Do ACE and CKMM gene variations have potent effects on physical performance in inactive male adolescents?

We studied to ascertain whether the ACE and/or CKMM genotypes independently influence the baseline level of some sport performances in 613 inactive male adolescents (mean ± SD age: 13.24 ± 0.28 years). All DNA samples were extracted and genotyped for ACE I/D and CKMM A/G polymorphisms using a PCR based procedure. One-way analysis of covariance was used to examine the discrepancies in the research phenotypes among various ACE and CKMM polymorphisms. The comparisons of genotype and allele frequencies between adolescents with the best and the worst performances were calculated and analyzed by the Chi square test. All procedures were approved by Medical University Ethics Committee. Written informed consent signed and approved by all subject`s parents were obtained. We observed the effect of the ACE and CKMM polymorphisms on VO2max (P = 0.001 & P = 0.001 respectively). ACE and CKMM genotypes differed between groups (< 90th vs. ≥ 90) in the multi-stage 20 m shuttle run (P = 0.001 and 0.001). ACE allele frequencies differed between groups (< 90th vs. ≥ 90) in the multi-stage 20-m shuttle run (P = 0.001). This study suggests that the ACE and CKMM polymorphisms influence the endurance performance phenotype in non-trained adolescent males.

Association between the PPARa and PPARGCA gene variations and physical performance in non-trained male adolescents.

The purpose of the research was to examine if some genetic variations are associated with some endurance, power and speed performances (multi-stage 20-m shuttle run, standing broad jump, 20 m sprint test and Abalakov jump) in a group of 586 non-trained male adolescents (mean ± SD age: 13.20 ± 0.25 years). Polymorphisms in PPARa and PPARGC1A implicated in physical performance traits were analyzed. DNA was extracted and the samples were genotyped for PPARa and PPARGC1A polymorphisms by a PCR based method followed by gel electrophoresis. The discrepancies in the study phenotypes among variations of the PPARa and PPARGC1A polymorphisms were analyzed by one-way analysis of covariance (ANCOVA), after age, weight and height adjustment. To examine whether the genotype and allele frequencies between adolescents with high and low performances were different, we divided them into two groups: ≥ 90th and < 90th of the percentile. The genotype and allele frequencies between adolescents with high and low performances were compared with the Chi square test. Our analysis demonstrated the effects of the PPARa and PPARGC1A polymorphisms only on [Formula: see text] (p = 0.010 and p = 0.010 respectively). Also, we observed significant differences in PPARa and PPARGC1A genotypes (p = 0.034 and p = 0.024) or allele frequencies (p = 0.031 and p = 0.001) between groups for the multi-stage 20-m shuttle run test. Findings of this research suggest that both the PPARa and PPARGC1A polymorphisms are associated with estimating endurance-related phenotype and endurance capacity in male non-athletes adolescents.

The response of circulating omentin-1 concentration to 16-week exercise training in male children with obesity.

OBJECTIVES: The purpose of the present study was to investigate the effects of the 16-week exercise training program on serum omentin-1 in relation to change in insulin resistance in obese male children. METHODS: Thirty-two obese male children, aged 9-12 years, were randomly assigned into Exercise Group (ExG; n = 16) and Control Group (CG; n = 16). ExG participated in a 16-week exercise training program which combined various forms of aerobic activities and resistance training. Body composition, body mass index (BMI), waist circumference (WC), fasting glucose and insulin, homeostasis model assessment estimate of insulin resistance (HOMA2-IR), blood lipids and serum omentin-1 were assessed before and after 16 weeks of training. RESULTS: Exercise training significantly decreased body mass (7.5%), BMI (7.6%), WC (4.3%), body fat % (15%), fasting insulin (18.5%), total cholesterol (TC) (5.4%), low-density lipoprotein cholesterol (LDL-C) (17%) and triglyceride (TG) (7.4%) compared to CG. Between-groups comparison showed a considerable exercise-induced upregulation in omentin-1 (ES = 89; P < 0.05) levels. Furthermore, in ExG serum omentin-1 levels were significantly increased from 24.5 ± 8.4 to 35.9 ± 9.3 ng/ml (45%; P < 0.001) after the training program, which was accompanied with significantly decreased fasting insulin (P < 0.001). The changes in omentin-1 concentrations correlated with the changes in BMI (r = -0.67, P < 0.001), WC (r = -0.62, P = 0.002), body fat % (r = -0.50, P = 0.004), insulin (r = -0.65, P = 0.001), HOMA2-IR (r = -0.60, P = 0.004), TC (r = -0.53, P = 0.004) and LDL-C (r = -0.51, P = 0.004) in ExG. BMI (ß = -0.50, P = 0.009) and fasting insulin (ß = -0.54, P = 0.006) changes were found to be independent predictors of omentin-1 increment in multiple regression analysis. CONCLUSION: Exercise training resulted in a significant increase in serum omentin-1 concentrations in children with obesity. The findings suggest that exercise-induced changes in omentin-1 may be associated with the beneficial effects of exercise on reduced insulin and weight lost.