Document Detail

Long-term combined beneficial effects of physical training and metabolic treatment on atherosclerosis in hypercholesterolemic mice.
MedLine Citation:
PMID:  15169957     Owner:  NLM     Status:  MEDLINE    
The pathogenic mechanisms by which physical exercise influences atherosclerotic lesion formation remain poorly understood. Because vigorous physical training increases oxidative stress, this study tested the hypothesis that graduated and moderate physical exercise together with metabolic intervention (l-arginine and antioxidants) may contribute to increased vascular protection. Exercise training in mice was induced by graduated swimming. In hypercholesterolemic male mice on an atherogenic high-cholesterol diet, graduated and moderate exercise lowered plasma cholesterol and decreased atherosclerotic lesions compared with sedentary control mice. Antioxidants (1.0% vitamin E added to the chow and 0.05% vitamin C added to the drinking water) and l-arginine (6% in drinking water) supplementation to exercising hypercholesterolemic mice further and synergistically reduced atherosclerosis compared with untreated exercised mice. Arterial oxidation-specific epitopes and systemic oxidative stress were reduced by metabolic intervention. Graduated chronic exercise elicited an increase in production of nitric oxide through increased endothelial nitric oxide synthase expression and ameliorated scavenger activities. Thus, metabolic intervention with l-arginine and antioxidants together with graduated and moderate exercise training reduce atherosclerotic lesion formation.
Claudio Napoli; Sharon Williams-Ignarro; Filomena De Nigris; Lilach O Lerman; Loredana Rossi; Carmen Guarino; Gelsomina Mansueto; Francesco Di Tuoro; Orlando Pignalosa; Gaetano De Rosa; Vincenzo Sica; Louis J Ignarro
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-05-28
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  101     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-06-09     Completed Date:  2004-08-17     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8797-802     Citation Subset:  IM    
Department of General Pathology, Medicine, Clinical Pathology, and Human Pathology, University of Naples, 80131 Naples, Italy.
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MeSH Terms
Antioxidants / therapeutic use*
Arginine / therapeutic use
Arteriosclerosis / etiology,  metabolism,  prevention & control*
Ascorbic Acid / therapeutic use
Diet, Atherogenic
Hyperlipoproteinemia Type II / complications*,  metabolism,  therapy*
Mice, Knockout
Nitric Oxide Synthase / metabolism
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Oxidative Stress
Physical Conditioning, Animal*
Receptors, LDL / deficiency,  genetics
Vitamin E / therapeutic use
Grant Support
Reg. No./Substance:
0/Antioxidants; 0/Receptors, LDL; 1406-18-4/Vitamin E; 50-81-7/Ascorbic Acid; 74-79-3/Arginine; EC Oxide Synthase; EC Oxide Synthase Type II; EC Oxide Synthase Type III; EC protein, mouse; EC protein, mouse
Erratum In:
Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18262

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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