title: Enhanced external counterpulsation improves peripheral artery function and glucose tolerance in subjects with abnormal glucose tolerance.
abstract: BACKGROUND
  In coronary artery disease patients, enhanced external counterpulsation (EECP) improves peripheral arterial function and nitric oxide (NO) bioavailability, which have been implicated in the pathogenesis of abnormal glucose tolerance (AGT). We sought to evaluate the effects of EECP on outcomes of arterial function, glucose tolerance, and skeletal muscle morphology in subjects with AGT.
  
  
  RESULTS
  18 subjects with AGT were randomly (2:1 ratio) assigned to receive either 7 wk (35 1-h sessions) of EECP (n = 12) or 7 wk of standard care (control; n = 6). Peripheral vascular function, biochemical assays, glucose tolerance, and skeletal muscle morphology were evaluated before and after EECP or control. EECP increased normalized brachial artery (27%) and popliteal artery (52%) flow-mediated dilation. Plasma nitrite/nitrate (NOx) increased (30%) and 8-isoprostane-PGF-F(2α), a marker of lipid peroxidation in the plasma, decreased (-23%). Fasting plasma glucose declined (-16.9 ± 5.4 mg/dl), and the homeostasis model assessment of insulin resistance (HOMA-IR) decreased (31%) following EECP. Plasma glucose 120 min after initiation of oral glucose tolerance testing decreased (-28.3 ± 7.3 mg/dl), and the whole body composite insulin sensitivity index (C-ISI) increased (21%). VEGF concentrations increased (75%), and vastus lateralis skeletal muscle biopsies demonstrated improvements in capillary density following EECP. No change was observed in cellular signaling pathways, but there was a significant increase GLUT-4 protein expression (47%) following EECP.
  
  
  CONCLUSIONS
  Our findings provide novel evidence that EECP has a beneficial effect on peripheral arterial function and glucose tolerance in subjects with AGT.
authors.affiliation: Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, Florida, USA. martinjs@missouri.edu
authors.forename: J S
authors.initials: JS
authors.lastname: Martin
authors.forename: D T
authors.initials: DT
authors.lastname: Beck
authors.forename: J M
authors.initials: JM
authors.lastname: Aranda
authors.forename: R W
authors.initials: RW
authors.lastname: Braith
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D001916:Brachial Artery / Q000378:metabolism / Q000503:physiopathology*; D002196:Capillaries / Q000378:metabolism / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D015908:Counterpulsation / Q000379:methods*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005947:Glucose / Q000378:metabolism*; D018149:Glucose Intolerance / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D005951:Glucose Tolerance Test / Q000379:methods; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D038321:Glycemic Index / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000378:metabolism; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000503:physiopathology; D009569:Nitric Oxide / Q000097:blood; D010084:Oxidation-Reduction; D010766:Phosphorylation; D011150:Popliteal Artery / Q000378:metabolism / Q000503:physiopathology; D012039:Regional Blood Flow / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology
chemical_list: D051275:Glucose Transporter Type 4; D007328:Insulin; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D005947:Glucose