Forearm Vascular Resistance Research Articles

Immediate and 24-h blood pressure-lowering effects of arm crank exercise in patients with traumatic lower-limb amputation: a randomized cross-over study.

This study aimed to investigate the clinic and 24-h postexercise hypotension (PEH) after a moderate-intensity arm crank exercise session in individuals with traumatic lower-limb amputation. Nine men (46±17 years) with unilateral traumatic lower-limb amputation participated in two experimental sessions conducted randomly: an aerobic exercise (EXE: arm crank ergometer, 30 min) or a control session (CON: participants remained seated on the cycle ergometer, 30 min). Clinic and 24-h systolic, diastolic, and mean blood pressure (BP) response were measured after both sessions. The clinical measurements of blood flow and forearm vascular resistance (FVR) were also performed. Compared with the preintervention period, the BP levels did not change in the CON session. However, EXE resulted in a significant hypotensive effect in systolic (-10±0.9 mmHg, P≤0.05), diastolic (-11±1.5 mmHg, P≤0.05), and mean BP (-11±1.2 mmHg, P≤0.05) during the entire postexercise period. The PEH was accompanied by a decreased FVR over the entire postintervention period (P≤0.05). Significant reductions were found for 24-h average systolic, diastolic, and mean BP levels (P=0.03, 0.01, and 0.02, respectively) following EXE compared with the CON session. These results showed, for the first time, that individuals with traumatic lower-limb amputation presented immediate and 24-h PEH after a single bout of arm crank exercise testing. The PEH at the clinic condition was justified, at least in part, by the reduction in peripheral FVR.

Arterial stiffness and peripheral vascular resistance in offspring of hypertensive parents: influence of sex and other confounders.

Established essential hypertension is associated with increased arterial stiffness and peripheral resistance, but the extent of vascular changes in persons genetically predisposed for essential hypertension is uncertain. Participants from the Danish Hypertension Prevention Project (DHyPP) (both parents hypertensive) (n = 95, 41 ± 1 years, 53% men) were compared with available spouses (n = 45, 41 ± 1 years) using measurements of ambulatory blood pressure (BP), left ventricular mass index (LVMI), pulse wave velocity, central BP and augmentation index (AIx) in addition to forearm resting and minimal resistance [forearm resting vascular resistance (Rrest) and forearm minimal vascular resistance (Rmin)]. DHyPP patients with participating spouses had higher 24-h mean BP (94 ± 1 vs. 88 ± 1 mmHg, P < 0.01), LVMI (94 ± 3 vs. 80 ± 2 g/m, P < 0.01), central SBP (121 ± 2 vs. 111 ± 2 mmHg, P < 0.01) and AIx (16.0 ± 1.2 vs. 10.5 ± 1.7%, P < 0.01), but similar carotid-femoral pulse wave velocity (7.5 ± 0.2 vs. 7.1 ± 0.2 m/s), Rrest (53 ± 3 vs. 51 ± 3 mmHg/ml/min/100 ml) and log Rmin (0.58 ± 0.02 vs. 0.55 ± 0.02 mmHg/ml/min/100 ml) when compared with spouses. Using multiple linear regression analysis (adjusting for sex, age, BMI, creatinine clearance and 24-h BP, heart rate and sodium excretion) AIx and LVMI remained elevated in DHyPP patients [4.2% (0.7; 7.7), P = 0.02 and 6.3 g/m (0.7; 11.9), P = 0.03]. For the entire DHyPP cohort AIx, Rrest and Rmin were higher in women than men (P < 0.01), and the same was true for AIx and Rmin among spouses (P < 0.05). Furthermore, AIx was linearly associated with Rrest and Rmin. Young to middle-aged individuals genetically predisposed for essential hypertension display increased AIx and LVMI, although vascular stiffness and peripheral resistance are still normal.

Face cooling reveals a relative inability to increase cardiac parasympathetic activation during passive heat stress.

