Kasikcioglu Erdem, Kayserilioglu Abidin, Ciloglu Figen, Akhan Hulya, Oflaz Huseyin, Yildiz Safinaz, Peker Ismail
Sports Medicine Department, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Heart Vessels. 2004 Nov;19(6):287-93. doi: 10.1007/s00380-004-0783-7.
The mechanisms that regulate the development of human physiological cardiac hypertrophy remain poorly understood. The renin-angiotensin system, which is modulated by genetic polymorphism, plays an important role in the regulation of vascular tone and myocardial hypertrophy. Although a few studies have analyzed the association of angiotensin-converting enzyme (ACE) polymorphism and left ventricular (LV) hypertrophy in isotonic exercise-trained subjects who developed eccentric cardiac hypertrophy, there has been no research done in power athletes who developed concentric cardiac hypertrophy. We have hypothesized that ACE genotypic modulation characteristics may affect LV mass in power athletes. This study included 29 elite Caucasian wrestlers (mean age, 22.6 years) and 51 age-matched sedentary subjects. According to the absence or presence of the insertion segment in the polymerase chain reaction (PCR) product, the subjects were classified as homozygous deletion-deletion (DD), insertion-insertion (II), or heterozygous insertion-deletion (ID). The association of LV hypertrophy with ACE gene insertion/deletion (I/D) polymorphism was analyzed. Left ventricular mass and index were determined by echocardiography. Angiotensin-converting enzyme genotyping was performed on peripheral leukocytes using the polymerase chain reaction technique. The study and control group subjects were similar in height and weight. Left ventricular hypertrophy in the athletes was more apparent than in the controls. Angiotensin-converting enzyme genotype II frequency was 17.2% (5) in the athletes, 17.6% (9) in the controls; ID frequency was 51.7% (15) in the athletes, 56.8% (29) in the controls; and the DD frequency was 31% (9) in the athletes and 25.4% (13) in the controls. Left ventricular mass and mass index were found to be higher in genotype DD (126.2 +/- 2.9g/m2) than genotype II (85.5 +/- 4.0g/m2) or genotype ID (110.1 +/- 2.3g/m2) in the athletes (P < 0.001). Furthermore, maximal oxygen consumption in genotype DD was found to be higher than in II and ID. An association was found between ACE gene I/D polymorphism and LV hypertrophy in strength-trained athletes.
调节人类生理性心脏肥大发展的机制仍未被充分理解。肾素 - 血管紧张素系统受基因多态性调节,在血管张力和心肌肥大的调节中起重要作用。尽管有一些研究分析了在发生离心性心脏肥大的等张运动训练受试者中血管紧张素转换酶(ACE)多态性与左心室(LV)肥大的关联,但尚未对发生向心性心脏肥大的力量型运动员进行研究。我们推测ACE基因型调节特征可能影响力量型运动员的左心室质量。本研究纳入了29名精英白人摔跤运动员(平均年龄22.6岁)和51名年龄匹配的久坐不动的受试者。根据聚合酶链反应(PCR)产物中是否存在插入片段,受试者被分为纯合缺失 - 缺失(DD)、插入 - 插入(II)或杂合插入 - 缺失(ID)。分析了左心室肥大与ACE基因插入/缺失(I/D)多态性的关联。通过超声心动图测定左心室质量和指数。使用聚合酶链反应技术对外周血白细胞进行血管紧张素转换酶基因分型。研究组和对照组受试者的身高和体重相似。运动员的左心室肥大比对照组更明显。运动员中血管紧张素转换酶基因型II的频率为17.2%(5例),对照组为17.6%(9例);ID频率在运动员中为51.7%(15例),对照组为56.8%(29例);DD频率在运动员中为31%(9例),对照组为25.4%(13例)。在运动员中,发现基因型DD的左心室质量和质量指数(126.2±2.9g/m²)高于基因型II(85.5±4.0g/m²)或基因型ID(110.1±2.3g/m²)(P<0.001)。此外,发现基因型DD的最大耗氧量高于II和ID。在力量训练的运动员中发现ACE基因I/D多态性与左心室肥大之间存在关联。