Control of red blood cell mass in spaceflight

Alfrey, Clarence P.; Udden, Mark M.; Leach-Huntoon, C.; Driscoll, T. B.; Pickett, MaryT.

doi:10.1152/jappl.1996.81.1.98

Cited by 230 publications

(180 citation statements)

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“…This attenuation over time could have been caused by a reduction in blood volume and by a smaller cardiac muscle mass. 13,14 It is noteworthy that cardiac output and systemic vascular resistance after a week in weightlessness adapt to a level in between that of the ground-based seated and horizontal supine positions (Figure 2). This is similar as to how renal responses to saline and water loadings adapt to spaceflight.…”

Section: Discussionmentioning

confidence: 99%

Vasorelaxation in Space

et al. 2006

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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...

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Section: Discussionmentioning

confidence: 99%

Vasorelaxation in Space

et al. 2006

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“…A second concern with the current approach is that 3 days of diuretic administration could have resulted in as many as 3 days of hypovolemia, leading to altered red blood cell mass and hematocrit values. However, this effect is unlikely because hemoconcentration results in reduced red blood cell production (1).…”

Section: Discussionmentioning

confidence: 99%

Hypovolemia and neurovascular control during orthostatic stress

Kimmerly

Shoemaker

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Humans exposed to real or simulated microgravity experience decrements in blood pressure regulation during orthostatic stress that may be related to autonomic dysregulation and/or hypovolemia. We examined the hypothesis that hypovolemia, without the deconditioning effects of bed rest or spaceflight, would augment the sympathoneural and vasomotor response to graded orthostatic stress. Radial artery blood pressure (tonometry), stroke volume (SV), brachial blood flow (Doppler ultrasound), heart rate (electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA; microneurography), and estimated central venous pressure (CVP) were recorded during five levels (Ϫ5, Ϫ10, Ϫ15, Ϫ20 and Ϫ40 mmHg) of randomly assigned lower body negative pressure (LBNP) (n ϭ 8). Forearm (FVR) and total peripheral vascular resistance (TPR) were calculated. The test was repeated under randomly assigned placebo (normovolemia) or diuretic (spironolactone: 100 mg/day, 3 days) (hypovolemia) conditions. The diuretic produced an ϳ16% reduction in plasma volume. Compared with normovolemia, SV and cardiac output were reduced by ϳ12% and ϳ10% at baseline and during LBNP after the diuretic. During hypovolemia, there was an upward shift in the %⌬MSNA/⌬CVP, ⌬FVR/⌬CVP, and ⌬TPR/⌬CVP relationships during 0 to Ϫ20 mmHg LBNP. In contrast to normovolemia, blood pressure increased at Ϫ40 mmHg LBNP during hypovolemia due to larger gains in the %⌬MSNA/⌬CVP and ⌬TPR/⌬CVP relationships. It was concluded that acute hypovolemia augmented the neurovascular component of blood pressure control during moderate orthostasis, effectively compensating for decrements in SV and cardiac output.baroreflex; muscle sympathetic nerve activity; Doppler ultrasound; lower body negative pressure; vascular resistance; spironolactone EXPOSURE TO REAL OR SIMULATED MICROGRAVITY leads to cardiovascular deconditioning with the associated reductions in blood pressure regulation during orthostatic stress. The effect of this deconditioning on baroreflex neurovascular control in humans is not known, and the pathophysiology of postflight difficulties in blood pressure control remains a focus of debate.To maintain adequate blood pressure and cerebral perfusion during orthostatic stress, reflex adjustments occur to increase heart rate (HR) and peripheral vasoconstriction to compensate for a decreased venous return and stroke volume (SV). Primary contributors to the diminished ability to maintain blood pressure in many individuals after spaceflight or bed rest are believed to include reductions in plasma volume (PV) (3, 7, 10, 11), diminished baroreflex control of HR (10, 21), and/or vascular resistance (36,48). From these findings, two separate hypotheses have been proposed to explain difficulties in postural blood pressure control after spaceflight or bed rest.The first hypothesis recognizes the positive correlation between the duration of microgravity exposure and the degree of PV reduction reaching 12-15% or 350-500 ml (3). Hypovolemia leads to larger decreases in both venous return and ...

