title: The CAREGENE study: genetic variants of the endothelium and aerobic power in patients with coronary artery disease.
abstract: OBJECTIVE
  Aerobic phenotypes show a wide variability to similar aerobic training stimuli, which can be partly attributed to heritability. Endothelial function affects aerobic power. Various physiological pathways may influence the endothelial function. Therefore, we aimed to examine whether polymorphisms of the eNos gene, the CAT gene, the VEGF gene, the GPX1 gene, the subunit P22 phox of the NAD(P)H-odixase gene, the PPAR-alpha gene, and the PGC-alpha gene are associated with aerobic power or with its response to physical training in patients with coronary artery disease (CAD).
  
  
  METHODS
  935 biologically unrelated Caucasian patients with CAD who had exercised until exhaustion during graded bicycle testing at baseline and after completion of 3 months of training were included in the CAREGENE study (Cardiac Rehabilitation and GENetics of exercise performance). Polymorphisms were detected using the invader assay and MassARRAY technology. Haplotype analysis was performed on the polymorphisms of the eNos gene, the VEGF gene and the NAD(P)H-oxidase gene.
  
  
  RESULTS
  Physical training significantly increased aerobic power by 24.2 +/- 0.6% (P < 0.001). Associations of P < 0.05 were found between aerobic power and the eNOS 273C>T variant and the catalase -262C>T variant and aerobic power response. Haplotypes of the eNOS polymorhisms were predictive of aerobic power and its response to training (P < 0.05). After Bonferroni correction of multiple testing no significant differences remained.
  
  
  CONCLUSIONS
  We believe that genetic factors are very important in the explanation of the great variability of aerobic power and its response. However, after Bonferroni-correction, differences in these polymorphisms remained no longer statistically significant.
authors: Cardiovascular Rehabilitation Unit, Department of Rehabilitation Sciences, Katholieke Universiteit Leuven, Belgium.
authors: Steven
authors: S
authors: Onkelinx
authors: Veronique
authors: V
authors: Cornelissen
authors: Johan
authors: J
authors: Defoor
authors: Gert
authors: G
authors: Matthijs
authors: Tom
authors: T
authors: Thomaes
authors: Ellen
authors: E
authors: Coeckelberghs
authors: Roselien
authors: R
authors: Buys
authors: Dirk
authors: D
authors: Schepers
authors: Robert
authors: R
authors: Fagard
authors: Luc
authors: L
authors: Vanhees
mesh_terms: D002374:Catalase / Q000235:genetics; D003324:Coronary Artery Disease / Q000235:genetics*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D017079:Exercise Tolerance / Q000235:genetics*; D005260:Female; D005979:Glutathione Peroxidase / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D019255:NADPH Oxidases / Q000235:genetics; D052250:Nitric Oxide Synthase Type III / Q000235:genetics; D010101:Oxygen Consumption / Q000235:genetics; D047493:PPAR alpha / Q000235:genetics; D011110:Polymorphism, Genetic; D013482:Superoxide Dismutase / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics; D000094765:Glutathione Peroxidase GPX1
chemical_list: D047493:PPAR alpha; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D002374:Catalase; D005979:Glutathione Peroxidase; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase; D019255:NADPH Oxidases; D000094765:Glutathione Peroxidase GPX1; C000722067:GPX1 protein, human