Key pointsr Weightlessness in space induces initially an increase in stroke volume and cardiac output, accompanied by unchanged or slightly reduced blood pressure.r It is unclear whether these changes persist throughout months of flight. r Here, we show that cardiac output and stroke volume increase by 35-41% between 3 and 6 months on the International Space Station, which is more than during shorter flights.r Twenty-four hour ambulatory brachial blood pressure is reduced by 8-10 mmHg by a decrease in systemic vascular resistance of 39%, which is not a result of the suppression of sympathetic nervous activity, and the nightly dip is maintained in space.r It remains a challenge to explore what causes the systemic vasodilatation leading to a reduction in blood pressure in space, and whether the unexpectedly high stroke volume and cardiac output can explain some vision acuity problems encountered by astronauts on the International Space Station.Abstract Acute weightlessness in space induces a fluid shift leading to central volume expansion. Simultaneously, blood pressure is either unchanged or decreased slightly. Whether these effects persist for months in space is unclear. Twenty-four hour ambulatory brachial arterial pressures were automatically recorded at 1-2 h intervals with portable equipment in eight male astronauts: once before launch, once between 85 and 192 days in space on the International Space Station and, finally, once at least 2 months after flight. During the same 24 h, cardiac output (rebreathing method) was measured two to five times (on the ground seated), and venous blood was sampled once (also seated on the ground) for determination of plasma catecholamine concentrations. The 24 h average systolic, diastolic and mean arterial pressures (mean ± SE) in space were reduced by 8 ± 2 mmHg (P = 0.01; ANOVA), 9 ± 2 mmHg (P < 0.001) and 10 ± 3 mmHg (P = 0.006), respectively. The nightly blood pressure dip of 8 ± 3 mmHg (P = 0.015) was maintained. Cardiac stroke volume and output increased by 35 ± 10% and 41 ± 9% (P < 0.001); heart rate and catecholamine concentrations were unchanged; and systemic vascular resistance was reduced by 39 ± 4% (P < 0.001). The increase in cardiac stroke volume and output is more than previously observed during short duration flights and might be a precipitator for some of the vision problems encountered by the astronauts. The spaceflight vasodilatation mechanism needs to be explored further.

Abstract-During everyday life, gravity constantly stresses the cardiovascular system in upright humans by diminishing venous return. This decreases cardiac output and induces systemic vasoconstriction to prevent blood pressure from falling. We therefore tested the hypothesis that entering weightlessness leads to a prompt increase in cardiac output and to systemic vasodilatation and that these effects persist for at least a week of weightlessness in space. Cardiac output and mean arterial pressure were measured in 8 healthy humans during acute 20-s periods of weightlessness in parabolic airplane flights and on the seventh and eighth day of weightlessness in 4 astronauts in space. The seated 1-G position acted as reference. Entering weightlessness promptly increased cardiac output by 29Ϯ7%, from 6.6Ϯ0.7 to 8.4Ϯ0.9 L min Ϫ1 (meanϮSEM; Pϭ0.003), whereas mean arterial pressure and heart rate were unaffected. Thus, systemic vascular resistance decreased by 24Ϯ4% (Pϭ0.017). After a week of weightlessness in space, cardiac output was increased by 22Ϯ8% from 5.1Ϯ0.3 to 6.1Ϯ0.1 L min Ϫ1 (Pϭ0.021), with mean arterial pressure and heart rate being unchanged so that systemic vascular resistance was decreased by 14Ϯ9% (Pϭ0.047). In conclusion, entering weightlessness promptly increases cardiac output and dilates the systemic circulation. This vasorelaxation persists for at least a week into spaceflight. Thus, it is probably healthy for the human cardiovascular system to fly in space. Key Words: blood pressure Ⅲ cardiac output Ⅲ cardiovascular diseases Ⅲ heart rate Ⅲ vascular resistance T hroughout evolution of mankind, gravity has constantly stressed the cardiovascular system by diminishing venous return of blood to the heart. 1 This gravity-induced decrease in venous return, and, thus in cardiac output, is detected by cardiopulmonary and arterial baroreflexes, which initiate constriction of the vasculature to prevent blood pressure from falling. Therefore, gravity is a chronic systemic vasoconstrictor in upright humans during normal everyday life.Previous cardiovascular measurements in astronauts in space indicate that cardiac output is increased by some 18% by weightlessness compared with upright standing or sitting on the ground and more so during the initial days of flight than at the end. 2,3 In these studies, blood pressure was not measured. In another study, Fritsch-Yelle et al 4 observed in 12 astronauts over several flights that the mean 24-hour diastolic arterial pressure, but not systolic pressure, was significantly decreased in space by some 5 mm Hg. This decrease was evident at the beginning and at the end of flight. However, cardiac output was not measured. Therefore, it is not known whether the unchanged systolic and decreased diastolic pressure in space is accounted for by systemic vasodilatation and whether systemic vasodilatation is evident from the very beginning and to the end of flight.We therefore tested the hypothesis that the weightlessnessinduced increase in cardiac output leads to systemic vasodilata...