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      Artificial Gravity as a Countermeasure to the Cardiovascular Deconditioning of Spaceflight: Gender Perspectives

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          Abstract

          Space flight-induced physiological deconditioning resulting from decreased gravitational input, decreased plasma volume, and disruption of regulatory mechanisms is a significant problem in returning astronauts as well as in normal aging. Here we review effects of a promising countermeasure on cardiovascular systems of healthy men and women undergoing Earth-based models of space-flight. This countermeasure is produced by a centrifuge and called artificial gravity (AG). Numerous studies have determined that AG improves orthostatic tolerance (as assessed by various protocols) of healthy ambulatory men, of men deconditioned by bed rest or by immersion (both wet and dry) and, in one case, following spaceflight. Although a few studies of healthy, ambulatory women and one study of women deconditioned by furosemide, have reported improvement of orthostatic tolerance following exposure to AG, studies of bed-rested women exposed to AG have not been conducted. However, in ambulatory, normovolemic subjects, AG training was more effective in men than women and more effective in subjects who exercised during AG than in those who passively rode the centrifuge. Acute exposure to an AG protocol, individualized to provide a common stimulus to each person, also improved orthostatic tolerance of normovolemic men and women and of furosemide-deconditioned men and women. Again, men’s tolerance was more improved than women’s. In both men and women, exposure to AG increased stroke volume, so greater improvement in men vs. women was due in part to their different vascular responses to AG. Following AG exposure, resting blood pressure (via decreased vascular resistance) decreased in men but not women, indicating an increase in men’s vascular reserve. Finally, in addition to counteracting space flight deconditioning, improved orthostatic tolerance through AG-induced improvement of stroke volume could benefit aging men and women on Earth.

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          Most cited references65

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          From space to Earth: advances in human physiology from 20 years of bed rest studies (1986-2006).

          Bed rest studies of the past 20 years are reviewed. Head-down bed rest (HDBR) has proved its usefulness as a reliable simulation model for the most physiological effects of spaceflight. As well as continuing to search for better understanding of the physiological changes induced, these studies focused mostly on identifying effective countermeasures with encouraging but limited success. HDBR is characterised by immobilization, inactivity, confinement and elimination of Gz gravitational stimuli, such as posture change and direction, which affect body sensors and responses. These induce upward fluid shift, unloading the body's upright weight, absence of work against gravity, reduced energy requirements and reduction in overall sensory stimulation. The upward fluid shift by acting on central volume receptors induces a 10-15% reduction in plasma volume which leads to a now well-documented set of cardiovascular changes including changes in cardiac performance and baroreflex sensitivity that are identical to those in space. Calcium excretion is increased from the beginning of bed rest leading to a sustained negative calcium balance. Calcium absorption is reduced. Body weight, muscle mass, muscle strength is reduced, as is the resistance of muscle to insulin. Bone density, stiffness of bones of the lower limbs and spinal cord and bone architecture are altered. Circadian rhythms may shift and are dampened. Ways to improve the process of evaluating countermeasures--exercise (aerobic, resistive, vibration), nutritional and pharmacological--are proposed. Artificial gravity requires systematic evaluation. This review points to clinical applications of BR research revealing the crucial role of gravity to health.
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            Cardiac atrophy after bed rest and spaceflight.

            Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 (n = 5) and 12 (n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 +/- 2.2% (P = 0.005) after 6 wk with an additional atrophy of 7.6 +/- 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 +/- 12.2 vs. 153.4 +/- 12.1 g, P = 0.81). Mean wall thickness decreased (4 +/- 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 +/- 1.7% (P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 +/- 2.7% (P = 0.06) and RV end-diastolic volume by 16 +/- 7.9% (P = 0.06). After spaceflight, LV mass decreased by 12 +/- 6.9% (P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.
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              Effect of aging and physical activity on left ventricular compliance.

              Left ventricular compliance appears to decrease with aging, which may contribute to the high incidence of heart failure in the elderly. However, whether this change is an inevitable consequence of senescence or rather secondary to reduced physical activity is unknown. Twelve healthy sedentary seniors (69.8+/-3 years old; 6 women, 6 men) and 12 Masters athletes (67.8+/-3 years old; 6 women, 6 men) underwent pulmonary artery catheterization to define Starling and left ventricular pressure-volume curves. Data were compared with those obtained in 14 young but sedentary control subjects (28.9+/-5 years old; 7 women, 7 men). Pulmonary capillary wedge pressures and left ventricular end-diastolic volumes by use of echocardiography were measured at baseline, during decreased cardiac filling by use of lower-body negative pressure (-15 and -30 mm Hg), and after saline infusion (15 and 30 mL/kg). Stroke volume for any given filling pressure was greater in Masters athletes compared with the age-matched sedentary subjects, whereas contractility, as assessed by preload recruitable stroke work, was similar. There was substantially decreased left ventricular compliance in healthy but sedentary seniors compared with the young control subjects, which resulted in higher cardiac pressures for a given filling volume and higher myocardial wall stress for a given strain. The pressure-volume curve for the Masters athletes was indistinguishable from that of the young, sedentary control subjects. A sedentary lifestyle during healthy aging is associated with decreased left ventricular compliance, leading to diminished diastolic performance. Prolonged, sustained endurance training preserves ventricular compliance with aging and may help to prevent heart failure in the elderly.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                06 July 2018
                2018
                : 9
                : 716
                Affiliations
                [1] 1Department of Biomedical Engineering, University of Kentucky , Lexington, KY, United States
                [2] 2Physiology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Medical University of Graz , Graz, Austria
                Author notes

                Edited by: Lorenza Pratali, Istituto di Fisiologia Clinica (IFC), Italy

                Reviewed by: Francesca Lanfranconi, Institute of Sport, Exercise and Active Living (ISEAL), Australia; Marcel Egli, Lucerne University of Applied Sciences and Arts, Switzerland

                *Correspondence: Joyce M. Evans, jevans1@ 123456uky.edu Nandu Goswami, nandu.goswami@ 123456medunigraz.at

                This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology

                Article
                10.3389/fphys.2018.00716
                6043777
                30034341
                9dd0b008-c718-4bde-a724-cd79d86a1371
                Copyright © 2018 Evans, Knapp and Goswami.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 30 January 2018
                : 24 May 2018
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 72, Pages: 9, Words: 0
                Funding
                Funded by: Kentucky Space Grant Consortium 10.13039/100005742
                Award ID: KY EPSCoR NNX07AT58A
                Funded by: National Center for Research Resources 10.13039/100000097
                Award ID: UK1TR000117
                Categories
                Physiology
                Review

                Anatomy & Physiology
                orthostatic intolerance,microgravity,aging,spaceflight simulations,falls
                Anatomy & Physiology
                orthostatic intolerance, microgravity, aging, spaceflight simulations, falls

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