Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.

URL: http://www.clinicaltrials.gov. Unique identifier: NCT01643434.

-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...

The aim of this study is to evaluate the activity of sympathetic nerve sistem by microneurography in asymptomatic patients with aortic insufficiency (AoI) chronic important.Were included 10 asymptomatic patients with anatomically important AoI of rheumatic etiology with normal left ventricular function (ejection fraction>; 55%) by echocardiogram.Exclusion criteriadiabetes mellitus, renal failure, neuropathy, or beta‐blockers. A control group of normotensive volunteers (control group, n=11) with age, sex and body mass index‐ matched was included. MNSA by microneuragraphy, and blood pressure (BP) by FINOMETER® were evaluated in supine rest position. Continuous variables are described as mean ± SD and categorical variables as relative frequencies. Student t test and a multivariate analysis model were used, p <0.05 was considered statistically significant.AoI group and control group showed no statistically significant regarding age, sex and BMI. Systolic BP in AoI group was 148 +16 mmHg vs. 120±4 mmHg in control group (p = 0.0001), Diastolic BP was 60±6 mmHg in AoI and 73±3 mmHg in control group (p = 0.0001). The MSNA was in the AoI group 25±3 vs. 15±2 in the control group (p <0.001). Aortic insufficiency was associated independently with a higher MSNA (p = 0.02).AoI important chronic and asymptomatic is associated with increased MSNA.

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