title: Augmentation of endothelial function following exercise training is associated with increased L-arginine transport in human heart failure.
abstract: We have reported previously a decrease in the clearance of the NO (nitric oxide) precursor L-arginine in the forearm circulation of CHF (congestive heart failure) patients, suggesting a potential rate-limiting mechanism contributing to the common finding of endothelial dysfunction in CHF. Given data that show exercise training augments endothelial function in CHF, the aim of the present study was to investigate whether these improvements were due to an increase in L-arginine transport. Measures of L-arginine transport, endothelial function and exercise capacity were repeated before and after 8 weeks of "usual living" or exercise training in 21 CHF patients [NYHA (New York Heart Association) class II/III]. Exercise capacity (6-min walk test) increased following exercise training (496+/-21 to 561+/-17 m; P=0.005), whereas the control group demonstrated no change [488+/-18 to 484+/-21 m; P=ns (not significant)]. Basal FBF (forearm blood flow) remained stable following exercise training (2.68+/-0.55 to 2.46+/-0.32 ml.min(-1).100 ml(-1) of tissue) and "usual living" (2.16+/-0.37 to 2.91+/-0.55 min(-1).100 ml(-1) of tissue). FBF responses to ACh (acetylcholine) increased following exercise by 49.6+/-17.7% (area under curve; P=0.01) demonstrating augmented endothelial function. FBF responses to SNP (sodium nitroprusside) were also improved following exercise training (30.8+/-8.2%; P=0.02). There was no change in vascular function in the "usual living" group. The clearance of L-arginine was significantly increased following involvement in the exercise programme (69.4+/-7.8 to 101.0+/-9.5 ml/min; P=0.04), whereas there was no change in the "usual living" group (78.4+/-17.5 to 81.0+/-14.9 ml/min; P=ns). In conclusion, the augmentation in endothelial function observed following exercise may be due, in part, to an increase in the transport of L-arginine in CHF patients.
authors.affiliation: Wynn Department of Metabolic Cardiology, Baker Medical Research Institute, St Kilda Road Central, Melbourne, Victoria 8008, Australia.
authors.forename: Melinda M
authors.initials: MM
authors.lastname: Parnell
authors.forename: Diane P
authors.initials: DP
authors.lastname: Holst
authors.forename: David M
authors.initials: DM
authors.lastname: Kaye
mesh_terms: D000109:Acetylcholine; D000704:Analysis of Variance; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism*; D001692:Biological Transport; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000378:metabolism*; D017079:Exercise Tolerance; D005542:Forearm / Q000098:blood supply; D006333:Heart Failure / Q000378:metabolism* / Q000628:therapy; D006801:Humans; D008297:Male; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D009599:Nitroprusside; D010806:Physical Education and Training; D012039:Regional Blood Flow / Q000187:drug effects; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D014665:Vasodilator Agents; C487735:dimethylarginine; D009599:Nitroprusside; D001120:Arginine; D000109:Acetylcholine