No abstract

ACTN3 R577X polymorphism is associated with VO2. XX individuals have greater aerobic capacity. Endurance training eliminates differences in peak VO2 between XX and RR individuals. These findings suggest a ceiling-effect phenomenon, and, perhaps, trained individuals may not constitute an adequate population to explain associations between phenotypic variability and gene variations.

The polymorphic allele at position -786 and the haplotype containing polymorphic alleles at positions -786 and 894 in the endothelial nitric oxide gene were associated with decreased parasympathetic modulation after exercise training.

Rondon MU. Exercise training improves muscle vasodilatation in individuals with T786C polymorphism of endothelial nitric oxide synthase gene. Physiol Genomics 42A: 71-77, 2010. First published July 6, 2010; doi:10.1152/physiolgenomics.00145.2009.-Allele T at promoter region of the eNOS gene has been associated with an increase in coronary disease mortality, suggesting that this allele increases susceptibility for endothelial dysfunction. In contrast, exercise training improves endothelial function. Thus, we hypothesized that: 1) Muscle vasodilatation during exercise is attenuated in individuals homozygous for allele T, and 2) Exercise training improves muscle vasodilatation in response to exercise for TT genotype individuals. From 133 preselected healthy individuals genotyped for the T786C polymorphism, 72 participated in the study: TT (n ϭ 37; age 27 Ϯ 1 yr) and CTϩCC (n ϭ 35; age 26 Ϯ 1 yr). Forearm blood flow (venous occlusion plethysmography) and blood pressure (oscillometric automatic cuff) were evaluated at rest and during 30% handgrip exercise. Exercise training consisted of three sessions per week for 18 wk, with intensity between anaerobic threshold and respiratory compensation point. Resting forearm vascular conductance (FVC, P ϭ 0.17) and mean blood pressure (P ϭ 0.70) were similar between groups. However, FVC responses during handgrip exercise were significantly lower in TT individuals compared with CTϩCC individuals (0.39 Ϯ 0.12 vs. 1.08 Ϯ 0.27 units, P ϭ 0.01). Exercise training significantly increased peak VO 2 in both groups, but resting FVC remained unchanged. This intervention significantly increased FVC response to handgrip exercise in TT individuals (P ϭ 0.03), but not in CTϩCC individuals (P ϭ 0.49), leading to an equivalent FVC response between TT and CTϩCC individuals (1.05 Ϯ 0.18 vs. 1.59 Ϯ 0.27 units, P ϭ 0.27). In conclusion, exercise training improves muscle vasodilatation in response to exercise in TT genotype individuals, demonstrating that genetic variants influence the effects of interventions such as exercise training. genetics NITRIC OXIDE (NO) is synthesized in the endothelium by the endothelial isoform of nitric oxide synthase (eNOS) (27), a protein encoded in the long arm of chromosome 7 (19). NO is responsible for the maintenance of vascular tone due to its capability of inducing vasodilatation in response to shear stress (9, 26). A disruption of eNOS function or of its production can decrease NO bioavailability and, consequently, lead to deleterious effects on endothelial and vasomotor function. Recent findings suggest that, apart from classic risk factors such as smoking and diabetes, genetic variants are capable of altering eNOS expression and enzymatic activity (21,23,36).Among the genetic variants present in the eNOS gene, considerable attention has been focused on the T786C polymorphism, which is located on the 5=-flanking region of the promoter region of the eNOS gene. The C allele of this polymorphism has been associated with coronary spasm (23) and blunted vasodilato...

Exercise training not only improves the plasma lipid profile but also reduces risk of developing coronary heart disease. We investigate whether plasma lipids and high density lipoprotein (HDL) metabolism are affected by aerobic training and whether the high‐density lipoprotein cholesterol (HDL‐C) levels at baseline influence exercise‐induced changes in HDL. Seventy‐one male sedentary volunteers were evaluated and allocated in two subgroups, according to the HLD‐C levels (< or >40 mg/dL). Participants underwent an 18‐week aerobic training period. Blood was sampled before and after training for biochemical analysis. Plasma lipids, apolipoproteins, HDL diameter, and VO2 peak were determined. Lipid transfers to HDL were determined in vitro by incubating plasma samples with a donor lipid artificial nanoemulsion. After the 18‐week period of aerobic training, the VO2 peak increased, while the mean body mass index (BMI) decreased. HDL‐C concentration was higher after the training period, but low‐density lipoprotein cholesterol (LDL‐C) and non‐HDL‐C did not change. The transfer of esterified cholesterol and phospholipids was greater after exercise training, but the triacylglycerol and unesterified cholesterol transfers were unchanged. The HDL particle diameter increased after aerobic training in all participants. When the participants were separated in low‐HDL and normal‐HDL groups, the postaerobic exercise increment in HDL‐C was higher in the low‐HDL group, while the transfer of esterified cholesterol was lower. In conclusion, aerobic exercise training increases the lipid transfers to HDL, as measured by an in vitro method, which possibly contributes to the classical elevation of the HDL‐C associated with training.