Search

Background Lower perceived social support is associated with hopelessness in patients with ischemic heart disease (IHD). Higher perceived social support is associated with higher heart rate variability (HRV) in adults following a stressful event, but the relationship between HRV and hopelessness has not been examined in patients with IHD. The purpose of this research was to evaluate the relationships among HRV, perceived social support, and hopelessness in patients with IHD. Methods and Results Ninety‐four participants were enrolled while hospitalized for an IHD event at a large hospital in the United States. Data collection occurred 2 weeks after hospital discharge and included the State–Trait Hopelessness Scale, ENRICHD Social Support Inventory, Patient Health Questionnaire‐9, a demographic form, and a short‐term HRV measurement taken at rest. Linear models were used to assess associations between variables in unadjusted and adjusted models. Most participants were men (67%), married (75%), and non‐Hispanic White (96%) and underwent coronary artery bypass surgery (57%). There were inverse correlations between high frequency HRV and state hopelessness (r=−0.21, P=0.008) and root mean square of successive differences between normal heartbeats HRV and state hopelessness (r=−0.20, P=0.012) after adjusting for important covariates. High frequency and root mean square of successive differences between normal heartbeats did not show evidence of mediating the relationship between perceived social support and hopelessness. Conclusions There were significant inverse correlations between parasympathetic measures of HRV and hopelessness. Assessing high frequency and root mean square of successive differences between normal heartbeats during early recovery following an IHD event could provide promising evidence for understanding a possible precursor to hopelessness and targets for future interventions. Registration Information: clinicaltrials.gov. Identifiers: NCT03907891, NCT05003791.

Abstract Oxidative stress has been linked to reductions in vascular function during acute inflammation in young adults; however, the effect of acute inflammation on vascular function with aging is inconclusive. The aim of this study was to determine if oral antioxidant administration eliminates vascular dysfunction during acute inflammation in young and older adults. Brachial flow‐mediated dilation (FMD) and carotid‐femoral pulse wave velocity (PWV) were measured in nine young (3 male, 24 ± 4 yrs, 26.2 ± 4.9 kg/m2) and 16 older (13 male, 64 ± 5 yrs, 25.8 ± 3.2 kg/m2) adults before and 2‐h after oral consumption of 2 g of vitamin C. The vitamin C protocol was completed at rest and 24 h after acute inflammation was induced via the typhoid vaccine. Venous blood samples were taken to measure markers of inflammation and vitamin C. Both interleukin‐6 (Δ+0.7 ± 1.8 pg/ml) and C‐reactive protein (Δ+1.9 ± 3.1 mg/L) were increased at 24 h following the vaccine (p 0.05). FMD was lower in all groups during acute inflammation (Δ‐1.4 ± 1.9%, p 0.05). Vitamin C restored FMD back to initial values in young and older adults during acute inflammation (Δ+1.0 ± 1.8%, p 0.05). In conclusion, oral vitamin C restored endothelial function during acute inflammation in young and older adults, with no effect on aortic stiffness. The effect of vitamin C on endothelial function did not appear to be due to reductions in inflammatory markers. The exact mechanisms should be further investigated.

Abstract Introduction Individuals with Down syndrome (DS) have autonomic dysfunction, which impacts heart rate and blood pressure regulation. Initial evidence also suggests an impaired ability to peripherally vasoconstrict during lower body negative pressure (LBNP). Given the relationship between vessel caliber and wave reflection, this may alter central hemodynamics and hemodynamic load. We aimed to investigate aortic hemodynamics and wave reflection during LBNP in individuals with DS and controls. Methods Radial applanation tonometry was performed on 15 individuals with DS (male n = 12, age 24 ± 1 yrs, BMI 29.4 ± 2.0 kg/m2) and 21 control participants (male n = 12, age 24 ± 1 yrs, BMI 24.4 ± 1.0 kg/m2) before, during and after a 5-min LBNP stimulus of –20 mmHg. Waveforms were calibrated to mean and diastolic brachial pressures. Generalized transfer function was used to estimate aortic pressures (systolic aSBP, diastolic aDBP and mean pressure aMAP), augmentation index (Aix), augmentation index normalized for HR (Aix@HR75), augmentation pressure (AP), reflection index (Rix) and forward (Pf) and reflected wave magnitude (Pb). Results Interaction effects were observed for AP, Aix, AIX@75, Rix and Pb (p < 0.05) in which DS had reductions in the outcome during LBNP whereas controls had little or no change. Although trending towards a larger drop in aSBP in individuals with DS, no significant interaction effects were found for aSBP, aDBP, aMAP, HR or Pf in response to LBNP. Conclusion These results show individuals with DS exhibited greater reductions in aortic pressure waveform characteristics and wave reflections in response to LBNP, indicative of reduced sympathetic control resulting in less peripheral vasoconstriction.

Background: Individuals with Down Syndrome (DS) have autonomic dysfunction impacting regulation of heart rate, Blood Pressure (BP), and peripheral vasoconstriction. This may alter central hemodynamics through different wave reflections. We investigated central hemodynamics including wave reflection during rest and a sympathoexcitatory stimulus [Lower Body Negative Pressure (LBNP)] in individuals with DS and controls. Methods: Radial applanation tonometry was performed on participants with and without DS before and during 5-min LBNP stimulus of −20 mmHg. Waveforms were calibrated to mean and diastolic BP. Generalized transfer function was used to estimate aortic pressures [Systolic Blood Pressure (aSBP), Diastolic Blood Pressure (aDBP), mean pressure (aMAP), pulse pressure (aPP)], Augmentation Index (AIx), augmentation index normalized for HR (AIx@75), Augmentation Pressure (AP), Reflection Index (RIx), Time to Reflection (Tr), forward and reflected wave magnitude (Pf and Pb). Results: Fifteen individuals with DS (male n = 12, age 24 ± 4 years, BMI 28 ± 5 kg/m2) and 16 control participants (male n = 12, age 24 ± 4 years, BMI 25 ± 5 kg/m2) participated. Baseline differences showed greater AP, higher AIx and AIx@75, a greater RIx, shorter Tr and larger Pb in individuals with DS (p < 0.05). In response to LBNP, interaction effects were observed for AIx, AIx@75, AP, RIx and Pb, due to reductions in the outcomes in response to LBNP for individuals with DS with no change in the controls. Conclusion: These results show that central hemodynamics and wave reflections are different in individuals with DS at rest and in response to LBNP, probably as a result of anatomical differences and reduced peripheral vasoconstrictive control during LBNP. HIGHLIGHTS •Individuals with DS exhibit greater central hemodynamic load at rest. •Individuals with DS have greater indices of wave reflections at rest. •Individuals with DS maintained blood pressure during LBNP with reduced wave reflection.

Abstract Sympathetic vasoconstriction is attenuated in exercising muscles to assist in matching of blood flow with metabolic demand. This “functional sympatholysis” may be impaired in young obese individuals due to greater sympathetic activation and/or reduced local vasodilatory capacity of both small and large arteries, but this remains poorly understood. We tested the hypothesis that functional sympatholysis is impaired in obese individuals compared with normal‐weight counterparts. In 36 obese and normal‐weight young healthy adults (n = 18/group), we measured forearm blood flow and calculated forearm vascular conductance (FVC) responses to reflex increases in sympathetic nerve activity induced by lower body negative pressure (LBNP) at rest and during rhythmic handgrip exercise at 15% and 30% of the maximal voluntary contraction (MVC). FVC was normalized to lean forearm mass. In normal‐weight individuals, LBNP evoked a decrease in FVC (−16.1 ± 5.7%) in the resting forearm, and the reduction in FVC (15%MVC: −8.1 ± 3.3%; 30%MVC: −1.0 ± 4.0%) was blunted during exercise in an intensity‐dependent manner (P 0.05) and was intensity‐dependent (P

Acute inflammation is associated with increased risk for cardiovascular events and leads to reductions in conduit artery (flow-mediated dilation, FMD) and resistance vessel endothelial function. Whether this dysfunction during acute inflammation is further transmitted down the arterial tree to the microvasculature, inhibiting its ability to dilate or be recruited in response to a hypoxic stimulus, has yet to be investigated. Microvascular function and reactivity can be non-invasively measured using near-infrared spectroscopy (NIRS) during and following an occlusive stimulus. Purpose: To investigate whether acute inflammation impairs microvascular function. Methods: The typhoid vaccine was used to induce acute systemic inflammation in 16 young, healthy adults (8 male, 26.3 ± 3.0 years; 21.7 ± 2.4 kg/m2). Blood pressure, FMD of the brachial artery, and NIRS of the forearm flexor muscles were measured at baseline and 24-h following the vaccination. NIRS was analyzed during a 5-min arterial occlusion to obtain markers of microvascular function and reactivity from the tissue saturation index (TSI): occlusion slope (muscle oxidative capacity); and reperfusion slope, reperfusion magnitude, and peak hyperemic response (microvascular reactivity). Results: Mean arterial pressure did not change during the inflammatory episode (90 ± 9 mmHg to 90 ± 7 mmHg, p = 0.83) and FMD was significantly reduced at 24 h (5.6 ± 2.6% to 4.1 ± 1.7%, p = 0.03). No change was noted in the TSI occlusion slope, reperfusion slope, reperfusion magnitude, or peak hyperemic response (p > 0.05). Conclusion: Vaccination-induced acute inflammation reduced endothelial function. However, no differences were noted in microvascular reactivity or oxidative capacity. Further investigation with a larger sample size is necessary to confirm these results.

Background: Individuals with Down syndrome (DS) experience autonomic dysfunction, with reduced sympathetic and parasympathetic control. This results in alterations in resting heart rate and blood pressure and attenuated responses to sympathoexcitatory stimuli. It is unknown to what extent this impacts the regulation of peripheral blood flow in response to sympathetic stimuli, which is an important prerequisite to exercise and perform work. Purpose: To investigate differences in peripheral blood flow regulation in response to lower body negative pressure (LBNP) between individuals with and without DS. Methods: Participants (n = 10 males with DS and n = 11 male controls, mean age 23.7 years ± 3.2) underwent 5 min of LBNP stimulations (−20 mmHg), after resting supine for 10 min. One minute steady state blood pressure and blood flow at baseline, LBNP, and 5 min recovery were obtained for analysis. Mean flow velocity and arterial diameters were recorded with ultrasonography; foreram blood flow (FBF), shear rate and forearm vascular conductance (FVC) were calculated using brachial blood pressure measured right before ultrasound recordings. Results: Participants with DS responded differently (consistent with reduced vasoconstrictive control) to the LBNP stimulus (significant ConditionxGroup interaction effect) for mean velocity (p = 0.003), FBF (p = 0.008), shear rate (p = 0.004) and FVC (p = 0.017), compared to participants without DS (see table). Conclusion: Young males with DS exhibit reduced peripheral blood flow regulation of blood flow in response to LBNP compared to controls, indicating a blunted sympathetic control of blood flow. Further research is necessary to explore the impact of these findings on exercise and work capacity. Baseline LBNP Recovery DS Control DS Control DS Control MAP 90 ± 13 88 ± 10 85 ± 12 87 ± 10 92 ± 11 85 ± 10 Diameter (cm) 0.36 ± 0.05 0.43 ± 0.05 0.37 ± 0.05 0.43 ± 0.7 0.37 ± 0.04 0.42 ± 0.06 Mean velocity (cm/sec) 13 ± 7 21 ± 10 15 ± 7 17 ± 5 16 ± 9 16 ± 8 FBF (ml/min) 91 ± 64 176 ± 80 104 ± 67 146 ± 47 114 ± 91 138 ± 74 Shear Rate (sec-1) 20 ± 12 35 ± ± 16 23 ± 12 29 ± 8 25 ± 17 28 ± 14 FVC (ml/min/100 mmHg) 101 ± 67 203 ± 95 124 ± 84 171 ± 63 125 ± 101 162 ± 81.

Introduction: Individuals with multiple sclerosis (MS) exhibit impaired cerebrovascular function and have poor sleep quality. In the general population, poor sleep contributes to cerebrovascular dysfunction and is related to cardiovascular disease (CVD). Improving sleep quality may have beneficial effects in preventing CVD; however, the relationship between sleep quality and cerebrovascular function in MS has not been examined. Purpose: To examine the effect of sleep quality on cerebrovascular function in individuals with MS. Methods: Sixteen individuals with MS had sleep quality assessed with the Pittsburgh Sleep Quality Index. Individuals were categorized as having poor sleep quality (n = 6, score >5) or good sleep quality (n = 10, score ≤5). Cerebrovascular function was assessed via transcranial Doppler ultrasound with the following hemodynamic outcomes: mean middle cerebral artery velocity (mMCAv), pulsatility index (PI), and resistance index (RI). An automated blood pressure cuff was used to measure baseline blood pressure (systolic, diastolic, mean (SBP, DBP, MAP)) and heart rate in a seated position. End-tidal CO2 (EtCO2) was measured by gas capnography. Results: Those with poor sleep quality had greater PI and RI, and lower mMCAv compared to those with good sleep quality (p

Inflammation is associated with an increased risk of cardiovascular events and reduced endothelial function. Higher cardiorespiratory fitness is associated with lower risk of cardiovascular events and improved vascular function. Whether fitness plays a role during acute inflammation is unknown. Purpose: Evaluate the role of fitness in the endothelial response to acute inflammation in younger (YA) and older (OA) adults. Methods: Acute inflammation was induced using influenza vaccine in 23 YA (12 male, 26 ± 4 yrs, 24.0 ± 3.5 kg/m2) and 60 OA (20 male, 65 ± 5 yrs, 27.8 ± 5.0 kg/m2). Blood pressure, flow-mediated dilation (FMD) and inflammatory markers were measured before and 24-hours post-vaccination. VO2peak was measured via a treadmill test. A VO2peak greater than age- and sex-associated 50th percentile according to the American College of Sports Medicine was defined as Fit. Results: Fit OA reduced FMD more than low fit OA (p = 0.02) 24 h post-vaccination. High and low fit YA similarly decreased FMD at 24 h (p = 0.66). YA and high fit OA had a similar reduction (relative %) in FMD (pz0.05). Regression analyses indicated no association between VO2peak and change in FMD (β = −0.01, p = 0.98) in YA, but a significant association existed in OA (β = −0.36, p = 0.04) after adjusting for age, sex, BMI and baseline FMD. YA-high fit YA-low fit OA-high fit OA-low fit n 14 9 16 43 VO2Max, ml/kg/min 48.4 (5.6)* 35.6 (4.9) 32.3 (4.2)* 21.9 (4.3) Baseline SBP 113 (13) 115 (13) 125 (14) 125 (14) Baseline PP 47 (8) 47 (11) 54 (10) 53 (11) Baseline FMD, % 12.4 (2.7) 11.6 (5.5) 7.5 (3.9)* 5.4 (2.5) Baseline CRP, mg/1 1.1 (0.7) 0.6 (0.6) 2.4 (3.3) 2.5 (2.2) Baseline IL-6, pg/ml 1.0 (0.7) 0.8 (0.5) 1.7 (1.4) 1.6 (1.1) Change SBP, mmHg −3 (6) 2 (8) −2 (9) −2 (11) Change PP, mmHg 2 (6) 5 (7) 0 (7) 0 (8) Change FMD, % −3.2 (4.1) −2.3 (5.5) −3.7 (3.8)* −0.2 (3.5) Change CRP, mg/l 1.0 (1.5) 0.9 (0.8) 1.1 (2.2) 0.9 (1.4) Change IL, pg/ml 1.0 (1.5) 1.6 (2.3) 0.8 (2.6) 0.4 (1.0) FMD: flow mediated dilation, CRP: C-reactive protein, IL-6: interleukin-6, SBP: systolic blood pressure, PP: pulse pressure *P < 00.5 vs. low-fit of same age category Conclusion: In OA, higher fitness is associated with a greater decrease in endothelial function during acute inflammation; high fit OA had a similar endothelial response compared to YA. This suggests intact reactivity of the vasculature to inflammatory stress in high fit OA, which may indicate a healthier vessel versus low fit OA.