What is the central question of this study? Does passive heat stress attenuate the increase in cardiac parasympathetic stimulation, vascular resistance and blood pressure evoked by face cooling? What is the main finding and its importance? Passive heat stress attenuates the capacity to increase cardiac parasympathetic activation and impairs the ability to increase vascular resistance during sympathoexcitation, which ultimately results in a relative inability to increase blood pressure. These findings cast doubt on the efficacy of face cooling at augmenting blood pressure during orthostasis while heat stressed. We tested the hypothesis that passive heat stress attenuates the increase in cardiac parasympathetic stimulation, vascular resistance and blood pressure evoked by face cooling. During normothermia and when intestinal temperature was elevated by 1.0±0.2°C, 10 healthy young adults underwent 3min of face cooling. Face cooling was accomplished by placing a 2.5litre bag of ice water (0±0°C) over the cheeks, eyes and forehead. Primary variables included forehead skin temperature, mean arterial pressure and systemic, forearm and cutaneous vascular resistances. Indices of heart rate variability in the time domain provided an index of cardiac parasympathetic activity. The magnitude of reduction in forehead skin temperature during face cooling was slightly greater during normothermia (-17.6±1.9 versus -16.3±3.0°C, P=0.03). Increases in heart rate variability evoked by face cooling were attenuated during heat stress. Changes in systemic, forearm and cutaneous vascular resistances during face cooling were virtually abolished during heat stress (P<0.01). However, when forearm and vascular data were reported as conductance, differences between normothermia and heat stress were not apparent (P≥0.62). Nevertheless, the increase in mean arterial pressure was attenuated during heat stress with face cooling (at 3min: 2±7mmHg) compared with normothermia (at 3min: 19±7mmHg, P<0.01). These data indicate that passive heat stress attenuates face cooling-evoked increases in cardiac parasympathetic activation, vascular resistance and blood pressure. However, they also indicate that changes in indices of vascular resistance do not always reflect equivalent changes in conductance.

Effects of renal denervation on coronary flow reserve and forearm dilation capacity in patients with treatment-resistant hypertension. A randomized, double-blinded, sham-controlled clinical trial.

Microvascular impairment is well documented in hypertension. We investigated the effect of renal sympathetic denervation (RDN) on cardiac and peripheral microvasculature in patients with treatment-resistant essential hypertension (TRH). A randomized, single centre, double-blinded, sham-controlled clinical trial. Fifty-eight patients with TRH (ambulatory systolic BP (ASBP) ≥ 145mmHg) despite stable treatment were randomized to RDN or SHAM. RDN was performed with the unipolar Medtronic Flex catheter. Coronary flow reserve (CFR) and coronary- and forearm minimum vascular resistance (C-Rmin and F-Rmin) were determined using transthoracic Doppler echocardiography and F-Rmin with venous occlusion plethysmography at baseline and at six-months follow-up. RDN was performed with 5.3±0.2 lesions in the right renal artery and 5.4±0.2 lesions in the left. Baseline ASBP was 152±2mmHg (RDN, n=29) and 154±2mmHg (SHAM, n=29). Similar reductions in MAP were seen at follow up (-3.5±2.0 vs. -3.2±1.8, P=0.92). Baseline CFR was 2.9±0.1 (RDN) and 2.4±0.1 (SHAM), with no significant change at follow-up (0.2±0.2 vs. -0.1±0.2, P=0.57). C-Rmin was 1.9±0.3 (RDN) and 2.7±0.6 (SHAM) (mmHgmin/ml pr. 100g) and did not change significantly (0.3±0.5 vs. -0.4±0.8, P=0.48). F-Rmin was 3.6±0.2 (RDN) and 3.6±0.3 (SHAM) (mmHgmin/ml pr. 100ml tissue) and unchanged at follow-up (4.2±0.4 vs. 3.8±0.2, P=0.17). Left ventricular mass index was unchanged following RDN (-4±7 (RDN) vs. 3±5 (SHAM) (g/m2) P=0.38). The current study does not support positive effects of RDN on microvascular impairment in TRH.

THE PATHOPHYSIOLOGY OF CAROTID SINUS HYPERSENSITIVITY: SENSORY BLOCK OF THE STERNOCLEIDOMASTOID MUSCLES DOES NOT INCREASE RESPONSES TO CAROTID SINUS MASSAGE

The arterial baroreflex is crucial for short-term blood pressure control – abnormal baroreflex function predisposes patients to syncope and falling. Hypersensitive responses to stimulation of the carotid baroreceptors using carotid sinus massage (CSM) are common in older adults and may be associated with syncope1. While the pathophysiology of this hypersensitivity is unknown, chronic denervation of the sternocleidomastoid muscles (ScM) is common in elderly patients with carotid sinus hypersensitivity (CSH)2. This phenomenon is proposed to interfere with normal integration of neural information from the carotid baroreceptors with proprioceptive feedback from the ScM, producing large responses to CSM. We hypothesized that simulation of ScM “denervation” using pharmacological blockade would increase cardiovascular responses to CSM. In six participants (aged 29±2 years), tilted CSM was performed while cardiac (RRI; electrocardiography), systolic arterial pressure (SAP; Finometer), and forearm vascular resistance (FVR; mean arterial pressure [Finometer]/brachial blood flow velocity [Doppler ultrasound]) responses were recorded. Participants then received intramuscular injections (6-8ml distributed over 4 sites) of 2% lidocaine hydrochloride, and 0.9% saline (placebo) in contralateral ScM. EMG was recorded during maximal unilateral ScM contraction both pre- and post-injection to confirm neural block with lidocaine. CSM was repeated following injections and responses compared to pre-injection. Data are presented as mean±standard error. Following lidocaine injection, the EMG mean root mean square fell to 21±0.05% of the pre-injection value (p < 0.001), confirming neural block of the ScM. Pre-injection responses of RRI, SAP and FVR were small and not different between sides. Compared to pre-injection, responses were unchanged following lidocaine (RRI: +2±20ms, p=0.99; SAP: -2±2mmHg, p=0.69; FVR +4±5%, p=0.82) and saline injection (RRI: +20±20ms, p=0.75; SAP: -0.6±2mmHg, p=0.98; FVR: +1±5%, p=0.99). Post-injection comparisons between lidocaine and placebo were not different for RRI, SAP, or FVR responses. Neural block of the ScM does not increase cardiovascular responses to CSM. The pathophysiology of CSH remains unknown.

The role of increased glucose on neurovascular dysfunction in patients with the metabolic syndrome.

Metabolic syndrome (MetS) causes autonomic alteration and vascular dysfunction. The authors investigated whether impaired fasting glucose (IFG) is the main cause of vascular dysfunction via elevated sympathetic tone in nondiabetic patients with MetS. Pulse wave velocity, muscle sympathetic nerve activity (MSNA), and forearm vascular resistance was measured in patients with MetS divided according to fasting glucose levels: (1) MetS+IFG (blood glucose ≥100mg/dL) and (2) MetS-IFG (<100mg/dL) compared with healthy controls. Patients with MetS+IFG had higher pulse wave velocity than patients with MetS-IFG and controls (median 8.0 [interquartile range, 7.2-8.6], 7.3 [interquartile range, 6.9-7.9], and 6.9 [interquartile range, 6.6-7.2] m/s, P=.001). Patients with MetS+IFG had higher MSNA than patients with MetS-IFG and controls, and patients with MetS-IFG had higher MSNA than controls (31±1, 26±1, and 19±1 bursts per minute; P<.001). Patients with MetS+IFG were similar to patients with MetS-IFG but had higher forearm vascular resistance than controls (P=.008). IFG was the only predictor variable of MSNA. MSNA was associated with pulse wave velocity (R=.39, P=.002) and forearm vascular resistance (R=.30, P=.034). In patients with MetS, increased plasma glucose levels leads to an adrenergic burden that can explain vascular dysfunction.

Walking training at the heart rate of pain threshold improves cardiovascular function and autonomic regulation in intermittent claudication: A randomized controlled trial.

This study investigated the effects of walking training (WT) on cardiovascular function and autonomic regulation in patents with intermittent claudication (IC). Randomized controlled trial. Forty-two male patients with IC (≥50years) were randomly allocated into two groups: control (CG, n=20, 30min of stretching exercises) and WT (WTG, n=22, 15 bouts of 2min of walking interpolated by 2min of upright rest-walking intensity was set at the heart rate of pain threshold). Both interventions were performed twice/week for 12 weeks. Walking capacity (maximal treadmill test), blood pressure (auscultatory), cardiac output (CO2 rebreathing), heart rate (ECG), stroke volume, systemic vascular resistance, forearm and calf vascular resistance (plethysmography), and low (LF) and high frequency (HF) components of heart rate variability and spontaneous baroreflex sensitivity were measured at baseline and after 12 weeks of the study. WT increased total walking distance (+302±85m, p=0.001) and spontaneous baroreflex sensitivity (+2.13±1.07ms/mmHg, p=0.02). Additionally, at rest, WT decreased systolic and mean blood pressures (-10±3 and -5±2mmHg, p=0.001 and p=0.01, respectively), cardiac output (-0.37±0.24l/min, p=0.03), heart rate (-4±2bpm, p=0.001), forearm vascular resistance (-8.5±2.8U, p=0.02) and LF/HF (-1.24±0.99, p=0.001). No change was observed in the CG. In addition to increasing walking capacity, WT improved cardiovascular function and autonomic regulation in patients with IC.

Breathing 100% oxygen during water immersion improves postimmersion cardiovascular responses to orthostatic stress.

Physiological compensation to postural stress is weakened after long‐duration water immersion (WI), thus predisposing individuals to orthostatic intolerance. This study was conducted to compare hemodynamic responses to postural stress following exposure to WI alone (Air WI), hyperbaric oxygen alone in a hyperbaric chamber (O2 HC), and WI combined with hyperbaric oxygen (O2 WI), all at a depth of 1.35 ATA, and to determine whether hyperbaric oxygen is protective of orthostatic tolerance. Thirty‐two healthy men underwent up to 15 min of 70° head‐up tilt (HUT) testing before and after a single 6‐h resting exposure to Air WI (N = 10), O2 HC (N = 12), or O2 WI (N = 10). Heart rate (HR), blood pressure (BP), cardiac output (Q), stroke volume (SV), forearm blood flow (FBF), and systemic and forearm vascular resistance (SVR and FVR) were measured. Although all subjects completed HUT before Air WI, three subjects reached presyncope after Air WI exposure at 10.4, 9.4, and 6.9 min. HUT time did not change after O2 WI or O2 HC exposures. Compared to preexposure responses, HR increased (+10 and +17%) and systolic BP (−13 and −8%), and SV (−16 and −23%) decreased during HUT after Air WI and O2 WI, respectively. In contrast, HR and SV did not change, and systolic (+5%) and diastolic BP (+10%) increased after O2 HC. Q decreased (−13 and −7%) and SVR increased (+12 and +20%) after O2 WI and O2 HC, respectively, whereas SVR decreased (−9%) after Air WI. Opposite patterns were evident following Air WI and O2 HC for FBF (−26 and +52%) and FVR (+28 and −30%). Therefore, breathing hyperbaric oxygen during WI may enhance post‐WI cardiovascular compensatory responses to orthostatic stress.

Cross-Sectional Associations of Flow Reversal, Vascular Function, and Arterial Stiffness in the Framingham Heart Study.

Experimental studies link oscillatory flow accompanied by flow reversal to impaired endothelial cell function. The relation of flow reversal with vascular function and arterial stiffness remains incompletely defined. We measured brachial diastolic flow patterns along with vasodilator function in addition to tonometry-based central and peripheral arterial stiffness in 5708 participants (age 47±13 years, 53% women) in the Framingham Heart Study Offspring and Third Generation cohorts. Brachial artery diastolic flow reversal was present in 35% of the participants. In multivariable regression models, the presence of flow reversal was associated with lower flow-mediated dilation (3.9±0.2 versus 5.0±0.2%; P<0.0001) and reactive hyperemic flow velocity (50±0.99 versus 57±0.93 cm/s; P<0.0001). The presence of flow reversal (compared with absence) was associated with higher central aortic stiffness (carotid-femoral pulse wave velocity 9.3±0.1 versus 8.9±0.1 m/s), lower muscular artery stiffness (carotid-radial pulse wave velocity 9.6±0.1 versus 9.8±0.1 m/s), and higher forearm vascular resistance (5.32±0.03 versus 4.66±0.02 log dyne/s/cm5; P<0.0001). The relations of diastolic flow velocity with flow-mediated dilation, aortic stiffness, and forearm vascular resistance were nonlinear, with a steeper decline in vascular function associated with increasing magnitude of flow reversal. In our large, community-based sample, brachial artery flow reversal was common and associated with impaired vasodilator function and higher aortic stiffness. Our findings are consistent with the concept that flow reversal may contribute to vascular dysfunction.

