title: Exercise does not attenuate early CAD progression in a pig model.
abstract: OBJECTIVE
  This study was designed to examine the effects of high-fat (HF) diet and subsequent exercise training (Ex) on coronary arteries of an animal model of early stage CAD. We hypothesized that HF diet would induce early stage disease and promote a proatherogenic coronary phenotype, whereas Ex would blunt disease progression and induce a healthier anti-inflammatory environment reflected by the increased expression of antioxidant capacity and the decreased expression of inflammatory markers in both the macrovasculature and the microvasculature of the coronary circulation.
  
  
  METHODS
  Immunohistochemistry in left anterior descending and right coronary arteries and immunoblots in left anterior descending and left ventricular arterioles were used to characterize the effects of HF diet and Ex on the progression of coronary atherosclerosis.
  
  
  RESULTS
  Our results revealed that HF diet promoted a proatherogenic coronary endothelial cell phenotype as evidenced by the endothelial expression of inflammatory and oxidative stress markers. Ex did not significantly alter any of these immunohistochemical markers in conduit arteries; however, Ex did increase antioxidant protein content in left ventricular arterioles.
  
  
  CONCLUSIONS
  We conclude that, at this early stage of CAD, Ex did not seem to modify vascular cell phenotypes of conduit coronary arteries from proatherogenic to a more favorable antiatherogenic status; however, Ex increased antioxidant protein content in coronary arterioles. These findings also support the idea that endothelial phenotype expression follows different patterns in the macrovasculature and microvasculature of the coronary circulation.
authors.affiliation: Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA. arcea@missouri.edu
authors.forename: Arturo A
authors.initials: AA
authors.lastname: Arce-Esquivel
authors.forename: Kurt V
authors.initials: KV
authors.lastname: Kreutzer
authors.forename: James W E
authors.initials: JW
authors.lastname: Rush
authors.forename: James R
authors.initials: JR
authors.lastname: Turk
authors.forename: M Harold
authors.initials: MH
authors.lastname: Laughlin
mesh_terms: D000818:Animals; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology; D015415:Biomarkers / Q000032:analysis; D003324:Coronary Artery Disease / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology; D006937:Hypercholesterolemia / Q000503:physiopathology; D007249:Inflammation / Q000473:pathology; D008297:Male; D055806:Microvessels / Q000473:pathology / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D013552:Swine
chemical_list: D015415:Biomarkers