD.
Subjects exercised for 959±308 seconds at 71±31 Watts. PAPm rose from 18.8±3.3 mm Hg to 28.5±4.6, CO from 6.35±1.6 L/min to 13.4±2.9 L/min, and pulmonary artery wedge pressure (PAWP) from 14±3.3 mm Hg to 19.5±5. Percent BPAP metabolism (%M) fell from 74.7%±0.1 to 67.1±0.1, and FCSA/body surface area (FCSA/BSA) rose from 2939±640 to 5018±1032. In nine of the subjects, the relationship of FCSA/BSA to CO suggested principally capillary recruitment and not distention. In the tenth subject, an active marathon runner, resting CO and FCSA/BSA were high, and subsequent increases with exercise suggested distention.
Exercising humans demonstrate pulmonary capillary recruitment and distention. At moderate resting CO, increasing blood flow causes mostly recruitment. However, when exercise begins at high CO, further increases cause mostly distention. Supine gravitational flow gradients play a role and the posterior lung zones, already perfused at rest, may respond to flow with more distention than the anterior zones that are less perfused at rest. Our findings resolve an important physiologic question, and they may provide a means for further understanding the exercise limitation in pulmonary hypertension, and responses to therapy.