Short-Term Angiotensin Subtype 1 Receptor Blockade Does Not Alter the Circulatory Responses to Sympathetic Nervous System Modulation in Healthy Volunteers Before and During Sevoflurane Anesthesia: Results of a Pilot Study

The mechanism of perioperative hypotension in patients taking an angiotensin-receptor blocker up to the time of surgery remains unclear. This study tested the hypothesis that short-term angiotensin-receptor blocker treatment attenuated the sympathetic and vascular responses to autonomic stimuli in volunteers undergoing anesthesia. Randomized, crossover, blinded, pilot design. Zablocki Veterans Affairs Medical Center, Milwaukee, WI. The study comprised 8 male and 6 female healthy, young volunteers (age 23±1.2 years [mean±standard error of the mean]). Volunteers were studied after receiving oral placebo or 50 mg of losartan (angiotensin-receptor blocker) for 3 days before each test day. The effectiveness of angiotensin-receptor blocker treatment was confirmed using the mean arterial blood pressure response to intravenous angiotensin II (1-µg bolus). Eight volunteers underwent direct mean arterial pressure and forearm bloodflow measurements during conscious baseline, a cold pressor test, induction of anesthesia, tracheal intubation, maintenance of anesthesia with 1 minimum alveolar concentration of sevoflurane, and airway irritation with 12% desflurane. Six volunteers experienced mean arterial pressure responses to 0.1 mg of phenylephrine at baseline and during 1 minimum alveolar concentration of sevoflurane. Comparisons were made over time and across groups. Angiotensin-receptor blocker treatment significantly reduced-mean arterial pressure and forearm vascular resistance (forearm blood flow/mean arterial pressure) over time and blocked the mean arterial pressure response to angiotensin-II challenge. The changes in mean arterial pressure and forearm vascular resistance in response to all stressors did not differ between treatments. Mean arterial pressure increases from phenylephrine were preserved. In healthy, young volunteers, sympathetically-mediated responses from the short-term use of an angiotensin-receptor blocker were not altered and most likely did not contribute to perioperative hypotension during the intraoperative period.

Sustained increases in blood pressure elicited by prolonged face cooling in humans.

We tested the hypothesis that increases in blood pressure are sustained throughout 15 min of face cooling. Two independent trials were carried out. In the Face-Cooling Trial, 10 healthy adults underwent 15 min of face cooling where a 2.5-liter bag of ice water (0 ± 0°C) was placed over their cheeks, eyes, and forehead. The Sham Trial was identical except that the temperature of the water was 34 ± 1°C. Primary dependent variables were forehead temperature, mean arterial pressure, and forearm vascular resistance. The square root of the mean of successive differences in R-R interval (RMSSD) provided an index of cardiac parasympathetic activity. In the Face Cooling Trial, forehead temperature fell from 34.1 ± 0.9°C at baseline to 12.9 ± 3.3°C at the end of face cooling (P < 0.01). Mean arterial pressure increased from 83 ± 9 mmHg at baseline to 106 ± 13 mmHg at the end of face cooling (P < 0.01). RMSSD increased from 61 ± 40 ms at baseline to 165 ± 97 ms during the first 2 min of face cooling (P ≤ 0.05), but returned to baseline levels thereafter (65 ± 49 ms, P ≥ 0.46). Forearm vascular resistance increased from 18.3 ± 4.4 mmHg·ml-1·100 g tissue-1·min at baseline to 26.6 ± 4.0 mmHg·ml-1·100 g tissue-1·min at the end of face cooling (P < 0.01). There were no changes in the Sham Trial. These data indicate that increases in blood pressure are sustained throughout 15 min of face cooling, and face cooling elicits differential time-dependent parasympathetic and likely sympathetic activation.

Increased Pre- and Post-Meal Free Fatty Acid Levels in Black, Obese Adolescents.

Black adolescents are at increased risk of cardiometabolic disease but have lower fasting triglyceride, which is usually associated with decreased risk. No one has studied racial differences in triglycerides or free fatty acids (FFAs) after a high-fat meal. Oral glucose tolerance testing was used to assess insulin secretion, sensitivity, and disposition index (DI). Endothelial function, triglycerides, FFA, c-reactive protein, interleukin 6 (IL6), and adiponectin were measured both pre- and 3 hr postprandially (McDonald's Big Breakfast(®) and 12 ounce Sprite(®)) in obese adolescents (10-13 years, 9 black and 7 white). Endothelial function was assessed using reactive hyperemic changes in forearm vascular resistance (FVR). Oral glucose tolerance test (OGTT) showed no difference in insulin sensitivity, but blacks tended to have (P = 0.08) higher insulin secretion and had increased DI (P = 0.003). After a high-fat meal, triglycerides increased in both groups (P < 0.001), tended to be lower in blacks compared with whites preprandially (64 ± 33 mg/dL vs 110 ± 80, P = 0.064), and was lower postprandially (112 ± 63 vs 188 ± 112, P = 0.039). Pre- and postprandial FFA (Black: 0.58 ± 0.15 and 0.39 ± 0.18 vs. white: 0.44 ± 0.14 and 0.26 ± 0.06, P = 0.020) and adiponectin (P = 0.002) were increased in blacks. FFA decreased in both groups postprandially (P = 0.002). IL6 increased after the meal (P = 0.022). Endothelial function decreased postprandially (P < 0.02), but this was due to a decrease in preocclusion FVR. These results indicate that differences in fat metabolism are present in both black and white obese adolescents. How these differences explain higher rates of cardiometabolic disease in blacks is unclear.

