title: Microvascular and myocardial contractile responses to ischemia: influence of exercise training.
abstract: We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
authors.affiliation: Department of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis 95616, USA. jdsymons@ucdavis.edu
authors.forename: J D
authors.initials: JD
authors.lastname: Symons
authors.forename: S V
authors.initials: SV
authors.lastname: Rendig
authors.forename: C L
authors.initials: CL
authors.lastname: Stebbins
authors.forename: J C
authors.initials: JC
authors.lastname: Longhurst
mesh_terms: D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000494:pharmacology; D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D019332:Endothelin-1 / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D010805:Physical Conditioning, Animal / Q000502:physiology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D019332:Endothelin-1; D014662:Vasoconstrictor Agents; D002245:Carbon Dioxide; D009599:Nitroprusside; D011189:Potassium Chloride; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D000109:Acetylcholine; D010100:Oxygen