Background: Cardiovascular disease is a leading cause of disease progression and death in multiple sclerosis (MS). Obesity has a negative impact on vascular structure and function, but whether this contributes to worse vascular function similarly in individuals with MS and controls is unknown. Aim: To investigate the impact of obesity on vascular function and structure in a group with MS. Methods: In a sample of n = 133 participants (MS: n = 89, control n = 44), height and weight were measured to calculate BMI. After a 10 minute rest in the supine position, resting heart rate (HR) and brachial blood pressure (BP) were collected. Augmentation index (AIX), HR normalized AIX (AIX@HR75) and pulse wave velocity (PWV) and subendocardial viability ratio (SEVR) were measured with applanation tonometry. Carotid intima-media thickness (IMT) and beta-stiffness (beta) were measured with carotid ultrasound, and Forearm Blood Flow (FBF Baseline, Peak and Area Under the Curve (AUC)) was measured with strain gauge plethysmography. Data were analyzed with multiple linear regression analyses with group, sex, BMI and GroupxBMI as independent variables. Results: Higher BMI correlated with higher HR and PWV in both groups. In the MS group however, a higher BMI was also correlated with worse outcomes on the SEVR, FBF Baseline, Peak and AUC. Outcome variables Standardized beta1 Adjusted R2 Group Sex BMI Grp x BMI HR rest 1.081* 0.005 0.520* −0.944 0.11 AIX −0.019 −0.523* 0.040 0.045 0.26 AIX@HR75 0.341 −0.536* 0.235 −0.270 0.32 SEVR −1.292* 0.175* −0.565* 1.090* 0.22 PWVc 0.001 −0.003 0.321* 0.120 0.12 PWVc/MAP 0.324 −0.126 0.278 −0.122 0.11 IMT 0.715 0.164 0.385 −0.511 0.12 FBF Baseline 0.432 0.070 0.326* −1.090* 0.33 FBF Peak 0.580 0.318* 0.152 −1.035* 0.35 FBF AUC 0.746 0.230* 0.316 −1.174* 0.21 1Group (0 = control, 1 = multiple sclerosis), Sex (1 = Female, 2 = Male). *(p < 0.05). Conclusions: Having a higher BMI contributes even more to a worse vascular profile in MS patients than in controls, suggesting that reducing overweight and obesity in the MS population will benefit their vascular structure and function.

High-intensity resistance exercise (RE) acutely increases arterial stiffness and blood pressure (BP), coupled with reduced cerebral blood flow velocity (CBFv) and greater flow pulsatility in the cerebral circulation, which may be detrimental to cerebral microvasculature. Because females have different CV control mechanisms, it is important to assess potential sex differences in cerebrovascular responses to acute RE. Purpose: To examine the effect of sex on hemodynamics and cerebral vasculature following acute RE. Methods: Men (n = 18, 27 yrs, BMI = 24.2) and women (n = 14, 25 yrs, BMI = 23.8) performed RE (3 × 10, isokinetic knee flexion/extension). Measurements were obtained at baseline and post-exercise (1, 5, 30-minute). Beat-to-beat heart rate (HR), brachial BP, cardiac output (CO), stroke volume and end-tidal CO2 were collected. CBFv was measured by transcranial Doppler, carotid BP by applanation tonometry and central pulse wave velocity (PWV) by an automated ambulatory BP monitor. Results: Table 1. CBFv pulsatility increased following RE at 1-minute post (p < 0.05) in men and was elevated above baseline 5-minute post-exercise (p < 0.05) in both groups (Figure 1). Mean CBFv increased 1-min post-exercise and decreased below baseline 5-minute post-exercise (p < 0.05) in both sexes. PWV increased 1-minute post-exercise (p < 0.05) in both groups. Variables Baseline 1-minute 5-minute 30-minute Heart Rate(bpm)*† Men 63 ± 9 82 ± 9 71 ± 10 70 ± 8 Women 70 ± 7 93 ± 13 79 ± 10 76 ± 9 CO (L/min) * Men 4.9 ± 0.7 7.9 ± 1.3 6.1 ± 1.3 5.2 ± 0.9 Women 5.4 ± 1.0 8.2 ± 1.4 6.3 ± 1.0 5.7 ± 0.8 SV (ml/min)*‡ Men 77 ± 16ab 95 ± 17bc 85 ± 17c 72 ± 13 Women 80 ± 17a 91 ± 20bc 81 ± 14 76 ± 16 bSBP (mmHg)* Men 124 ± 10 140 ± 12 127 ± 10 127 ± 9 Women 124 ± 9 136 ± 15 122 ± 13 123 ± 9 bDBP (mmHg)* Men 72 ± 8 74 ± 7 72 ± 7 76 ± 6 Women 73 ± 5 76 ± 9 71 ± 7 73 ± 5 bMAP (mmHg)* Men 92 ± 8 100 ± 8 93 ± 8 96 ± 7 Women 95 ± 6 101 ± 11 93 ± 8 95 ± 6 cSBP (mmHg)* Men 120 ± 12 129 ± 18 125 ± 13 126 ± 10 Women 1 22 ± 12 124 ± 13 119 ± 18 123 ± 8 cDBP (mmHg)* Men 75 ± 7 74 ± 7 75 ± 7 79 ± 6 Women 74 ± 6 73 ± 6 75 ± 7 74 ± 5 cMAP (mniHg)* Men 93 ± 8 94 ± 8 94 ± 7 97 ± 7 Women 94 ± 6 93 ± 8 95 ± 9 96 ± 5 PWV (m/s)* Men 5.2 ± 0.5 5.6 ± 0.5 5.4 ± 0.5 5.2 ± 0.3 Women 5.0 ± 0.4 5.3 ± 0.5 5.1 ± 0.3 5.0 ± 0.3 CBFv Mean (cm/s)*† Men 55.8 ± 7.6 63.9 ± 9.6 51.4 ± 6.9 53.7 ± 7.9 Women 69.8 ± 14.4 81.0 ± 23.1 63.7 ± 12.9 65.8 ± 12.0 CBFv Pulsatility Index*†‡ Men 0.91 ± 0.12ab 1.10 ± 0.16* 1.13 ± 0.17c 0.89 ± 0.13 Women 0.81 ± 0.09b 0.90 ± 0.18 0.95 ± 0.13c 0.81 ± 0.11 End-Tidal CO2 (%)* Men 4.86 ± 0.48 5.72 ± 0.66 4.64 ± 0.51 4.51 ± 0.58 Women 4.41 ± 0.60 5.44 ± 0.65 4.26 ± 0.39 4.24 ± 0.50 Table 1All Data are mean ± SD; *Exercise effect, p < 0.05. †Group effect. p < 0.05. ‡Interaction effect. p < 0.05. a Significantly different from 1-minute, b Significantly different from 5-minute. c Significantly different from 30-minute. p < 0.05). Brachial systolic BP (bSBP), brachial diastolic BP (bDBP), brachial mean BP (bMAP), Carotid systolic BP (cSBP),carotid diastolic BP (cDBP), cardiac output (CO), stroke volume (SV) and central pulse wave velocity (PWV), cerebral blood flow velocity (CBFv). Figure 1All Data are mean ± SD, *Exercise effect, p < 0.05. †Group effect, p < 0.05. ‡Interaction effect, p < 0.05. a Significantly different from 1-minute, b Significantly different from 5-minute. c Significantly different from 30-minute, p < 0.05). Conclusion: Men increased CBFv pulsatility at 1-minute post-RE compared to women, demonstrating a sex difference in cerebral vascular reactivity. RE increased central arterial stiffness, mean CBFv, HR, and BP similarly for both sexes. CO was also elevated at 5-minute, but CBFv dropped below baseline and pulsatility continued to rise above baseline. This temporary disruption in cerebral autoregulation may impact brain health in both sexes.

