Alves Guilherme B, Oliveira Edilamar M, Alves Cleber R, Rached Heron R S, Mota Glória F A, Pereira Alexandre C, Rondon Maria U, Hashimoto Nara Y, Azevedo Luciene F, Krieger José Eduardo, Negrão Carlos Eduardo
Heart Institute (InCor), University of São Paulo, São Paulo, Brazil.
Eur J Cardiovasc Prev Rehabil. 2009 Aug;16(4):487-92. doi: 10.1097/HJR.0b013e32832c5a8a.
The allele threonine (T) of the angiotensinogen has been associated with ventricular hypertrophy in hypertensive patients and soccer players. However, the long-term effect of physical exercise in healthy athletes carrying the T allele remains unknown. We investigated the influence of methionine (M) or T allele of the angiotensinogen and D or I allele of the angiotensin-converting enzyme on left-ventricular mass index (LVMI) and maximal aerobic capacity in young healthy individuals after long-term physical exercise training.
Prospective clinical trial.
Eighty-three policemen aged between 20 and 35 years (mean+/-SD 26+/-4.5 years) were genotyped for the M235T gene angiotensinogen polymorphism (TT, n = 25; MM/MT, n = 58) and angiotensin-converting enzyme gene insertion/deletion (I/D) polymorphism (II, n = 18; DD/DI, n = 65). Left-ventricular morphology was evaluated by echocardiography and maximal aerobic capacity (VO2peak) by cardiopulmonary exercise test before and after 17 weeks of exercise training (50-80% VO2peak).
Baseline VO2peak and LVMI were similar between TT and MM/MT groups, and II and DD/DI groups. Exercise training increased significantly and similarly VO2peak in homozygous TT and MM/MT individuals, and homozygous II and DD/DI individuals. In addition, exercise training increased significantly LVMI in TT and MM/MT individuals (76.5+/-3 vs. 86.7+/-4, P = 0.00001 and 76.2+/-2 vs. 81.4+/-2, P = 0.00001, respectively), and II and DD/DI individuals (77.7+/-4 vs. 81.5+/-4, P = 0.0001 and 76+/-2 vs. 83.5+/-2, P = 0.0001, respectively). However, LVMI in TT individuals was significantly greater than in MM/MT individuals (P = 0.04). LVMI was not different between II and DD/DI individuals.
Left-ventricular hypertrophy caused by exercise training is exacerbated in homozygous TT individuals with angiotensinogen polymorphism.
血管紧张素原的苏氨酸（T）等位基因与高血压患者及足球运动员的心室肥厚有关。然而，对于携带T等位基因的健康运动员进行体育锻炼的长期影响仍不清楚。我们研究了血管紧张素原的甲硫氨酸（M）或T等位基因以及血管紧张素转换酶的D或I等位基因对年轻健康个体长期体育锻炼训练后左心室质量指数（LVMI）和最大有氧能力的影响。
前瞻性临床试验。
对83名年龄在20至35岁之间（平均±标准差26±4.5岁）的警察进行血管紧张素原M235T基因多态性（TT，n = 25；MM/MT，n = 58）和血管紧张素转换酶基因插入/缺失（I/D）多态性（II，n = 18；DD/DI，n = 65）的基因分型。在17周的运动训练（50 - 80%最大摄氧量峰值）前后，通过超声心动图评估左心室形态，通过心肺运动试验评估最大有氧能力（VO2peak）。
TT组与MM/MT组之间，以及II组与DD/DI组之间，基线VO2peak和LVMI相似。运动训练使纯合子TT和MM/MT个体以及纯合子II和DD/DI个体的VO2peak显著且相似地增加。此外,运动训练使TT和MM/MT个体的LVMI显著增加（分别为76.5±3对86.7±4，P = 0.00001和76.2±2对81.4±,2，P = 0.00001），以及II和DD/DI个体的LVMI显著增加（分别为77.7±4对81.5±4，P = 0.0001和76±2对83.5±2，P = 0.0001）。然而，TT个体的LVMI显著大于MM/MT个体（P = 0.04）。II和DD/DI个体之间的LVMI没有差异。
血管紧张素原多态性的纯合子TT个体因运动训练导致的左心室肥厚加剧。
