title: Effects of high-cholesterol diet and parallel exercise training on the vascular function of rabbit aortas: a time course study.
abstract: It is plausible to assume that exercise training, when applied early enough, can completely correct atherosclerotic defects. Using rabbit aortic specimens, we examined the effects of chronic exercise and high-cholesterol diet feeding on vascular function for different time periods. Male New Zealand White rabbits were divided into four groups: the normal diet groups with or without exercise training and the high-cholesterol diet groups with or without exercise training. Animals in high-cholesterol diet groups were fed 2% cholesterol rabbit chow for 2, 4, or 6 wk. Those in exercise training groups ran on a treadmill at 0.88 km/h for up to 40 min/day, 5 days/wk for the same period of time as the diet feeding. Thoracic aortas were isolated for functional and immunohistochemical analyses. We found that 1). although high-cholesterol diet feeding (>or=2 wk) elevated serum cholesterol levels and impaired acetylcholine-evoked vasorelaxation, only the latter effect was reversed by exercise training; 2). the effects of diet and exercise on acetylcholine-evoked vasorelaxation were mainly due to altered release of nitric oxide and endothelium-derived hyperpolarizing factor; and 3). diet feeding for 4 or 6 wk caused significant lipid deposition and expression of P-selectin, VCAM-1, monocyte chemoattractant protein-1, and inducible nitric oxide synthase, which were largely reduced by exercise training. In conclusion, parallel exercise training almost completely reverses the early-stage endothelial dysfunction caused by high-cholesterol diet feeding.
authors.affiliation: Department of Physiology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
authors.forename: Ai-Lun
authors.initials: AL
authors.lastname: Yang
authors.forename: Chauying J
authors.initials: CJ
authors.lastname: Jen
authors.forename: Hsiun-ing
authors.initials: HI
authors.lastname: Chen
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D001161:Arteriosclerosis / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D002791:Cholesterol, Dietary / Q000009:adverse effects*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000096:biosynthesis / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011817:Rabbits; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013997:Time Factors; D014664:Vasodilation / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D015815:Cell Adhesion Molecules; D018932:Chemokine CCL2; D002791:Cholesterol, Dietary; D004791:Enzyme Inhibitors; D013757:Tetraethylammonium Compounds; D014665:Vasodilator Agents; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester