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1 Departments of Medicine and Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033; 2 Life Sciences Division, National Aeronautics and Space Administration Ames Research Center, Moffett Field, California 94035; and 3 Department of Health and Kinesiology, Texas A&M University, and 4 Department of Medical Physiology, and the Cardiovascular Research Institute, Texas A&M Health Science Center, College Station, Texas 77843
The purpose of this study was to test the hypothesis that exposure to short-term microgravity or long-term hindlimb unloading induces cardiac atrophy in male Sprague-Dawley rats. For the microgravity study, rats were subdivided into four groups: preflight (PF, n = 12); flight (Fl, n = 7); flight cage simulation (Sim, n = 6), and vivarium control (Viv, n = 7). Animals in the Fl group were exposed to 7 days of microgravity during the Spacelab 3 mission. Animals in the hindlimb-unloading study were subdivided into three groups: control (Con, n = 20), 7-day hindlimb-unloaded (7HU, n = 10), and 28-day hindlimb-unloaded (28HU, n = 19). Heart mass was unchanged in adult animals exposed to 7 days of actual microgravity (PF 1.33 ± 0.03 g; Fl 1.32 ± 0.02 g; Sim 1.28 ± 0.04 g; Viv 1.35 ± 0.04 g). Similarly, heart mass was unaltered with hindlimb unloading (Con 1.40 ± 0.04 g; 7HU 1.35 ± 0.06 g; 28HU 1.42 ± 0.03 g). Hindlimb unloading also had no effect on the peak rate of rise in left ventricular pressure, an estimate of myocardial contractility (Con 8,055 ± 385 mmHg/s; 28HU 8,545 ± 755 mmHg/s). These data suggest that cardiac atrophy does not occur after short-term exposure to microgravity and that neither short- nor long-term simulated microgravity alters cardiac mass or function.
heart; deconditioning; cardiac atrophy
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