The effect of training and detraining on ACE, ADRβ3 and UCP1 polymorphism in younger adult male
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In this study, we examined whether this effect was mediated by improvements in cardiovascular fitness capacity and body composition in 136 homozygous for the angiotensin-converting enzyme(ACE) genotype, β3-Adrenergic Receptor (ADRβ3) gene and Uncoupled Protein-1(UCP1) gene during 24 week training and after 24 week detraining consecutively. Body mass index(BMI), skinfold thickness(SKT), percent body fat(%fat), maximal oxygen uptake(VO2max), and 2km running record were measured with standard methods, Genotyping was determined by the I/D polymorphism of ACE gene, A/T of ADRβ3 A/G of UCP1. An exercise protocol was used to performing 60min running at heart rate reserve(HRR) 70∼85%. ACE, ADRβ3 and UCP1 genes were not correlated with each gene. The distributions of ACE genotypes were 22.8% DD, 45.8% ID, and 31.6% II. The distributions of UCP-1 genotypes were aa type 24.3%, ag type 46.3% and gg type 29.4% and those of ADRβ3 were aa type 4.4%, at type 16.9% and tt type 78.7%. There was not significant intergroup difference in changes of VO2max, SKT and %fat. However, VO2max was grater for the II subjects compared to DD subjects[mean 1.5ml/kg/min, respectively; P=0.02 for mean difference]. Body weight and %fat were lower for the II subjects compared to DD subjects[mean 4.6kg, respectively; P=0.02 for mean difference] [4.0%, respectively; P=0.01 for mean difference]. There was relationship between the body composition(%fat and BMI) and cardiovascular fitness level(VO2max) in the genotypes of the ACE gene I/D polymorphism of younger adult man. However, the ACE gene I/D polymorphism may not play a role in main enhanced endurance performance and this is not mediated by differences in VO2max, body weight and % fat in response to training and detraining.
Abstract
In this study, we examined whether this effect was mediated by improvements in cardiovascular fitness capacity and body composition in 136 homozygous for the angiotensin-converting enzyme(ACE) genotype, β3-Adrenergic Receptor (ADRβ3) gene and Uncoupled Protein-1(UCP1) gene during 24 week training and after 24 week detraining consecutively. Body mass index(BMI), skinfold thickness(SKT), percent body fat(%fat), maximal oxygen uptake(VO2max), and 2km running record were measured with standard methods, Genotyping was determined by the I/D polymorphism of ACE gene, A/T of ADRβ3 A/G of UCP1. An exercise protocol was used to performing 60min running at heart rate reserve(HRR) 70∼85%. ACE, ADRβ3 and UCP1 genes were not correlated with each gene. The distributions of ACE genotypes were 22.8% DD, 45.8% ID, and 31.6% II. The distributions of UCP-1 genotypes were aa type 24.3%, ag type 46.3% and gg type 29.4% and those of ADRβ3 were aa type 4.4%, at type 16.9% and tt type 78.7%. There was not significant intergroup difference in changes of VO2max, SKT and %fat. However, VO2max was grater for the II subjects compared to DD subjects[mean 1.5ml/kg/min, respectively; P=0.02 for mean difference]. Body weight and %fat were lower for the II subjects compared to DD subjects[mean 4.6kg, respectively; P=0.02 for mean difference] [4.0%, respectively; P=0.01 for mean difference]. There was relationship between the body composition(%fat and BMI) and cardiovascular fitness level(VO2max) in the genotypes of the ACE gene I/D polymorphism of younger adult man. However, the ACE gene I/D polymorphism may not play a role in main enhanced endurance performance and this is not mediated by differences in VO2max, body weight and % fat in response to training and detraining.
참고문헌 (41)
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