title: Exercise-induced improvement in endothelial dysfunction is not mediated by changes in CV risk factors: pooled analysis of diverse patient populations.
abstract: We have pooled data from a series of our exercise training studies undertaken in groups with a broad range of vascular (dys) function to the examine the hypothesis that exercise-induced improvements in the conduit and/or resistance vessel function are related to improvements in risk factors for cardiovascular (CV) disease. Endothelium-dependent and -independent conduit vessel function were assessed by using wall tracking of high-resolution ultrasound images of the brachial artery response to flow-mediated dilation (FMD) and glyceryl trinitrate. Resistance vessel function was assessed using intrabrachial administration of acetylcholine (ACh), sodium nitroprusside, and NG-monomethyl-l-arginine. Randomized cross-over studies of 8-wk exercise training were undertaken in untreated hypercholesterolemic (n = 11), treated hypercholesterolemic (n = 11), coronary artery disease (n = 10), chronic heart failure (n = 12), Type 2 diabetic (n = 15), and healthy control subjects (n = 16). Exercise training did not significantly alter plasma lipids, blood pressure, blood glucose, waist-to-hip ratio, or body mass index values, despite significant improvement in both FMD and ACh responses. There were no correlations between changes in any risk factor variables and indexes of either resistance or conduit vessel function. We conclude that, in these subjects with antecedent vascular dysfunction, the beneficial effects of relatively short-term exercise training on vascular function are not solely mediated by the effects of exercise on CV risk factors.
authors.affiliation: School of Human Movement and Exercise Science, The University of Western Australia, and Department of Cardiology, Royal Perth Hospital, Crawley, Western Australia 6009, Australia.
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Green
authors.forename: Jennifer H
authors.initials: JH
authors.lastname: Walsh
authors.forename: Andrew
authors.initials: A
authors.lastname: Maiorana
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Best
authors.forename: Roger R
authors.initials: RR
authors.lastname: Taylor
authors.forename: J Gerard
authors.initials: JG
authors.lastname: O'Driscoll
mesh_terms: D000109:Acetylcholine; D003324:Coronary Artery Disease / Q000453:epidemiology* / Q000503:physiopathology*; D018592:Cross-Over Studies; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D015444:Exercise; D006333:Heart Failure / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D006937:Hypercholesterolemia / Q000453:epidemiology* / Q000503:physiopathology*; D008875:Middle Aged; D012307:Risk Factors; D014655:Vascular Resistance; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D000109:Acetylcholine