Elevated Resting Blood Pressure Research Articles

Actigraphy-Based Sleep and Muscle Sympathetic Nerve Activity in Humans.

Short and insufficient sleep are prevalent and associated with cardiovascular disease, with the sympathetic nervous system as a suspected mediator. The purpose of the present study was to investigate the association between objective, actigraphy-based total sleep time (TST), sleep efficiency (SE) and cardiovascular and sympathetic regulation in healthy adults. We hypothesized that short TST and low SE would be associated with elevated resting blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA). Participants included 94 individuals (46 males, 48 females, age: 30±15 years, body mass index (BMI): 26±4 kg/m2). All participants underwent at least 7 days of at-home, wristwatch actigraphy monitoring (avg: 10 ± 3 days). Seated blood pressures were assessed using brachial blood pressure measurements, followed by a 10-minute supine autonomic testing session consisting of continuous HR (electrocardiogram), beat-by-beat blood pressure (finger plethysmograph), and MSNA (microneurography) monitoring. Partial correlations were used to determine the relationship between sleep and cardiovascular parameters while accounting for the influence of age, sex, and BMI. TST was not associated with MAP (R=-0.105, p=0.321), HR (R=0.093, p=0.383), or MSNA burst frequency (BF; R=-0.168, p=0.112) and incidence (BI; R=-0.162, p=0.124). Similarly, SE was not associated with MAP (R=-0.088, p=0.408), HR (R=-0.118, p=0.263), MSNA BF (R=0.038, p=0.723), or MSNA BI (R=0.079, p=0.459). In contrast to recent preliminary findings, our results do not support a significant association between actigraphy-based sleep duration or efficiency and measures of resting blood pressure, heart rate, and MSNA.

AKAP150 and Caveolin 1 Facilitate the Formation of Distinct TRPV4 Signaling Microdomains in Vascular Smooth Muscle Cells

Ca2+ influx through transient receptor potential vanilloid 4 (TRPV4) channel is a well-established pathway in vascular smooth muscle cells (SMCs). We recently discovered two separate SMC TRPV4 (TRPV4SMC) channel subpopulations: constrictor TRPV4SMC channels that are activated by α1 adrenergic receptors (a1AR) through protein kinase C (PKC), and dilator TRPV4SMC channels that are activated by intraluminal pressure and couple with Ca2+-activated K+ (BK) channels. However, the underlying mechanism for the formation of these TRPV4SMC signaling microdomains is unclear. AKAP150 (A kinase anchoring protein 150), a PKC-anchoring protein, is essential for PKC activation of TRPV4SMC channels, and Caveolin-1 (Cav1) has been linked to enhanced activity of TRPV4 and BK channels. We hypothesized that distinct anchoring proteins facilitate the formation of spatially separated TRPV4SMC signaling microdomains. Therefore, we tested the possibility that AKAP150 mediates α1AR-induced activation of constrictor TRPV4SMC channels, and Cav1 provides a signaling scaffold for the intraluminal pressure-activated TRPV4SMC-BK channel signaling. Radiotelemetric recordings showed lower resting blood pressure in tamoxifen-inducible, SMC-specific AKAP150KO (AKAP150SMCKO) mice, suggesting that AKAP150SMC increases the resting blood pressure. On the contrary, Cav1SMCKO mice showed elevated resting blood pressure, suggesting that Cav1SMC decreases blood pressure. Furthermore, phenylephrine (PE, a1AR agonist)-induced TRPV4SMC currents and increase in blood pressure (1 mg/kg PE, intraperitoneal), and nerve stimulation-induced (electrical pulses; 50–150 V, 0.25-ms pulse, 15 Hz) TRPV4SMC channel activity were absent in AKAP150SMCKO mice, but not in Cav1SMCKO mice. TRPV4 channel-activated BK current was abrogated in SMCs from Cav1SMCKO mice, but not in SMCs from AKAP150SMCKO mice. Together, these data supported the concept that AKAP150 and Cav1 are required for the formation of constrictor and dilator TRPV4SMC signaling microdomains, respectively. Studies in other cell types have shown that mechanosensitive Piezo1 channels can increase the activity of TRPV4 channels. Therefore, we determined whether Piezo1 is required for intraluminal pressure- activation of the dilator TRPV4SMC channels. We postulated that intraluminal-pressure activates Cav1-scaffolded Piezo1SMC-TRPV4SMC-BK channel signaling. Piezo1SMCKO mice showed a loss of intraluminal pressure-induced TRPV4SMC channel activity and increased myogenic constriction in MAs. Importantly, Yoda1 (Piezo1 activator)-induced increase in BK current was absent in SMCs from Cav1SMCKO, TRPV4SMCKO, and Piezo1SMCKO mice, but not AKAP150SMCKO mice. Together, our results suggest that AKAP150SMC and Cav1SMC facilitate constrictor α1AR-PKC-TRPV4SMC and dilator Piezo1SMC-TRPV4SMC-BK channel signaling, respectively. Collectively, our data identify the anchoring proteins involved in the formation of distinct Ca2+ signaling microdomains with opposite effects on blood pressure. This work was supported by funding from the American Heart Association to YLC (POST833691), the National Institutes of Health to SKS (HL146914, HL142808, and HL147555). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The Impact of Ketone Salt Supplementation on Blood Pressure and Health Parameters in Adults Diagnosed with PTSD – A Pilot Stud

"Post-traumatic stress disorder (PTSD) is a condition associated with high levels of stress often linked to elevated resting blood pressure (BP). Beta-hydroxybutyrate, a fuel source and signaling molecule, has been shown to improve metabolic and neurological conditions, as well as decrease systolic BP in healthy populations. The purpose of this study was to determine if longterm beta-hydroxybutyrate administration via ketone salt (KS) supplementation alters BP, complete blood count (CBC), or comprehensive metabolic panel (CMP) results in adults diagnosed with PTSD. Sixteen adults (ages 21-65; 12 women/4 men) with PTSD completed this randomized, double-blinded, and placebo-controlled study by taking KS or a placebo supplement for 6 weeks. Blood was collected (for CMP and CBC assessment) and BP measurements were taken before and after the intervention period. None of the variables changed significantly based on the condition (p > .05 for all interaction effects). The reduction in BP measures following the KS supplementation, though non-significant, may be clinically meaningful in PTSD populations and others subject to increased cardiovascular mortality risk. Chronic KS supplementation did not negatively impact BP, CBC, or CMP measures in adults with PTSD. Further investigation of KS as a hypertension treatment approach is warranted in this population."

Hemodynamic responses to handgrip and metaboreflex activation are exaggerated in individuals with metabolic syndrome independent of resting blood pressure, waist circumference, and fasting blood glucose.

Introduction: Prior studies report conflicting evidence regarding exercise pressor and metaboreflex responses in individuals with metabolic syndrome (MetS). Purpose: To test the hypotheses that 1) exercise pressor and metaboreflex responses are exaggerated in MetS and 2) these differences may be explained by elevated resting blood pressure. Methods: Blood pressure and heart rate (HR) were evaluated in 26 participants (13 MetS) during 2min of handgrip exercise followed by 3min of post-exercise circulatory occlusion (PECO). Systolic (SBP), diastolic (DBP), and mean arterial pressure (MAP), along with HR and a cumulative blood pressure index (BPI), were compared between groups using independent samples t-tests, and analyses of covariance were used to adjust for differences in resting blood pressure, fasting blood glucose (FBG), and waist circumference (WC). Results: ΔSBP (∼78% and ∼54%), ΔMAP (∼67% and ∼55%), and BPI (∼16% and ∼20%) responses were significantly exaggerated in individuals with MetS during handgrip and PECO, respectively (all p ≤ 0.04). ΔDBP, ΔMAP, and BPI responses during handgrip remained significantly different between groups after independently covarying for resting blood pressure (p < 0.01), and after simultaneously covarying for resting blood pressure, FBG, and WC (p ≤ 0.03). Likewise, peak SBP, DBP, MAP, and BPI responses during PECO remained significantly different between groups after adjusting for resting blood pressure (p ≤ 0.03), with peak SBP, MAP, and BPI response remaining different between groups after adjusting for all three covariates simultaneously (p ≤ 0.04). Conclusion: These data suggest that exercise pressor and metaboreflex responses are significantly exaggerated in MetS independent of differences in resting blood pressure, FBG, or WC.

