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Am J Physiol Heart Circ Physiol 288: H1747-H1755, 2005. First published December 2, 2004; doi:10.1152/ajpheart.00966.2004
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Vascular adaptation to 4 wk of deconditioning by unilateral lower limb suspension

Michiel W. P. Bleeker,1,2 Patricia C. E. De Groot,1 Fleur Poelkens,1 Gerard A. Rongen,2,3 Paul Smits,2,3 and Maria T. E. Hopman1

Departments of 1Physiology, 2General Internal Medicine, and 3Pharmacology-Toxicology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Submitted 17 September 2004 ; accepted in final form 29 November 2004

Physical inactivity or deconditioning is an independent risk factor for atherosclerosis and cardiovascular disease. In contrast to exercise, the vascular changes that occur as a result of deconditioning have not been characterized. We used 4 wk of unilateral lower limb suspension (ULLS) to study arterial and venous adaptations to deconditioning. In contrast to previous studies, this model is not confounded by denervation or microgravity. Seven healthy subjects participated in the study. Arterial and venous characteristics of the legs were assessed by echo Doppler ultrasound and venous occlusion plethysmography. The diameter of the common and superficial femoral artery decreased by 12% after 4 wk of ULLS. Baseline calf blood flow, as measured by plethysmography, decreased from 2.1 ± 0.2 to 1.6 ± 0.2 ml·min–1·dl tissue–1. Both arterial diameter and calf blood flow returned to baseline values after 4 wk of recovery. There was no indication of a decrease in flow-mediated dilation of the superficial femoral artery after ULLS deconditioning. This means that functional adaptations to inactivity are not simply the inverse of adaptations to exercise. The venous pressure-volume curve is shifted downward after ULLS, without any effect on compliance. In conclusion, deconditioning by 4 wk of ULLS causes significant changes in both the arterial and the venous system.

plethysmography; echo Doppler ultrasound; leg suspension; venous compliance; flow-mediated dilation



Address for reprint requests and other correspondence: M. T. E. Hopman, Dept. of Physiology 237, Radboud Univ. Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands (E-mail: M.Hopman{at}fysiol.umcn.nl)




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