-Besides neuronal plasticity, the neurotrophin brain-derived neurotrophic factor (BDNF) is also important in vascular function. The BDNF has been associated with angiogenesis through its specific receptor tropomyosin-related kinase B (TrkB). Additionally, Val66Met polymorphism decreases activity-induced BDNF. Since BDNF and TrkB are expressed in vascular endothelial cells and aerobic exercise training can increase serum BDNF, this study aimed to test the hypotheses: 1) Serum BDNF levels modulate peripheral blood flow; 2) The Val66Met BDNF polymorphism impairs exercise training-induced vasodilation. We genotyped 304 healthy male volunteers (Val66Val, n ϭ 221; Val66Met, n ϭ 83) who underwent intense aerobic exercise training on a running track three times/wk for 4 mo. We evaluated pre-and post-exercise training serum BDNF and proBDNF concentration, heart rate (HR), mean blood pressure (MBP), forearm blood flow (FBF), and forearm vascular resistance (FVR). In the pre-exercise training, BDNF, proBDNF, BDNF/proBDNF ratio, FBF, and FVR were similar between genotypes. After exercise training, functional capacity (V O2 peak) increased and HR decreased similarly in both groups. Val66Val, but not Val66Met, increased BDNF (interaction, P ϭ 0.04) and BDNF/proBDNF ratio (interaction, P Ͻ 0.001). Interestingly, FBF (interaction, P ϭ 0.04) and the FVR (interaction, P ϭ 0.01) responses during handgrip exercise (HG) improved in Val66Val compared with Val66Met, even with similar responses of HR and MBP. There were association between BDNF/proBDNF ratio and FBF (r ϭ 0.64, P Ͻ 0.001) and FVR (r ϭ Ϫ0.58, P Ͻ 0.001) during HG exercise. These results show that peripheral vascular reactivity and serum BDNF responses to exercise training are impaired by the BDNF Val66Met polymorphism and such responsiveness is associated with serum BDNF concentrations in healthy subjects.BDNF Val66Met polymorphism; exercise training; vascular reactivity EXERCISE TRAINING HAS BEEN considered a key element in the improvement in brain-derived neurotrophic factor (BDNF) levels (39), which is the strongest factor linking exercise with cognitive benefits. However, the variability of individual responses may be linked to genetic differences.While BDNF promotes neuronal survival and enhanced synaptic plasticity by activating the tropomyosin kinase B (TrkB) receptor, the action of its precursor proBDNF results in apoptosis by interacting with the p75 neurotrophin receptor (p75NTR), and both are significantly involved in different physiological functions (15,53).Considering the fact that the BDNF gene and its TrkB receptor are expressed in several tissues, such as brain, heart, lungs, and endothelial cells (12, 28), besides neuronal plasticity, it is possible that the neurotrophin BDNF also is involved in the health of other tissues. Indeed, besides the hippocampus, the circulating BDNF is produced by a number of peripheral nonneuronal tissues, including vascular endothelial cells (28,53). Moreover, the neurotrophin BDNF has been associated with angiogenesis thro...
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.
Peripheral blood cells are an accessible environment in which to visualize exercise-induced alterations in global gene expression patterns. We aimed to identify a peripheral blood mononuclear cell (PBMC) signature represented by alterations in gene expression, in response to a standardized endurance exercise training protocol. In addition, we searched for molecular classifiers of the variability in oxygen uptake (V̇o2). Healthy untrained policemen recruits (n = 13, 25 ± 3 yr) were selected. Peak V̇o2 (measured by cardiopulmonary exercise testing) and total RNA from PBMCs were obtained before and after 18 wk of running endurance training (3 times/wk, 60 min). Total RNA was used for whole genome expression analysis using Affymetrix GeneChip Human Gene 1.0 ST. Data were normalized by the robust multiarray average algorithm. Principal component analysis was used to perform correlations between baseline gene expression and V̇o2peak. A set of 211 transcripts was differentially expressed (ANOVA, P < 0.05 and fold change > 1.3). Functional enrichment analysis revealed that transcripts were mainly related to immune function, cell cycle processes, development, and growth. Baseline expression of 98 and 53 transcripts was associated with the absolute and relative V̇o2peak response, respectively, with a strong correlation (r > 0.75, P < 0.01), and this panel was able to classify the 13 individuals according to their potential to improve oxygen uptake. A subset of 10 transcripts represented these signatures to a similar extent. PBMCs reveal a transcriptional signature responsive to endurance training. Additionally, a baseline transcriptional signature was associated with changes in V̇o2peak. Results might illustrate the possibility of obtaining molecular classifiers of endurance capacity changes through a minimally invasive blood sampling procedure.
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.
Aim: The purpose of this study was to identify a PBMC gene expression signature in response to endurance training. We also aimed to identify transcripts associated with changes in peak oxygen uptake (VO2peak). Methods: Healthy untrained policemen recruits (n=13; 25 ± 3 yrs; BMI 27.0 ± 2.8 kg∙m‐2) were selected. VO2peak (cardiopulmonary exercise test) and total RNA were obtained before and after 18 weeks of running endurance training (3 times/wk; 60min), for whole‐genome expression analysis (GeneChip® Human Gene 1.0 ST). Results: Training induced changes (Δ) in VO2peak (0.27±0.28 l∙min‐1, P=0.09) and a differential regulation of 211 transcripts (P<0.05; fold change>1.3). Baseline expression levels of 98 transcripts were strongly correlated with absolute ΔVO2peak (r>0.75; P<0.01). Differentially regulated transcripts were mostly represented in immune response of heat shock proteins and cytokines (HSPA1A, IL‐1), cell cycle regulation of differentiation and post‐translational modification processes (Histone H1, PLK1, SUMO‐1) and growth factors (EGR1, GH) activation and signalling. Conclusions: We describe a transcriptional map regulated by endurance training, ocurring in easily accessed PBMCs. Future research will focus on establishing transcriptional markers of trainability. Grant Funding Source: Supported by FAPESP #2005/59740‐7; CNPq #482863/2011‐0
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