Post-Exercise Hypotension Is Mediated by a Decrease in Sympathetic Nerve Activity in Stages 2-3 CKD

Background: This study aimed at evaluating the after effects of a single bout of aerobic exercise on muscle sympathetic nerve activity (MSNA), peripheral vascular resistance and blood pressure (BP) in stages 2-3 chronic kidney disease (CKD) patients. We hypothesized that CKD patients present a greater decline in these variables after the exercise than healthy individuals. Methods: Nine patients with stages 2-3 CKD (50 ± 8 years) and 12 healthy volunteers (50 ± 5 years) underwent 2 sessions, conducted in a random order: exercise (45 min, cycle ergometer, 50% of peak oxygen uptake) and rest (seated, 45 min). Sixty minutes after either intervention, MSNA (by microneurography), BP (by oscillometry), and forearm vascular resistance (FVR) were measured. A 2-way analysis of variance with group (between) and session (within) as main factors was employed, accepting p < 0.05 as significant. Results: Diastolic BP and MSNA were higher in the CKD than the control group in both sessions. Responses after exercise were similar in both groups. Systolic BP, diastolic BP, MSNA and FVR were significantly lower after the exercise than after the rest session in both the CKD and the control groups (162 ± 15 vs. 152 ± 23 and 155 ± 11 vs. 145 ± 16 mm Hg, 91 ± 11 vs. 85 ± 14 and 77 ± 5 vs. 71 ± 10 mm Hg, 38 ± 4 vs. 31 ± 4 and 34 ± 2 vs. 27 ± 4 burst/min, 59 ± 29 vs. 41 ± 29 and 45 ± 20 vs. 31 ± 8 U, respectively, all p < 0.05). Conclusion: These results showed that aerobic exercise may produce hemodynamic and neural responses that can be beneficial to these patients in spite of CKD.

Increased peripheral vascular resistance in male patients with traumatic lower limb amputation: one piece of the cardiovascular risk puzzle.

The increased morbidity and mortality in traumatic lower limb amputees can be explained by the development of risk factors, among which high blood pressure plays an important role. However, the possible mechanisms underlying increased blood pressure levels observed in this population remain unclear. Thus, we aimed to test the hypothesis that peripheral vascular resistance is increased at rest in patients with traumatic lower limb amputation. In a cross-sectional study, eight patients with traumatic unilateral lower limb amputation (amputee group) and eight healthy individuals without amputation (control group) were included. Resting blood pressure, heart rate, and forearm blood flow were recorded simultaneously and thus, forearm vascular resistance was calculated. The amputee group showed higher systolic (126±2 vs. 118±5 mmHg, P<0.01), diastolic (78±2 vs. 63±3 mmHg, P<0.01), mean blood pressure (94±2 vs. 81±3 mmHg, P<0.01), and heart rate (74±5 vs. 65±8 bpm, P=0.02) compared with the control group. Despite the similar forearm blood flow response between groups, patients with traumatic lower limb amputation presented increased peripheral vascular resistance at rest compared with the control group (31.3±3.8 vs. 25.7±6.5 U, P=0.05). Patients with traumatic amputation present increased peripheral vascular resistance. Our findings clarify one possible mechanism underlying the higher blood pressure levels observed in this population.

Peripheral vascular reactivity and serum BDNF responses to aerobic training are impaired by the BDNF Val66Met polymorphism.

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 = 221; Val66Met, n = 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 (V̇o2 peak) increased and HR decreased similarly in both groups. Val66Val, but not Val66Met, increased BDNF (interaction, P = 0.04) and BDNF/proBDNF ratio (interaction, P < 0.001). Interestingly, FBF (interaction, P = 0.04) and the FVR (interaction, P = 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 = 0.64, P < 0.001) and FVR (r = -0.58, P < 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.

