In 1915 Krogh first reported that the breathholding pulmonary diffusing capacity for carbon monoxide (DL) is increased during exercise (1). Although change in the volume of blood in the pulmonary capillary bed (Vc), as determined by change in DL, can be produced by several mechanisms, it is during exercise that the greatest changes are observed. Yet, in a previous investigation in which some of the physiologic changes of exercise were simulated, such as alterations in alveolar ventilation, alveolar volume, cardiac output, mixed venous Pco2, and mixed venous Po2, there was little change in breath-holding DL (2).Rosenberg and Forster (3), studying isolated cat lungs, concluded that the pressure across the walls of the pulmonary blood vessels is a primary factor in controlling the size of the pulmonary capillary bed as measured by DL. Observations by other investigators have agreed with this hypothesis (4). Breath-holding DL is increased by central venous engorgement with elevated pulmonary vascular pressure induced by pressure suit inflation (2,5,6). In addition, changes in gravitational orientation from the supine to erect position result in a small decrease in DL and Vc (7), which can be prevented by pressure suit inflation.Head-down tilt increases right atrial pressure and also increases DL and Vc (8). Atropine diminishes central venous pressure (9, 10) and pulmonary blood volume and decreases DL and Vc in