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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2782.)
© 1999 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Exercise Training Increases Basal Nitric Oxide Production From the Forearm in Hypercholesterolemic Patients

Tamara V. Lewis; Anthony M. Dart; Jaye P. F. Chin-Dusting; Bronwyn A. Kingwell

From the Alfred and Baker Medical Unit, Baker Medical Research Institute, Prahran, Australia.

Correspondence Dr Bronwyn Kingwell, Alfred and Baker Medical Unit, Baker Medical Research Institute, Commercial Rd, Prahran 3181, Australia. E-mail b.kingwell{at}alfred.org.au

Abstract—The objective of this study was to investigate the effects of cycle training on basal nitric oxide (NO) production and endothelium-dependent dilator capacity in hypercholesterolemic patients in whom acetylcholine responsiveness is impaired. Nine sedentary hypercholesterolemic volunteers (total plasma cholesterol >6.0 mmol/L; 2 female) aged 44±3 years (mean±SEM) participated in the study. Subjects remained sedentary for 4 weeks and performed 4 weeks of home-based cycle training (3x30 minutes/week at 65% maximum oxygen consumption [VO₂max]) in a randomized order. Arteriovenous nitrate/nitrite (NO_x) gradient was assessed and plethysmography was used to measure the forearm blood flow responses to arterial infusions of acetylcholine, sodium nitroprusside, and N^Gmono methyl L-arginine. Training increased VO₂max from 30.4±1.9 to 34.3±1.4 mL · kg^-1 · min^-1 (P=0.01). Intrabrachial diastolic blood pressure was reduced from 70±3 to 68±3 mm Hg (P=0.02) with training, whereas systolic pressure did not change. Plasma triglycerides and total, LDL, and HDL cholesterol were not different between interventions. In the sedentary state, there was a positive forearm arteriovenous difference in plasma NO_x indicating net extraction (6.8±4.0 nmol · 100 mL^-1 · min^-1), whereas in the trained state this difference was negative, indicating net production (-5.8±5.8 nmol · 100 mL^-1 · min^-1; P=0.03). N^Gmono methyl L-arginine, at a dose of 4 µmol/min, caused a greater vasoconstriction after training (79.6±3.4% versus 69.9±6.8%; P=0.05). Acetylcholine and sodium nitroprusside induced dose-dependent elevations in forearm blood flow that were unaffected by training. These data suggest that basal release of endothelium-derived NO is increased with 4 weeks of home based training in hypercholesterolemic patients, independently of lipid profile modification. This may contribute to the cardiovascular protective effects of exercise training, including reduced blood pressure.

Key Words: exercise • endothelium-dependent vasodilation • acetylcholine • lipids • hyperlipidemia

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