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J Appl Physiol 98: 648-654, 2005. First published October 22, 2004; doi:10.1152/japplphysiol.01332.2003
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Long-term bed rest-induced reductions in stroke volume during rest and exercise: cardiac dysfunction vs. volume depletion

Jonas Spaak, Stéphanie Montmerle, Patrik Sundblad, and Dag Linnarsson

Department of Physiology and Pharmacology, Section of Environmental Physiology, Karolinska Institutet, Stockholm, Sweden

Submitted 11 December 2003 ; accepted in final form 19 October 2004

Long-term head-down-tilt bed rest (HDT) causes cardiovascular deconditioning, attributed to reflex dysfunctions, plasma volume reduction, or cardiac impairments. Our objective with the present study was to evaluate the functional importance and relative contribution of these during rest and exercise in supine and upright postures. We studied six subjects before (baseline), during [days 60 (D60) and 113 (D113)], and after [recovery days 0 (R0), 3 (R3), and 15 (R15)] 120 days of –6° HDT. We determined cardiac output, stroke volume (SV), mean arterial pressure, and heart rate during rest and exercise in supine and upright postures. Cardiac output and SV decreased significantly in all four conditions, but the time courses differed for rest and exercise. Upright resting SV was decreased by 24 ± 9% at D60 compared with baseline but had recovered already at R3. Supine exercise SV decreased more slowly (by 5 ± 8% at D60 and by 18 ± 4% at D113) and recovered more slowly after HDT termination. Steady-state mean arterial pressure showed no changes. Heart rate had increased by 18 ± 4% at D60 and had recovered partially at R3. Our data indicate that long-term HDT causes both a rapid, preload-dependent reduction in SV, most evident during rest in the upright position, and a more slowly developing cardiac dysfunction, most evident during supine exercise. However, the ability to maintain blood pressure and to perform sustained low levels of dynamic exercise is not influenced by HDT.

hypokinesia; microgravity; deconditioning; head-down tilt; orthostasis



Address for reprint requests and other correspondence: J. Spaak, Sect. of Environmental Physiology, Dept. of Physiology and Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden (E-mail: Jonas.Spaak{at}fyfa.ki.se)




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