Background: Multiple sclerosis (MS) is associated with increased risk of cardiovascular disease (CVD) and approximately 25–54% of patients report poor sleep quality. There is evidence from the general population of an association between poor sleep and increased CVD risk, but this is poorly understood in MS. Purpose: This study examined the association between self-reported sleep quality and arterial health in persons with MS. Methods: MS subjects (n = 31) and control subjects (n = 23) were recruited. Control subjects were age and body size matched. All subjects were administered the Pittsburgh Sleep Quality Index (PSQI) to assess self-reported sleep quality. Subjects with a global score >5 were classified as “poor sleepers”. Blood pressure, arterial stiffness, and the forearm blood flow responses following 5-min ischemic occlusion (endothelial function) were measured. Results: Nineteen MS subjects and 5 control subjects were classified as “poor sleepers”. AIx was significantly higher in MS subjects who had poor sleep quality (32.5 ± 8.8 vs 22.0 ± 13.2; P < 0.05). Conclusions: Markers of arterial dysfunction were significantly higher in MS subjects with poor sleep quality compared to those with good sleep quality. This study suggests novel evidence for the association of CVD risk and sleep quality in MS.

Background: Autonomic dysfunction, with increased sympathetic activity at rest has been reported in obese individuals. Indices of blood pressure variability (BPV) and baroreceptor sensitivity (BRS) can provide insight into aspects of autonomic function, particularly following an aerobic exercise bout. Purpose: To examine BPV and BRS in normotensive obese individuals in response to aerobic exercise. Methods: Normal-weight (n=8; 25 yr; 23.0 kg/m2) and obese individuals (n=9; 27 yrs; 32.2 kg/m2) performed a 60-min leg cycling exercise at 60% of VO2peak. Beat-by-beat blood pressure was recorded at baseline, immediately post-exercise and 30 min into passive recovery using finger plethysmography. R-R intervals were obtained at 1,000 Hz with a digital acquisition system. Power spectral analysis was conducted using WinCPRS software for estimates of BPV (very low and low frequency (VLF, LF), and systolic and diastolic deviation (SDev, DDev)). BRS was estimated using the sequence technique. Natural log-transformed was performed on LF BPV (LnLF) to account for non-normal distribution. Results: HR increased from baseline similarly in both groups (p

Introduction: Peak prevalence of multiple sclerosis (MS) is approaching 60 years of age, suggesting an aging patient population compared to past reports. Aging is independently associated with increased cardiovascular disease risk. Additionally, arterial function is compromised with aging. Carotid artery stiffness serves as a non-invasive method to quantify aspects of arterial function. As MS patients increase their average lifespan, it is unclear if they may experience differential changes in aspects of carotid artery function compared to their healthy age-matched peers. Objective: To compare carotid artery structure and function between young and older subjects with and without MS. Methods: After 10 minutes of supine rest, 120 subjects (MS=89, Control=31) underwent applanation tonometry and ultrasonography of the carotid artery. Subjects were classified as young or older (

