PetersenLG, Damgaard M, Petersen JCG, Norsk P. Mechanisms of increase in cardiac output during acute weightlessness in humans. J Appl Physiol 111: 407-411, 2011. First published June 2, 2011 doi:10.1152/japplphysiol.01188.2010.-Based on previous water immersion results, we tested the hypothesis that the acute 0-Ginduced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects (n ϭ 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 Ϯ 0.4 l/min (P Ͻ 0.001). This increase was diminished to 0.8 Ϯ 0.4 l/min (P ϭ 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G ϩ CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50% of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 Ϯ 0.7 to 7.9 Ϯ 0.8 l/min (P ϭ 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects. regional blood flow; blood pressure; vascular resistance; gravity GRAVITY CONSTANTLY STRESSES the cardiovascular system in upright humans by diminishing venous return. It decreases stroke volume (SV) and thus cardiac output (CO) and, through the baroreflex system, induces arteriolar constriction and an increase in heart rate (HR) to counteract a fall in blood pressure (4,21,30). Compared with the upright 1-G position, sudden entry into weightlessness (0 G) causes a redistribution of blood from the lower vascular beds to the central circulation (4, 29), leading to an increase in venous return, and thus in SV and CO, and, through stimulation of the baroreflexes, to arteriolar vasodilatation and a decrease in HR (18,21,23,29).Our laboratory has previously observed that, in upright seated humans, short-term 0 G created by parabolic airplane flights increases CO by as much as 1.8 l/min, which corresponds to some 0.6 liters over the 20-s period of 0 G (21). Bailliart et al. (2) estimated that, in standing humans, some 165 ml of fluid disappeared from each leg during 20 s of 0 G. These and our observations collectively suggest that the contribution of blood from the legs to the acute 0-G-induced increase in CO amounts to some 50%. In another study from our laboratory, we have, however, observed that water immersion in humans, which is used to simulate the effects of 0 G, increases the diameter of the left atrium to the same degree, whethe...