The aim of this study was to determine the distribution of ACTN3 R577X gene polymorphism in soccer players and sedentary individuals, and to investigate the relationship of this distribution with performance tests. A total of 100 soccer players and 101 sedentary individuals were enrolled in the study. Standing long jump and countermovement jump (with arm swing, without arm swing and repeated) scores were recorded, using a jump meter. Maximum VO2 levels were measured using a treadmill-connected cardiopulmonary exercise device, Masterscreen CPX. ACTN3 R577X polymorphism was evaluated by real-time PCR. ACTN3 R577X genotype distribution was found to be similar in soccer players and controls (p>0.05). The only statistically significant finding was a shorter countermovement jump with arm swing scores in the RR-genotyped soccer players, compared with their RX genotyped counterparts (p<0.05). In the soccer player group, RX-genotyped subjects were observed to have lower respiratory threshold values compared with RR-genotyped subjects (p<0.05). No significant correlation was detected between this distribution and performance test results. ACTN3 R577X genotype distribution was found to have no effect on sprint and endurance characteristics in amateur soccer players. The ACTN3 R577X polymorphism may not be a specific enough genetic marker to determine athletic performance in soccer.
The main purpose of this research is to determine the relationship between angiotensin converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and maximal oxygen consumption (maxVO2) in soccer players and sedentary subjects. To prove possible association of telomerase enzyme activity with maxVO2, was a secondary aim.A total of 104 healthy soccer players and 103 healthy sedentary individuals who are aged between 18-30 yrs, and have similar characteristics were included in the study. Participants’ medical histories were taken and physical examinations were performed. Regional fat measurement by skinfold calliper and body composition measurements by bioimpedance were made. MaxVO2 measurements were performed with a cardiopulmonary exercise testing device (Masterscreen CPX) in connexion to a treadmill. Blood samples were taken into EDTA tubes for ACE I/D gene polymorphism determination, which was performed using the polymerase chain reaction (PCR) method. In an attempt to relate maxVO2 with leucocyte telomere length, telomerase enzyme activity was also searched. Apart from descriptive statistical analysis, 2 x 3 factorial ANOVA analysis was performed to see the effect of both sports participation and gene polymorphism. Hardy-Weinberg analysis was made to determine gene distribution. For statistical significance, the p < 0.05 level was used.Soccer players’ body composition, body mass index (BMI), body fat ratio (BFR), and all skinfold thicknesses were lower than the controls’. Total (ml/min) and per body weight (ml/min/kg) maxVO2 and ventilatory threshold (VT) levels of the control group were found to be significantly lower than those of the soccer players. ACE I/D gene polymorphism distribution in all subjects was 21.7% for ACE I/I, 45.5% for ACE I/D and 32.8% for ACE D/D; I and D alleles amounting to 44.4% and 55.6%. Soccer players and controls had similar gene distribution. ACE I/D gene polymorphism and maxVO2 were not associated. However, average maxVO2 score of all individuals with ACE I/I polymorphism (52.1 ± 10.3 ml/min/kg) was found to be higher than those with I/D (50.5 ± 9.6 ml/min/kg) and D/D (50.9 ± 10.8 ml/min/kg) polymorphism, the difference failing statistical significance. In the present study, no effect of ACE I/D gene polymorphism on body weight, BMI, BFR and skinfold measurements -apart the subscapular- were determined. Leucocyte telomerase activity was not detectable in the blood samples.According to the present investigation, ACE I/D gene polymorphism is not associated with maxVO2 and body composition measurements in soccer players and sedentary subjects. No leucocyte telomerase activity was detected in the blood samples, failing to prove association of maxVO2 with telomere length.AcknowledgmentThe authors would like to express their gratitude for the support of Ege University Research Fund (BAP TIP2012)
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