Background: Elevations in muscle sympathetic nerve activity (MSNA) and sympathetic vasoconstrictor responsiveness to sympathoexcitation are associated with increased cardiovascular risks, which affect hemodynamics, and have been reported in obese adults with metabolic syndrome (1–3). It remains unclear whether this observation may also be present in young metabolically healthy obese adults. Purpose: To compare sympathetic vasoconstrictor and hemodynamic responsiveness to lower body negative pressure (LBNP, −20 mmHg) in young normal-weight (NW) vs. obese (OB) adults. Method: Eleven NW (female=6; 25±2 yrs; 22.4±0.6 kg/m2) and 13 OB adults (female=6; 27±1 yrs; 32.7±0.6 kg/m2) underwent 2-min of LBNP in the supine position. Ultrasonography [brachial diameter, forearm blood flow (FBF), forearm vascular conductance (FVC)], MSNA [burst frequency, total MSNA, sympathetic vascular transduction], and beat-to-beat hemodynamics [heart rate (HR), mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO), stroke volume (SV), systemic compliance (SC)] were reported. FBF and FVC were normalized to lean forearm mass, and TPR, CO, SV, and SC to body surface area. Results: Baseline MAP was lower in OB (P

Individuals with Down syndrome (DS) experience premature aging. Arterial stiffness increases with advancing biological age and predicts cardiovascular disease. However, only limited studies investigated arterial function in individuals with DS. Thus, the impact of DS on vascular function still remains poorly understood. Purpose: To compare vascular function between individuals with and without DS (control). Methods: Twenty-seven volunteers (DS=13, Control=14) participated in this study. Central arterial stiffness indices (β-stiffness, Ep and circumferential strain) were measured by carotid ultrasonography and analyzed with B-mode, echo tracking and strain analysis. Cardio-ankle Vascular Index (CAVI) and carotid blood pressure (carBP) were measured using a limb cuff system and applanation tonometry (SphygmoCor), respectively. In addition, heart rate (HR) was recorded by finger photoplethymography. Results: There were significant differences in CAVI (lower) and circumferential strain (higher) in individuals with DS compared to individuals without DS (p

Background: Poor sleep quality has been related to poor vascular function and higher risk of cardiovascular disease in the general population. Persons with multiple sclerosis (MS) exhibit a high cardiovascular risk, and report poor sleep quality. To date, the association between sleep quality and vascular health in MS has not been investigated. Objective: To investigate differences in vascular health between good and poor quality sleepers with MS. Methods: After a 10 minute rest in the supine position, resting heart rate (HR) and brachial blood pressure (BP) were collected.Aortic SBP, augmentation index (AIX), HR normalized AIX (AIX@HR75), subendocardial viability ratio (SEVR), end systolic pressure (ESP), and central pulse wave velocity (PWVc) were measured with applanation tonometry in individuals with MS (n=49). Carotid intima-media thickness (IMT) and beta-stiffness were measured with carotid ultrasound, and peak forearm blood flow (FBF Peak) was measured with strain gauge plethysmography. Sleep quality was measured with the Pittsburgh Sleep Quality Index (>5 was categorized as poor sleep quality). Age was used as a covariate. Results: AIX@HR75 and SEVR were different between groups, even with age as a covariate, suggesting higher vascular risk for the poor quality sleepers with MS. Conclusions: This study shows that within the MS population, poor quality sleepers have a higher cardiovascular risk than good quality sleepers. Whether poor sleep raises their cardiovascular risk more than in the general population is an area of future investigation. Good quality sleepers with MS (n=23) Poor quality sleepers with MS (n=26) Effect of sleep quality Effect of age Mean (SD) Mean (SD) p Partial Eta2 p Partial Eta2 N Female (%) 18 (75%) 22 (82%) PSQI score 2.9 (1.5) 9.7 (3.1) Age 44 ±13 52 ±10 BMI 26.9 ±5.4 28.1± 5.6 .582 0.007 .584 0.007 HR 64 ±10 65± 8 .136 0.048 .014* 0.125 SBP 116 ±14 122 ±14 .384 0.017 .025* 0.105 DBP 72 ±9 74 ±10 .457 0.012 .559 0.007 MAP 86± 10 90 ±11 .403 0.015 .175 0.040 Aortic SBP 106 ±14 114 ±14 .223 0.032 .001** 0.200 AIX 21.1 ±13.7 30.0± 9.0 .082 0.064

Background: Arterial stiffness and large artery function are independent risk factors for cardiovascular disease.(1) Individuals with Down Syndrome (DS) have autonomic dysfunction and known to have lower incidence of cardiovascular disease.(2) Limited literatures showed no difference in arterial stiffness in DS compared to a healthy, non-DS population using a longitudinal view of the carotid artery.(3,4) However, it is unknown if individuals with DS exhibit different circumferential strain compared to individuals without DS at rest or during a sympathoexcitation stimulus. Purpose: To examine the differences in the carotid artery strain and its responsiveness to sympathoexcitation by hypovolemic lower body negative pressure (LBNP) in individuals with and without DS. Methods: Twenty four volunteers (DS=11, 23 yrs Control=13, 23 yrs) participated in this study. Circumferential strain was measured by ultrasonography B-mode and radial strain from the longitudinal view was calculated using echo tracking analysis at rest, during and after sympathoexcitatory stimulation by LBNP. Changes in hemodynamics (HR, BP) were recorded continuously. Results: Compared with controls, individuals with DS have significantly higher strain values at all stages (p < 0.05) with no group interaction with hypovolemic sympathoexcitation stimulation. However, there were no differences in β-Stiffness or EP, suggesting that the differences in strain were due to differences in blood pressure. Conclusions: Our results demonstrate significantly higher strain value, which indicates greater arterial movement in individuals with DS. However, these differences were likely due to higher BP in persons with DS.

Background: Aging is associated with increased arterial stiffness and wave reflection, which is predictive of all-cause cardiovascular (CV) mortality (1–3). Firefighters have the highest cardiovascular mortality of any occupational group (4). High levels of heat stress, physical exertion, and elevated arterial stiffness (5) during/following firefighting provide a susceptible milieu for CV events. Purpose: To describe the differential effects of age following live firefighting on cardiac, arterial function and wave reflection. Methods: Firefighters aged 18–37yrs (n=18, YA) or 38–55yrs (n=17, MA) participated in a staged 12-minute live firefighting scenario. Blood pressures (BP), pulse wave analysis, pulse wave velocity (PWV) and hemodynamic measurements were obtained at rest, immediate and 30 minutes post-firefighting using an automated ambulatory blood pressure monitor (Mobil-O-Graph, I.E.M, Germany). Results: YA increased heart rate and PWV more than MA in response to live firefighting (p0.05). Conclusions: Young and MA firefighters exhibit differential cardiovascular responses to live firefighting. Although MA had higher PWV, diastolic BP and higher peripheral resistance they exhibited attenuated changes following live firefighting. Thus, arterial and hemodynamic parameters in younger firefighters appeared to change in a direction associated with increased risk to a greater degree than observed in older firefighters.

Changing from supine to a seated position creates an orthostatic challenge due to the effects of gravity on the distribution of blood. This redistribution of volume unloads baroreceptors and may evoke sympathetic activation. The sympathetic activation may lead to increases in arterial stiffness, but it is unknown as to how different demographic variables may impact these changes. Objective: To investigate whether the change in arterial stiffness parameters between two positions is influenced by factors such as age, sex, or body mass index (BMI). Methods: Thirty healthy, young adults (24±4 years) were randomly positioned supine or semi-supine, at two different angles (0°,72°) on an adjustable table. After 5 minutes rest, arterial stiffness parameters of the common carotid artery were obtained via ultrasound: beta stiffness index, elastic modulus (Ep), arterial compliance (AC), and distensibility, as well as cardio-ankle vascular index (CAVI) from the VaSera (Fukuda Denshi, Tokyo, Japan). Linear regression was used on the change value for each arterial stiffness parameter adjusting for age, sex, BMI, and baseline values of each outcome measure. Results: BMI was a significant independent predictor of changes in each measured arterial stiffness parameter after controlling for age and sex. Increasing BMI is related to greater changes in beta stiffness (β=0.55,p=0.001) and Ep (β=0.58,p=0.001) with change in position. Concomitantly, increasing BMI is associated with smaller changes in AC (β=−0.31,p=0.03), distensibility (β=−0.54,p=0.001), and CAVI (β=−0.48,p=0.001). Sex was only a significant independent predictor when assessing change in CAVI (β=−0.44,p=0.001). Conclusion: When measuring arterial stiffness parameters in different positions, it is important to account for the effect of BMI in the analyses. Although obesity is associated with increased baseline sympathetic activity and reduced baroreceptor sensitivity, the change in position creates a larger change in arterial stiffness which may relate to the greater displacement of blood volume with a larger body size.

Objectives: Cardiovascular disease is a leading cause of death in multiple sclerosis (MS), and recent data showed that subclinical markers of atherosclerosis are higher in MS as well. Prevalence of MS in men is much lower than in women, but their prognosis is much worse. Men with MS also have higher rates of hypertension and diabetes than women with MS. Whether vascular function and structure differs in men than in women with MS, and whether potential sex differences are similar to those in healthy controls, is unknown. Aim: To compare vascular function and structure between men and women in a group with MS and in healthy controls. Methods: After a 10 minute rest in the supine position, resting heart rate (HR) and brachial blood pressure (BP) were collected. Augmentation index (AIX), HR normalized AIX (AIX@HR75) and pulse wave velocity were measured with applanation tonometry. Carotid intima-media thickness (IMT) and beta-stiffness were measured with carotid ultrasound, and Forearm Blood Flow (Baseline, Peak and Area Under the Curve) was measured with strain gauge plethysmography. Data were analyzed with a two-way independent ANOVA for factors group, sex and group*sex. Results: In both groups, men were taller and heavier than the women, had higher SBP, lower AIX and AIX@HR75, larger IMT and higher baseline and peak FBF. Different patterns were observed in the sex differences for AIX and AIX@HR75 (in women similar in MS and controls, in men higher in MS than in controls). Conclusions: People with MS demonstrate a vascular profile consistent with a higher cardiovascular risk compared to controls. Sex differences were similar in subjects with and without MS, except for the significantly higher AIX and AIX@HR75 in men with MS vs male controls, suggesting males with MS may be particularly at risk for cardiovascular disease. Control MS p-values factors # Female (n=21) Male (n=18) Female (n=52) Male (n=18) Group Sex Inter-action Age 49 ± 10 41 ± 9 48 ± 12 48 ± 13 0.228 0.126 0.109 Height (cm) 164 ± 6 177 ± 5 163 ± 7 179 ± 6 0.867