Sedentary behaviour is associated with heightened cardiovascular, inflammatory and cortisol reactivity to acute psychological stress

BackgroundSedentary behaviour is a risk factor for cardiovascular disease (CVD), but the underlying mechanisms remain unclear. Exaggerated psychobiological responses to acute psychological stress increase CVD risk. Sedentary behaviour is associated with characteristics that can predict large psychobiological stress response patterns (e.g., elevated resting blood pressure and systemic inflammation), but it is currently unknown whether sedentary behaviour and stress reactivity are directly linked. The aim of this study was to examine associations between device-assessed sedentary behaviour and measures of stress reactivity. MethodsSixty-one healthy adults wore an activPAL (thigh) and ActiGraph (wrist) for seven days to measure habitual levels of sedentary behaviour (mean ± SD = 9.96 ± 1.48 h/day) and moderate-to-vigorous physical activity (mean ± SD = 101.82 ± 42.92 min/day). Participants then underwent stress reactivity testing, where beat-to-beat cardiovascular (e.g., blood pressure, total peripheral resistance), inflammatory (plasma interleukin-6, leukocytes) and salivary cortisol measurements were taken in response to an 8-minute socially evaluative Paced Auditory Serial Addition Test. ResultsHigher volumes of daily sedentary behaviour were associated with larger stress responses for diastolic blood pressure (Β=1.264, 95%CI=0.537—1.990, p = .005), total peripheral resistance (Β=40.563, 95%CI=19.310—61.812, p < .001), interleukin-6 (Β=0.219, 95%CI=0.109—0.329, p < .001) and cortisol (Β=1.844, 95%CI=1.139—2.549, p < .001). These findings emerged independent of a priori determined covariates, including daily levels of moderate-to-vigorous physical activity and adiposity. DiscussionExaggerated stress reactivity is characteristic of high sedentary behaviour and could be a novel mechanism linking sedentary behaviour with CVD. Future work should examine the impact of reducing sedentary behaviour on measures of stress reactivity, as this may have clinical relevance for preventing CVD.

Significance of extended sports cardiology screening of elite handball referees.

The significance of cardiology screening of referees is not well established. Cardiovascular risk factors and diseases were examined in asymptomatic Hungarian elite handball referees undergoing extended screening: personal/family history, physical examination, 12-lead ECG, laboratory tests, body-composition analysis, echocardiography, and cardiopulmonary exercise testing. Holter-ECG (n = 8), blood pressure monitorization (n = 10), cardiac magnetic resonance imaging (CMR; n = 27) and computer tomography (CCT; n = 4) were also carried out if needed. We examined 100 referees (age: 29.6±7.9years, male: 64, training: 4.3±2.0 hours/week), cardiovascular risk factors were: positive medical history: 24%, overweight: 10%, obesity: 3%, dyslipidaemia: 41%. Elevated resting blood pressure was measured in 38%. Stress-ECG was positive due to ECG-changes in 16%, due to elevated exercise blood pressure in 8%. Echocardiography and/or CMR identified abnormalities in 19%. A significant number of premature ventricular contractions was found on the Holter-ECG in two cases. The CCT showed myocardial bridge or coronary plaques in one-one case. We recommended lifestyle changes in 58%, new/modified antihypertensive or lipid-lowering therapy in 5%, iron-supplementation in 22%. By our results, a high percentage of elite Hungarian handball referees had cardiovascular risk factors or diseases, which, combined with physical and psychological stress, could increase the possibility of cardiovascular events. Our study draws attention to the importance of cardiac screening in elite handball referees.

