Endurance training produces physiological left ventricular (LV) hypertrophy and bradycardia. However, similarity training athletes do not have same ventricular size, suggesting that genetic factors may affect ventricular mass. Therefore, we studied whether left ventricular mass in athletes associated with polymorphisms in renin-angiotensin system genes.
Polymerase chain reaction with genomic DNA samples of 21 male distance runners was used to detect genotype of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and angiotensinogen (AGT) gene M235T polymorphism. Genotype frequencies of the ACE and AGT gene polymorphisms were found by 9.5%, 42.9% and 47.6% for DD, DI and II, and by 52.4% and 47.6% for TT and MT, respectively. Bradycardia (49.4±7.7/min) and high voltage in LV were shown in electrocardiography (ECG) and massive LV (263.3±47.3g) were observed in echocardiography. However, there was no significant relationship between athlete's heart and genotypes of the ACE and AGT polymorphisms. Holter ECG showed bradycardia, atrioventricular block and many long cardiac pauses, but there was no correlation without minimal heart rate (HR) between arrhythmias and genotypes of the ACE and AGT polymorphisms. TT genotype of AGT polymorphisms showed lower minimal HR (34.3±15.4/min) than that of MT genotype (38.2±5.9/min) (P<0.05). We also examined maximal oxygen consumption (VO_2 max) to detect whether the ACE and AGT gene polymorphisms affected athlete's performance. Subjects showed high VO_2 max (68.1 ± 5.4ml/kg/min), but there was no correlation to the ACE and AGT genotypes. In conclusion, we could not find significant relationship without minimal HR between athlete's heart and genotypes of the ACE and AGT polymorphisms.