It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Recent observations strongly connect high-density lipoproteins (HDL) function and levels with coronary heart disease outcomes and risk for infections and sepsis. To date, our knowledge of factors determining this connection is still very limited. The immobility associated with prolonged bedrest is detrimental to health, affecting several systems, including the cardiovascular, pulmonary, gastrointestinal, musculoskeletal and urinary. Effects of prolonged bedrest on the composition and functional properties of HDL remain elusive. We evaluated metrics of HDL composition and function in healthy male volunteers participating in a randomized, crossover head-down bedrest study. We observed that HDL cholesterol efflux capacity was profoundly decreased during bedrest, mediated by a bedrest associated reduction in plasma levels of HDL-cholesterol and major apolipoproteins (apo) apoA-I and apoA-II. Paraoxonase activity, plasma anti-oxidative capacity and the activities of lecithin-cholesterol acyltransferase and cholesteryl ester transfer protein were not affected. No change was observed in the content of HDL-associated serum amyloid A, a sensitive marker of inflammation. Resistive vibration exercise countermeasure during bedrest did not correct impaired cholesterol efflux capacity and only tended to increase arylesterase activity of HDL-associated paraoxonase. In conclusion, prolonged bedrest reduces plasma HDL levels linked to markedly suppressed HDL cholesterol efflux capacity. Resistive vibration exercise during bedrest did not correct HDL levels and impaired cholesterol efflux capacity.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Medical University of Graz, Division of Pharmacology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Graz, Austria (GRID:grid.11598.34) (ISNI:0000 0000 8988 2476)
2 Medical University of Graz, Institute of Medical and Chemical Laboratory Diagnostics, Graz, Austria (GRID:grid.11598.34) (ISNI:0000 0000 8988 2476)
3 Medical University of Graz, Division of Pharmacology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Graz, Austria (GRID:grid.11598.34) (ISNI:0000 0000 8988 2476); BioTechMed Graz, Graz, Austria (GRID:grid.452216.6)
4 Medical University of Graz, Division of Physiology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Graz, Austria (GRID:grid.11598.34) (ISNI:0000 0000 8988 2476)