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“…Thus, when altitude natives, or even altitude sojourners, return to sea level, there is a suppression of erythropoietin (Faura et al, 1969;Jelkman, 1992;Richalet et al, 1993;Gunga et al, 1996;Levine and Stray-Gundersen, 1997;Chapman et al, 1998), a dramatic reduction in iron turnover and bone marrow production of erythroid cell lines (Huff et al, 1951;Reynafarje et al, 1959), and a marked decrease in red cell survival time (Reynafarje et al, 1959). This increase in red cell destruction with suppression of EPO levels has been termed neocytolysis and has been observed under other conditions of a relative increase in oxygen content (Alfrey et al, 1996a(Alfrey et al, , 1996b(Alfrey et al, , 1997Rice and Alfrey, 2000;Rice et al, 2001). Both the rapid ubiquitination and destruction of HIF-1a and neocytolysis (which may be its clinical manifestation) may compromise the ability of short-duration, intermittent hypoxic exposures to induce a sustained increase in the red cell mass.…”

Section: Erythropoietic Effect Of High Altitudementioning

confidence: 97%

Intermittent Hypoxic Training: Fact and Fancy

Levine

2002

High Altitude Medicine & Biology

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LTITUD E TRAINING has been used frequently by endurance athletes to enhance performance. However, not all athletes or teams have the resources to travel to high altitude environments on a regular basis. Moreover, issues such as availability of adequate training facilities have limited the use of mountain-based altitude training. In the last few years, there has been a remarkable increase in the number of techniques designed to "bring the mountain to the athlete." Nitrogen houses, hypoxia tents, and special breathing apparatuses to provide inspired hypoxia at rest and during exercise, all have been developed and promoted to simulate what are perceived as the critical elements of altitude training.Intermittent hypoxic training (IHT) refers to the discontinuous use of normobaric or hypobaric hypoxia, in an attempt to reproduce some of these key features of altitude acclimatization, with the ultimate goal to improve sea-level athletic performance. In general, IHT can be divided into two different strategies: (1) providing hypoxia at rest with High Alt Med Biol. 3:177-193, 2002.-Intermittent hypoxic training (IHT) refers to the discontinuous use of normobaric or hypobaric hypoxia, in an attempt to reproduce some of the key features of altitude acclimatization, with the ultimate goal to improve sea-level athletic performance. In general, IHT can be divided into two different strategies: (1) providing hypoxia at rest with the primary goal being to stimulate altitude acclimatization or (2) providing hypoxia during exercise, with the primary goal being to enhance the training stimulus. Each approach has many different possible application strategies, with the essential variable among them being the "dose" of hypoxia necessary to achieve the desired effect. One approach, called living high-training low, has been shown to improve sea-level endurance performance. This strategy combines altitude acclimatization (2500 m) with low altitude training to ensure high-quality training. The opposite strategy, living low-training high, has also been proposed by some investigators. The primacy of the altitude acclimatization effect in IHT is demonstrated by the following facts: (1) living high-training low clearly improves performance in athletes of all abilities, (2) the mechanism of this improvement is primarily an increase in erythropoietin, leading to increased red cell mass, V O 2max , and running performance, and (3) rather than intensifying the training stimulus, training at altitude or under hypoxia leads to the opposite effect-reduced speeds, reduced power output, reduced oxygen flux-and therefore is not likely to provide any advantage for a well-trained athlete.

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Control of red blood cell mass in spaceflight

Cited by 230 publications

References 0 publications

Vasorelaxation in Space

Vasorelaxation in Space

Hypovolemia and neurovascular control during orthostatic stress

Intermittent Hypoxic Training: Fact and Fancy

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