Onkelinx Steven, Cornelissen Veronique, Defoor Johan, Matthijs Gert, Thomaes Tom, Coeckelberghs Ellen, Buys Roselien, Schepers Dirk, Fagard Robert, Vanhees Luc
Cardiovascular Rehabilitation Unit, Department of Rehabilitation Sciences, Katholieke Universiteit Leuven, Belgium.
Acta Cardiol. 2011 Aug;66(4):407-14. doi: 10.1080/ac.66.4.2126586.
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).
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.
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.
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.
有氧代谢表型对相似的有氧训练刺激表现出广泛的变异性，这部分可归因于遗传因素。内皮功能影响有氧能力。多种生理途径可能影响内皮功能。因此，我们旨在研究内皮型一氧化氮合酶（eNos）基因、过氧化氢酶（CAT）基因、血管内皮生长因子（VEGF）基因、谷胱甘肽过氧化物酶1（GPX1）基因、NAD（P）H氧化酶基因的亚基P22 phox、过氧化物酶体增殖物激活受体α（PPAR-α）基因和过氧化物酶体增殖物激活受体γ共激活因子1α（PGC-α）基因的多态性是否与冠心病（CAD）患者的有氧能力或其对体育锻炼的反应相关。
CAREGENE研究（心脏康复与运动表现遗传学研究）纳入了935名无生物学亲缘关系的白种CAD患者，这些患者在基线时进行了分级自行车测试直至力竭，并在完成3个月训练后再次进行测试。使用入侵检测法和飞行质谱技术检测多态性。对eNos基因、VEGF基因和NAD（P）H氧化酶基因的多态性进行单倍型分析。
体育锻炼使有氧能力显著提高24.2±0.6%（P<0.001）。有氧能力与eNOS 273C>T变异体、过氧化氢酶-262C>T变异体以及有氧能力反应之间存在P<0.05的相关性。eNOS多态性的单倍型可预测有氧能力及其对训练的反应（P<0.05）。经过多重检验的Bonferroni校正后，未发现显著差异。
我们认为遗传因素在解释有氧能力及其反应的巨大变异性方面非常重要。然而，经过Bonferroni校正后，这些多态性的差异不再具有统计学意义。