UNLABELLED:Caucasian populations have a higher prevalence of cardiovascular disease (CVD) when compared with their Chinese counterparts and CVD is associated with autonomic function. It is unknown whether autonomic function during exercise recovery differs between Caucasians and Chinese. The present study investigated autonomic recovery following an acute bout of treadmill exercise in healthy Caucasians and Chinese. Sixty-two participants (30 Caucasian and 32 Chinese, 50% male) performed an acute bout of treadmill exercise at 70% of heart rate reserve. Heart rate variability (HRV) and baroreflex sensitivity (BRS) were obtained during 5-min epochs at pre-exercise, 30-min, and 60-min post-exercise. HRV was assessed using frequency [natural logarithm of high (LnHF) and low frequency (LnLF) powers, normalized high (nHF) and low frequency (nLF) powers, and LF/HF ratio] and time domains [Root mean square of successive differences (RMSSD), natural logarithm of RMSSD (LnRMSSD) and R-R interval (RRI)]. Spontaneous BRS included both up-up and down-down sequences. At pre-exercise, no group differences were observed for any HR, HRV and BRS parameters. During exercise recovery, significant race-by-time interactions were observed for LnHF, nHF, nLF, LF/HF, LnRMSSD, RRI, HR, and BRS (up-up). The declines in LnHF, nHF, RMSSD, RRI and BRS (up-up) and the increases in LF/HF, nLF and HR were blunted in Chinese when compared to Caucasians from pre-exercise to 30-min to 60-min post-exercise. Chinese exhibited delayed autonomic recovery following an acute bout of treadmill exercise. This delayed autonomic recovery may result from greater sympathetic dominance and extended vagal withdrawal in Chinese. TRIAL REGISTRATION:Chinese Clinical Trial Register ChiCTR-IPR-15006684.

Post-exercise hypotension (PEH) is widely observed in Caucasians (CA) and is associated with histamine receptors 1- and 2- (H1R and H2R) mediated post-exercise vasodilation. However, it appears that blacks (BL) may not exhibit PEH following aerobic exercise. Hence, this study sought to determine the extent to which BL develop PEH, and the contribution of histamine receptors to PEH (or lack thereof) in this population. Forty-nine (22 BL, 27 CA) young and healthy subjects completed the study. Subjects were randomly assigned to take either a combined H1R and H2R antagonist (fexofenadine and ranitidine) or a control placebo. Supine blood pressure (BP), cardiac output and peripheral vascular resistance measurements were obtained at baseline, as well as at 30 min, 60 min and 90 min after 45 min of treadmill exercise at 70% heart rate reserve. Exercise increased diastolic BP in young BL but not in CA. Post-exercise diastolic BP was also elevated in BL after exercise with histamine receptor blockade. Moreover, H1R and H2R blockade elicited differential responses in stroke volume between BL and CA at rest, and the difference remained following exercise. Our findings show differential BP responses following exercise in BL and CA, and a potential role of histamine receptors in mediating basal and post-exercise stroke volume in BL. The heightened BP and vascular responses to exercise stimulus is consistent with the greater CVD risk in BL.

Background: Aging is associated with increased arterial stiffness and chronic low-grade inflammation. Acute inflammatory stimulus in the presence of low-grade chronic inflammation briefly increases the risk of cardiovascular events. The risk of cardiovascular events also increases substantially in older compared to younger women, therefore the relationship between sex and aging is important to understand. Purpose: To describe the differential effects of age following induced systemic inflammation on arterial function, endothelial function, and wave reflection. Method: Healthy volunteers aged 18–35 yrs (n = 18, ≈26yr, male = 6) or 55–75 yrs (n = 21, ≈64yr, male = 9) participated. Ultrasound of the common carotid and brachial artery was performed, Beta-stiffness (β) and flow mediated dilation (FMD) were calculated. Aortic mean arterial (aMAP), pulse wave analysis with wave separation, pulse wave velocity (PWV) measurements were obtained in the supine position at rest using applanation tonometry. Participants received an influenza vaccine to induce acute inflammation following baseline measurements and returned for 24-hour follow-up. Results: C-reactive protein and interlukin-6 increased pre-to-post similar in all groups (p < 0.05). β was higher for older adults pre/post. (p < 0.05). Older males exhibited decreased MAP and reflected wave pressure (RP), but increased PWV following vaccination (p < 0.05). However, FMD significantly decreased only in young males. Conclusion: The results suggest that differential responses occur between young and older adults and between males and females in response to acute inflammation. Although inflammation increased similarly, inflammation had limited effects on vascular function in both young and old females, suggesting there are significant sex effects for arterial function in response to acute inflammation.

We aimed to determine the effects of 6 wks of exercise on inflammatory markers in mice concomitantly fed either high-fat (HF) or normal chow (NC) diets in young mice. C57BL/6 mice were randomized into (/group) an NC/sedentary (NC/SED), NC/exercise (NC/EX), HF/SED, and HF/EX groups. Treadmill exercise was performed 5 d/wk at 12 m/min, with 12% grade for 40 min/d. Liver triglycerides and gene expression of F4/80, MCP-1, TNF-α, leptin, and VEGF in visceral white adipose were determined. NC groups had lower body weights after 6 wks versus the HF groups ( versus g) (). F4/80 gene expression (indicator of macrophage infiltration) and liver triglycerides were greatest amongst the HF/SED group, with no differences between the remaining groups. VEGF (indicator of angiogenesis) was greatest in the HF/EX versus the other 3 groups (). Exposure of an HF diet in sedentary young mice increased visceral adipose depots and liver triglycerides versus an NC diet. Exercise training while on the HF diet protected against hepatic steatosis and possibly macrophage infiltration within white adipose tissue. This suggests that moderate exercise while on an HF diet can offer some level of protection early on in the development of obesity.

Background: The aim of this study was to assess resistance artery function in short-term chronic cigarette smokers and non-smoking control subjects. Methods: Reactive hyperemia was assessed in 19 cigarette smokers (age 23±1 years) and 19 non-smokers (age 23±1 years). Results: Cigarette smokers demonstrated a 23% lower peak forearm blood flow response compared with non-smokers (15.81±0.66 vs. 20.58±1.26mL/min/100mL, p