Abstract 17258: Effects of Aerobic Exercise Intensity on Ambulatory Blood Pressure Monitoring and Vascular Responses in Resistant Hypertension: A Cross-over Trial

Introduction: Patients with resistant hypertension are usually exposed to poor blood pressure (BP) control, resulting in clinical vulnerability, possibility of device-based procedures (denervation), and cumulative costs with drug therapy. Regular aerobic exercise promotes marked benefits in hypertension, including the subset of resistant patients. However, little is known about acute effects of exercise on patients with resistant hypertension. Hypothesis: We hypothesized that a single aerobic session would reduce BP and improve vascular variables. Thus, we compared ambulatory BP and vascular parameters in response to two intensities of aerobic sessions and a non-exercise control session in patients with resistant hypertension. Methods: After a maximal exercise test, 18 patients (54±6 years, 30.2±4.9 kg/m2) participated in three interventions in random order, crossover design, and on separate days: control session (45’ of rest), light intensity (LI) and moderate intensity (MI) sessions (45’ of aerobic exercise at 50% and 75% of HRmax, respectively). Ambulatory BP monitoring (Space Labs, 90702) comprised a 19h period after each session. Vascular variables were measured at the non-dominant forearm by venous occlusion plethysmography (Hokanson Inc) before and up to 1h after all sessions. Results: Compared with control session, both exercise sessions reduced ambulatory systolic BP in a 5h period (LI: -7.7±2.4mm Hg and MI: -9.4±2.8mm Hg, p&lt;0.01), whereas only LI session reduced diastolic BP (-5.7±2.2mm Hg, p&lt;0.01). In addition, LI induced lower values in systolic and diastolic BP during 10h-daytime (-3.8±1.3mm Hg and -4.0±1.3mm Hg, respectively, p&lt;0.02), nighttime (-6.0±2.4 mm Hg and -6.1±1.6mm Hg, respectively, p&lt;0.05) and in diastolic BP during 19h (-4.8±1.2mm Hg, p&lt;0.01). Forearm blood flow decreased only at minute 50 after LI (p&lt;0.05), with no other changes. In control and LI sessions, forearm vascular resistance increased at the end of 1h recovery period and in MI session, it decreased immediately after the intervention (p&lt;0.05). Conclusions: A single aerobic exercise session in light or moderate intensities induces beneficial changes in ambulatory BP in resistant hypertension, with advantages in effect length for lighter intensities.

Vascular function and brain-derived neurotrophic factor: The functional capacity factor.

Brain-derived neurotrophic factor (BDNF) is essential for neurocognitive function. This study aims at establishing a plausible link between level of serum BDNF, functional capacity (FC), and vascular function in 181 young (age 25.5±9.1 years old), apparently healthy adults. Fasting blood samples were drawn from participants' antecubital veins into plain glass tubes while they were in a sitting position to evaluate serum BDNF using enzyme-linked immunosorbent assay (ELISA). Mercury-in-silastic strain-gauge plethysmography was used to determine arterial function indices, blood flow and vascular resistance at rest and following 5 minutes of arterial ischemia. The 6-minute walk distance (6MWD) test was used to determine FC, according to the American Thoracic Society Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories guidelines. It was conducted in an enclosed corridor on a flat surface with a circular track 33 meters long. The walking course was demarcated with bright colored cones. The 6MWD correlated with BDNF (r=0.3, p=0.000), as well as with forearm blood inflow (r=0.5, p=0.000) and vascular resistance (r = -0.4, p=0.000). Subsequent comparison showed that BDNF and blood inflow were greater (p<0.05) while vascular resistance was less (p<0.05) in participants who achieved a longer 6MWD. Similarly, BDNF correlated with forearm blood inflow (r=0.4, p=0.000) and vascular resistance (r = -0.4, p=0.000). Subsequent comparison showed improved vascular function (p<0.05) in the participants with greater BDNF. In conclusion, these findings might suggest that improved vascular function in individuals with greater FC is mediated, at least partially, by an enhanced serum BDNF level.

Endothelial dysfunction and negative emotions in adolescent girls.

Endothelial dysfunction predicts adult cardiovascular disorder and may be associated with negative emotions in adolescents. This study was conducted to determine if hopelessness, hostility, and depressive, anxiety, or conduct disorders were associated with compromised endothelial function and whether those associations were mediated by health risk behaviors. Endothelial function, assessed through brachial artery reactive hyperemia, was measured in a psychopathology enriched sample of 60 15-18-year-old girls. The correlations between hopelessness, hostility, and depressive, anxiety, or conduct disorders and the percent change in forearm vascular resistance (PCFVR) were measured. Possible mediation effects of health risk behaviors were tested. Hopelessness was negatively associated with PCFVR, controlling for race and body mass index. Conduct disorder without any anxiety disorder was associated with better endothelial function. The other negative emotions were not associated with PCFVR. Risky health behaviors were associated with conduct disorder and hopelessness, but not with PCFVR, so there was no evidence of mediation. The main finding was that hopelessness in adolescent girls was associated with endothelial dysfunction. This may indicate that when present, hopelessness places a girl at risk for later cardiovascular disease, whether she has a psychiatric disorder or not. Possible mechanisms for this finding are examined and the surprising finding that conduct disorder is associated with better endothelial function is also discussed. Suggestions for future research are presented.

Acute vascular effects of waterpipe smoking: Importance of physical activity and fitness status

ObjectiveWhile new forms of tobacco, including waterpipe (WP) smoking, continue to gain popularity, limited literature has examined the vascular health consequences. The purpose of the current study was to examine: (i) the acute WP-induced changes in vascular function; (ii) whether acute changes in vascular function are modified by lifestyle behaviors (habitual physical activity, physical fitness). MethodsFifty three (22.7 y, 36% F, 23.4 kg/m2) otherwise healthy WP smokers were recruited. Strain-gauge plethysmography was used to measure forearm blood flow, vascular resistance, venous capacitance, and venous outflow at rest and following occlusion. Habitual physical activity was determined using the Arabic version of short-form international physical activity questionnaire, while physical fitness was assessed using the 6 min walk test and handgrip strength. Partial correlations were used to examine the relationships between post-smoking vascular function and lifestyle behaviors, controlling for pre-smoking vascular measures. Results(i) WP had a small effect on forearm post-occlusion blood flow (d = −0.19), a moderate effect on venous outflow (d = 0.30), and a moderate effect on post-occlusion vascular resistance (d = 0.32). (ii) Total habitual physical activity strongly correlated with resting blood flow (r = 0.50) and moderately with vascular resistance (r = −0.40). Handgrip strength moderately correlated with venous capacitance (r = 0.30) and post-occlusion blood flow (r = 0.30), while 6 min walked distance moderately correlated with resting venous capacitance (r = 0.30). ConclusionWaterpipe smoking is associated with immediate changes in vascular function, which are exacerbated in individuals with low habitual physical activity and physical fitness levels in young otherwise healthy individuals.

Resistance exercise with different volumes: blood pressure response and forearm blood flow in the hypertensive elderly

BackgroundThe purpose of this study was to evaluate the effect of two sessions of resistance exercise with different volumes on post-exercise hypotension, forearm blood flow, and forearm vascular resistance in hypertensive elderly subjects.MethodsThe study was conducted with ten hypertensive elderly (65±3 years, 28.7±3 kg/m2) subjected to three experimental sessions, ie, a control session, exercise with a set (S1), and exercise with three sets (S3). For each session, the subjects were evaluated before and after intervention. In the pre-intervention period, blood pressure, forearm blood flow, and forearm vascular resistance were measured after 10 minutes of rest in the supine position. Thereafter, the subjects were taken to the gym to perform their exercise sessions or remained at rest during the same time period. Both S1 and S3 comprised a set of ten repetitions of ten exercises, with an interval of 90 seconds between exercises. Subsequently, the measurements were again performed at 10, 30, 50, 70, and 90 minutes of recovery (post-intervention) in the supine position.ResultsPost-exercise hypotension was greater in S3 than in S1 (systolic blood pressure, −26.5±4.2 mmHg versus −17.9±4.7 mmHg; diastolic blood pressure, −13.8±4.9 mmHg versus −7.7±5 mmHg, P<0.05). Similarly, forearm blood flow and forearm vascular resistance changed significantly in both sessions with an increase and decrease, respectively, that was more evident in S3 than in S1 (P<0.05).ConclusionResistance exercises with higher volume were more effective in causing post-exercise hypotension, being accompanied by an increase in forearm blood flow and a reduction of forearm vascular resistance.