Conditioned Pain Modulation And Blood Pressure Responses To Cold Pressor Test Among Resistance Exercisers

Conditioned pain modulation (CPM) examines central pain inhibitory processing by assessing changes of sensitivity to the first pain stimulus after exposure to the second pain stimulus compared to baseline, and serves as risk factor of chronic pain. Aerobically-trained individuals typically show greater CPM compared to controls, but little is known regarding CPM among resistance exercisers (REs) who habitually engage in resistance exercise/strength training. REs often show elevated resting blood pressure (BP), which is associated with greater BP responses to cold pressor test (CPT) of immersing a hand into a cold water bath. Given past research showing the positive association between CPM and BP responses to CPT as the second pain stimulus, REs may exhibit greater CPM, along with augmented BP responses to CPT. PURPOSE: To compare CPM and BP responses to CPT between REs and controls. METHODS: REs were primarily recruited from weight lifting and power lifting teams (n = 15). Controls were healthy, normally active individuals (NAs) (n = 15). The participants completed the CPM test to evaluate changes in pain ratings (0-100) to electrical stimuli delivered to the ankle after CPT for a maximum of 2 minutes compared to baseline. The magnitude of CPM was calculated as change scores: post-CPT pain ratings - baseline pain ratings, with smaller pain ratings indicating greater pain inhibition. BP was assessed at baseline and every minute during CPT. CPM and BP data were analyzed using a mixed model ANOVA. The relationship between CPM and BP was tested using a correlational analysis. RESULTS: Each group consisted of young, 9 men and 6 women (REs: 23 ± 5 yrs vs. NAs: 22 ± 2 yrs, p > 0.05). REs reported spending 9.1 ± 4.5 hours/week for resistance exercise. REs and NAs exhibited comparable CPM (Change scores. REs: -12 ± 12 vs. NAs: -14 ± 12, p > 0.05), but REs showed greater systolic BP responses to CPT compared to NAs (Mean SBP. REs: 129 ± 11 mmHg vs. NAs: 119 ± 14 mmHg, p < 0.05). No significant association was found between systolic BP and CPM in REs (Resting: r = 0.2, p > 0.05 & Reactivity: r = -0.2, p > 0.05), but resting systolic BP was positively associated with CPM in NAs (Resting: r = 0.5, p < 0.05 & Reactivity: r = -0.1, p > 0.05). CONCLUSION: The role of BP in CPM is likely complex, and the potential role of exercise in central pain processing needs to be studied.

Blood pressure-associated emotional dampening and risky behavior: Elevated resting blood pressure predicts risky simulated driving in women

Elevated resting blood pressure (BP) is associated with dampened responses to emotionally meaningful stimuli. This BP-associated emotional dampening may also influence threat appraisal and, hence, motivation to avoid risk. The present study was designed to determine if resting BP is associated with risky driving behavior assessed in a high fidelity driving simulator. Fifty-one healthy women (n = 20) and men (n = 31) rested for BP determinations both before and after a simulated driving scenario in a DriveSafety automotive simulator with six visual channels, single-axis motion, and functioning controls and instrumentation. Resting systolic (SBP) and diastolic (DBP) BPs were obtained systematically with a calibrated GE Dinamap Pro V100. Risky driving was assessed by speed relative to the posted speed limit, and a speed-adjusted time to collision index of tailgating. Regression analyses indicated that sex interacted with resting BP, with significant associations between BP and risk in women, but not men. For example, risky driving in women was associated with higher resting DBP (p = .006), with similar but less reliable effects for resting SBP (p = .058). These results provide some partial, preliminary support for the notion that BP-associated emotional dampening may reduce threat appraisal and thereby decrease motivation for risk avoidance, but these effects are confined to women in this simulated driving scenario. Interacting central nervous system (CNS) mechanisms controlling BP and emotional responsivity may mediate the relationship between BP and risk-taking behavior. Relative expression of this relationship in women and men may depend on multiple psychosocial and physiological mechanisms. The association of higher BP with increased risk-taking behaviors may have relevance to the early pathogenesis of essential hypertension.

Sympathoexcitation and impaired arterial baroreflex sensitivity are linked to vascular inflammation in individuals with elevated resting blood pressure.

Elevated Resting Blood Pressure (ERBP) in the prehypertensive range is associated with increased risk of hypertension and cardiovascular disease, the mechanisms of which remain unclear. Prior studies have suggested that ERBP may be associated with overactivation and dysregulation of the sympathetic nervous system (SNS). We hypothesized that compared to normotensives (≤120/80 mmHg), ERBP (120/80–139/89 mmHg) has higher SNS activity, impaired arterial baroreflex sensitivity (BRS), and increased vascular inflammation. Twenty‐nine participants were studied: 16 otherwise healthy individuals with ERBP (blood pressure (BP) 130 ± 2/85 ± 2 mmHg) and 13 matched normotensive controls (mean BP 114 ± 2/73 ± 2 mmHg). We measured muscle sympathetic nerve activity (MSNA), beat‐to‐beat BP, and continuous electrocardiogram at rest and during arterial BRS testing via the modified Oxford technique. Blood was analyzed for the following biomarkers of vascular inflammation: lipoprotein‐associated phospholipase A2 (Lp‐PLA2), E‐selectin, and intercellular adhesion molecule 1 (ICAM‐1). Resting MSNA burst frequency (22 ± 2 vs. 16 ± 2 bursts/min, P = 0.036) and burst incidence (36 ± 3 vs. 25 ± 3 bursts/100 heart beats, P = 0.025) were higher in ERBP compared to controls. Cardiovagal BRS was blunted in ERBP compared to controls (13 ± 2 vs. 20 ± 3 msec/mmHg, P = 0.032), while there was no difference in sympathetic BRS between groups. Lp‐PLA2 (169 ± 8 vs. 142 ± 9 nmol/min/mL, P = 0.020) and E‐selectin (6.89 ± 0.6 vs. 4.45 ± 0.51 ng/mL, P = 0.004) were higher in ERBP versus controls. E‐selectin (r = 0.501, P = 0.011) and ICAM‐1 (r = 0.481, P = 0.015) were positively correlated with MSNA, while E‐selectin was negatively correlated with cardiovagal BRS (r = −0.427, P = 0.030). These findings demonstrate that individuals with ERBP have SNS overactivity and impaired arterial BRS that are linked to biomarkers of vascular inflammation.

Elevated resting blood pressure augments autonomic imbalance in posttraumatic stress disorder.

Posttraumatic stress disorder (PTSD) is characterized by increased sympathetic nervous system (SNS) activity, blunted parasympathetic nervous system (PNS) activity, and impaired baroreflex sensitivity (BRS), which contribute to accelerated cardiovascular disease. Patients with PTSD also have chronic stress-related elevations in resting blood pressure (BP), often in the prehypertensive range; yet, it is unclear if elevated resting blood pressure (ERBP) augments these autonomic derangements in PTSD. We hypothesized that compared with normotensive PTSD (N-PTSD), those with ERBP (E-PTSD) have further increased SNS, decreased PNS activity, and impaired BRS at rest and exaggerated SNS reactivity, PNS withdrawal, and pressor responses during stress. In 16 E-PTSD and 17 matched N-PTSD, we measured continuous BP, ECG, muscle sympathetic nerve activity (MSNA), and heart rate variability (HRV) markers reflecting cardiac PNS activity [standard deviation of R-R intervals (SDNN), root mean square of differences in successive R-R intervals (RMSSD), and high frequency power (HF)] during 5 min of rest and 3 min of mental arithmetic. Resting MSNA ( P = 0.943), sympathetic BRS ( P = 0.189), and cardiovagal BRS ( P = 0.332) were similar between groups. However, baseline SDNN (56 ± 6 vs. 78 ± 8 ms, P = 0.019), RMSSD (39 ± 6 vs. 63 ± 9 ms, P = 0.018), and HF (378 ± 103 vs. 693 ± 92 ms2, P = 0.015) were lower in E-PTSD versus N-PTSD. During mental stress, the systolic blood pressure response ( P = 0.011) was augmented in E-PTSD. Although MSNA reactivity was not different ( P > 0.05), the E-PTSD group had an exaggerated reduction in HRV during mental stress ( P < 0.05). PTSD with ERBP have attenuated resting cardiac PNS activity, coupled with exaggerated BP reactivity and PNS withdrawal during stress.

Blood Pressure, Emotional Dampening, and Risk Behavior: Implications for Hypertension Development.

Elevated resting blood pressure (BP) is associated with risk for hypertension and emotional dampening, including reduced responses to emotionally meaningful stimuli. Perception of threat is a critical motivator in avoidance of risky health-damaging behavior. We hypothesize that BP-associated dampening of threat appraisal may increase risk-taking behavior. We measured resting BP, perception of affect, and risk behavior in 92 healthy women (n = 49) and men (n = 43) recruited from university students and staff as well as members of the surrounding community. Mean (SE) age for the sample was 21.5 (4.3) year. BP was measured using an automated BP monitor, and risk behavior was assessed with a modified National College Health Risk Behavior Survey. We also measured recognition of affect using the Perception of Affect Task (PAT). Risk-taking behavior was positively correlated with both systolic (r(89) = .278, p = .008) and diastolic BP (r(89) = .309, p < .003). Regression analyses indicated that the association between risk-taking behavior and BP was not mediated by PAT scores. Results show that persons with higher resting BP levels report increased risk-taking behavior. PAT scores, while correlated with systolic BP, did not mediate the relationship between BP and risk. The relationship between BP and risk behavior reflects the potential involvement of central nervous system regulation of both BP and emotional responsivity, and its relationship to health-damaging behavior and risk for hypertension.

Is Resolution of Chronic Pain Associated With Changes in Blood Pressure-related Hypoalgesia?

In healthy individuals, elevated resting blood pressure (BP) is associated with reduced pain responsiveness and lower temporal summation. Prior work indicates that this BP-related hypoalgesia is reduced in individuals with chronic pain. This study evaluated whether resolution of chronic pain was associated with greater BP-related hypoalgesia compared to nonresolution. From a prospective sample of adolescents and young adults diagnosed with chronic functional abdominal pain an average of 9 years earlier, 99 individuals in whom the condition had resolved and 51 individuals with ongoing abdominal pain were studied. Resting systolic BP was assessed, followed by evaluation of thermal pain threshold and tolerance, and assessment of temporal summation to thermal pain stimuli. Higher resting systolic BP was significantly associated with higher pain threshold and tolerance, and lower temporal summation only in the group with resolved functional abdominal pain (p < .05). Hierarchical regressions revealed that interactions between BP and resolution of chronic pain were significant only for pain tolerance (p < .05). Analyses by sex indicated that interactions between BP and resolution status were significant for the temporal summation outcome in males but not in females. Results suggest that BP-related hypoalgesic mechanisms may be more effective in individuals in whom chronic pain has resolved compared to those with ongoing chronic pain. Findings hint at sex differences in the extent to which resolution of chronic pain is associated with BP-related hypoalgesia. Whether greater BP-related hypoalgesia is a consequence of, or alternatively a contributor to, resolution of chronic pain warrants further investigation.

Exercise and Lifestyle Therapy Improves Weight Maintenance in Young People with Psychosis

INTRODUCTION Young people with psychosis typically have higher rates of premature cardiovascular disease and metabolic disorders compared to non-psychotic peers. This has been primarily due to a sedentary lifestyle, poor diet composition, misuse of harmful substances and higher rates of obesity and smoking. When prescribed obesogenic antipsychotic medication, a weight gain of >12 kg within 2 years is typical. PURPOSE: To examine the benefits of a 12 wk exercise and lifestyle intervention entitled ‘Supporting Health and Promoting Exercise’ (SHAPE) for young people recently diagnosed with psychosis. METHODS Participants (n=26; 8 females; mean age 27.7 ± 5.1) engaged in weekly 45’ education sessions on healthy lifestyle behaviors, including: managing anxiety and depression, mindfulness and relaxation training, substance misuse, smoking cessation, healthy eating and nutritional advice, dental and sexual health care. This was followed by a 45’ exercise session including activities such as circuit and resistance training, yoga, and badminton, led by qualified exercise instructors. Anthropometric data were measured at baseline, 12 wk and 12 month post-intervention. Lifestyle behaviors and clinical measurements, including resting heart rate, blood pressure, total cholesterol, triglycerides, HbA1c and prolactin, were assessed at baseline and 12 months post-intervention as part of their routine clinical care plan. Significant differences over time were assessed using Paired Sample t-tests. RESULTS SHAPE participants (n=26) presented with first episode psychosis (n=11), schizophrenia (n=11), bipolar disorder (n=2), at risk mental state (n=1), and persistent delusion disorder (n=1) of which 52% were prescribed highly obesogenic antipsychotic medications (Clozapine and Olanzepine). Mean baseline data suggests participants were at an increased health risk due to elevated values in mean BMI (70% were overweight or obese), waist circumference, resting heart rate, and triglycerides (see Table 1 & 2). Over 50% reported smoking daily and 85% had elevated resting blood pressure (>120/80 mm Hg). At 12 wk post-intervention, no changes were observed in mean BMI or waist circumference (see Table 1); 19 participants either maintained (mean 0.5 kg: range ± 2 kg) or decreased (mean -5.7 kg: range 2-7 kg) weight; 7 participants increased weight (mean 4.9 kg: range 2.0-9.6 kg). At 12 month post-intervention (n=16), no change was evident in mean BMI, waist circumference, or any other clinical variable (see Table 2). Positive impacts on lifestyle behaviors included 7 participants eating ~400g of fruit/vegetables daily, 2 ceased substance use, 2 ceased alcohol use, 4 ceased smoking and 5 were less sedentary. CONCLUSION At the start of the programme, participants were already at an increased risk for cardiometabolic disorders. Findings suggest that SHAPE supported young people with psychosis to: -attenuate their physical health risk following a 12 wk exercise and lifestyle intervention which were sustained at 12 months follow up. -make positive lifestyle behavior changes leading to sustained improvements in weight maintenance and physical health.

(186) Relationship between central pain mechanisms and arterial blood pressure in pain free subjects

Studies in humans suggest an interrelationship between blood pressure and pain regulation, where elevated resting blood pressure is associated with decreased pain sensitivity in pain free normotensives. However, it is still unclear whether: 1) this interrelationship involves peripheral and central arterial blood pressure, or 2) central pain mechanisms are involved. We classified 13 pain-free subjects (mean age = 47.46; SD= 7.32) as normotensive (n = 6) or prehypertensive (n = 7) using a systolic blood pressure >135 mm Hg as the cutoff. Heart rate (HR) and peripheral and central blood pressures were measured non-invasively before, during and after experimental pain procedures. Suprathreshold heat pain responses (SHPR) were generated with repeated thermal stimuli, and conditioned pain modulation (CPM) was assessed using SHPR as the experimental stimulus and cold pressor task (7 °C) as the conditioning stimulus. Repeated measures ANOVA showed significant increases (pre, during and post pain) in all measures of peripheral and central blood pressure; however, the time*group (normotensive vs prehypertensive) interaction was significant only for peripheral systolic pressure (F (2,18)=6.07, p=0.01) and central systolic pressure (F(2,18)=3.84, p=0.04). Significant positive associations were found between SHPR and arterial blood pressure (peripheral and central, p< 0.01) only in prehypertensive subjects. There was a significant positive association between the magnitude of CPM and HR difference in all subjects. These preliminary results imply that: 1) the acute response of peripheral and central systolic pressure differs between normotensive and prehypertensive individuals, where normotensives have a more pronounced response to pain induction, and 2) inhibitory (CPM) and facilitatory (SHPR) central pain mechanisms are related to different cardiovascular mechanisms in response to acute pain induction. Further analyses in a larger sample and in chronic pain patients will provide stronger evidence about the interrelationship between blood pressure and central pain mechanisms. Supported by Charlotte Zietlow Research Grant, Indiana State University.

The Effect of Low Volume Interval Training on Resting Blood Pressure in Pre-hypertensive Subjects: A Preliminary Study

ABSTRACTObjectives: Clinically pre-hypertensive adults are at a greater risk of developing hypertension, stiffened arteries, and other cardiovascular risks. Endurance exercise training has been shown to improve elevated resting blood pressure and C-reactive protein (CRP) levels. However, a primary barrier preventing individuals from engaging in regular physical activity is a lack of time. The purpose of our study was to determine if a high-intensity interval training (HIIT) protocol would be as effective as continuous aerobic endurance training (ET) on resting blood pressure in pre-hypertensive participants. Additionally, this study investigated the effects of HIIT vs. ET on CRP.Methods: Twelve pre-hypertensive participants (33.3±6.1 yrs; 3M/9W) participated in 8 weeks of cycle ergometer exercise training. The ET exercised for 30 continuous min/day, 4 days/week at 40% reserve. The HIIT exercised at a 1:1 work-to-rest for 20 min/day, 3 days/week at 60% peak power. Resting mean arterial pressure and CRP were compared throughout the study.Results: Both groups showed decreases (p<0.001) in mean arterial pressure (ET: -11.5 ± 5.9 mmHg; HIIT: -8.6 ± 4.8 mmHg) following the 8 weeks. For CRP, there was a significant decrease (p=0.014) as a main effect of time. increased (p<0.001) approximately 25% for both HIIT and ET.Conclusion: These preliminary data suggest HIIT and ET similarly decreased resting blood pressure and increased .

Shoulder arthroscopy and complications: Can we afford to relax?

Shoulder arthroscopy and complications: Can we afford to relax?

Role of the ovarian cycle on neural cardiovascular control in sleep-deprived women

The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women.

The association of elevated resting blood pressure with greater conditioned pain modulation is present for men but not women

Elevated resting blood pressure (BP) is consistently associated with hypoalgesia (i.e., diminished pain responsiveness) in healthy normotensive individuals. It has been suggested that sex might moderate BP-related hypoalgesia, such that BP-related hypoalgesia may be stronger in men compared to women. At this time it remains unclear whether resting BP is also associated with conditioned pain modulation (CPM), an endogenous, opioid-mediated pain inhibitory process that is often mechanistically associated with hypoalgesia.

Decreased Cognitive/CNS Function in Young Adults at Risk for Hypertension: Effects of Sleep Deprivation

Hypertension has been linked to impaired cognitive/CNS function, and some of these changes may precede development of frank essential hypertension. The stress and fatigue of sleep deprivation may exacerbate these cognitive changes in young adults at risk. We hypothesize that individuals at risk for hypertension will show significant declines in cognitive function during a night of sleep deprivation. Fifty-one young adults were recruited for 28-hour total sleep deprivation studies. Hypertension risk was assessed by mildly elevated resting blood pressure and by family history of hypertension. A series of cognitive memory tasks was given at four test sessions across the sleep deprivation period. Although initially comparable in cognitive performance, persons at risk showed larger declines across the night for several indices of working memory, including code substitution, category, and order recall. These results suggest that cognitive/CNS changes may parallel or precede blood pressure dysregulation in the early stages of hypertension development. The role of CNS changes in the etiology of essential hypertension is discussed.

Metabolically exaggerated cardiac reactions to acute psychological stress: The effects of resting blood pressure status and possible underlying mechanisms

The study aimed to: confirm that acute stress elicits metabolically exaggerated increases in cardiac activity; test whether individuals with elevated resting blood pressure show more exaggerated cardiac reactions to stress than those who are clearly normotensive; and explore the underlying mechanisms. Cardiovascular activity and oxygen consumption were measured pre-, during, and post-mental stress, and during graded sub-maximal cycling exercise in 11 young men with moderately elevated resting blood pressure and 11 normotensives. Stress provoked increases in cardiac output that were much greater than would be expected from contemporary levels of oxygen consumption. Exaggerated cardiac reactions were larger in the relatively elevated blood pressure group. They also had greater reductions in total peripheral resistance, but not heart rate variability, implying that their more exaggerated cardiac reactions reflected greater β-adrenergic activation.