title: The flow-mediated dilation response to acute exercise in overweight active and inactive men.
abstract: OBJECTIVE
  Inflammation has been found to play a role in the etiology of cardiovascular disease as well as provoke endothelial dysfunction. Inflammatory cytokines associated with endothelial function are interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). IL-6 is exercise intensity dependent and has been shown to inhibit TNF-alpha expression directly. The aim of this study was to investigate the interaction of IL-6 and TNF-alpha on endothelial function in response to acute exercise in overweight men exhibiting different physical activity profiles.
  
  
  METHODS
  Using a randomized mixed factorial design, 16 overweight men (8 active, maximal exercise capacity (VO(2)peak) = 34.2 +/- 1.7, BMI = 27.4 +/- 0.7 and 8 inactive, VO(2)peak = 30.9 +/- 1.2, BMI = 29.3 +/- 1.0) performed three different intensity acute exercise treatments. Brachial artery flow-mediated dilation (FMD) and subsequent blood samples were taken pre-exercise and 1 h following the cessation of exercise.
  
  
  RESULTS
  Independent of exercise intensity, the active group displayed a 24% increase (P = 0.034) in FMD following acute exercise compared to a 32% decrease (P = 0.010) in the inactive group. Elevated (P < 0.001) concentrations of IL-6 following moderate (50% VO(2)) and high (75% VO(2)) intensity acute exercise were observed in both groups; however, concentrations of TNF-alpha were unchanged in response to acute exercise (P = 0.584).
  
  
  CONCLUSIONS
  The FMD response to acute exercise is enhanced in active men who are overweight, whereas inactive men who are overweight exhibit an attenuated response. The interaction of IL-6 and TNF-alpha did not provide insight into the physiological mechanisms associated with the disparity of FMD observed between groups.
authors.affiliation: Clinical Exercise Physiology Laboratory, Department of Kinesiology, School of Health, Physical Education and Recreation, Indiana University, Bloomington, IN, USA. harrisra@indiana.edu
authors.forename: Ryan A
authors.initials: RA
authors.lastname: Harris
authors.forename: Jaume
authors.initials: J
authors.lastname: Padilla
authors.forename: Kevin P
authors.initials: KP
authors.lastname: Hanlon
authors.forename: Lawrence D
authors.initials: LD
authors.lastname: Rink
authors.forename: Janet P
authors.initials: JP
authors.lastname: Wallace
mesh_terms: D000368:Aged; D001794:Blood Pressure; D015992:Body Mass Index; D001916:Brachial Artery / Q000378:metabolism / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D015444:Exercise; D006339:Heart Rate; D006801:Humans; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D050177:Overweight / Q000378:metabolism / Q000503:physiopathology*; D010101:Oxygen Consumption; D005082:Physical Exertion; D012039:Regional Blood Flow; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*; D014664:Vasodilation
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein