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Introduction: Non-invasive cuffless blood pressure devices have shown promising results in accurately estimating blood pressure when comparing measurements at rest. However, none of commercially available or prototype cuffless devices have yet been validated according to the appropriate standards. The aim of the present study was to bridge this gap and evaluate the ability of a prototype cuffless device, developed by Aidee Health AS, to track changes in blood pressure compared to a non-invasive, continuous blood pressure monitor (Human NIBP or Nexfin) in a laboratory set up. The performance was evaluated according to the metrics and statistical methodology described in the ISO 81060-3:2022 standard. However, the present study is not a validation study and thus the study was not conducted according to the ISO 81060-3:2022 protocol, e.g., non-invasive reference and distribution of age not fulfilled. Method: Data were sampled continuously, beat-to-beat, from both the cuffless and the reference device. The cuffless device was calibrated once using the reference BP measurement. Three different techniques (isometric exercise, mental stress, and cold pressor test) were used to induce blood pressure changes in 38 healthy adults. Results: The mean difference (standard deviation) was 0.3 (8.7) mmHg for systolic blood pressure, 0.04 (6.6) mmHg for diastolic blood pressure, and 0.8 (7.9) mmHg for mean arterial pressure, meeting the Accuracy requirement of ISO 81060-3:2022 (≤6.0 (10.0) mmHg). The corresponding results for the Stability criteria were 1.9 (9.2) mmHg, 2.9 (8.1) mmHg and 2.5 (9.5) mmHg. The acceptance criteria for the Change requirement were achieved for the 85th percentile of ≤50% error for diastolic blood pressure and mean arterial pressure but were higher than the limit for systolic blood pressure (56% vs. ≤50%) and for all parameters for the 50th percentile (32%–39% vs. ≤25%). Conclusions: The present study demonstrated that the cuffless device could track blood pressure changes in healthy adults across different activities and showed promising results in achieving the acceptance criteria from ISO 81060-3:2022. [ABSTRACT FROM AUTHOR]

Arterial vasodilation is dependent on nitric oxide synthesized from L-arginine by endothelial nitric oxide synthase. Triathletes are reported to display altered serum concentrations of nitric oxide metabolites such as L-arginine, asymmetric dimethyl arginine (ADMA) and symmetric dimethyl arginine (SDMA) shortly after completing long-distance triathlon races. In other populations, similar changes to nitric oxide metabolites are established risk markers of cardiovascular disease. The objective of this study was to assess serum concentrations of metabolites for endothelial nitric oxide synthesis in triathletes one week following a long-distance triathlon race. In this prospective observational study, we used high-performance liquid chromatography to measure circulating concentrations of L-arginine, ADMA, and SDMA in triathletes. Venous blood samples were collected before, immediately after, day one, and one week following the triathlon race. Serum concentrations and L-arginine/ADMA ratio were determined for each time-point and compared to baseline. L-arginine/ADMA ratio was reduced on day one (147 ± 32 vs 163 ± 40, p < 0.02). ADMA was reduced immediately after and increased at day one and remained elevated at one week (0.29 ± 0.05 mM, p < 0.001, 0.44 ± 0.08 mM, p < 0.001 and 0.42 ± 0.07 μM, p = 0.04, respectively vs 0.40 ± 0.05 μM). SDMA was increased at all time-points when compared to baseline (0.48 ± 0.10 μM, p < 0.001, 0.53 ± 0.11 μM, p < 0.001 and 0.42 ± 0.08 μM, p = 0.048 vs 0.38 ± 0.05 μM). L-arginine was only decreased immediately after (46.0 ± 9.3 μM vs. 64.6 ± 16.1 μM, p < 0.001). Long-distance triathlon racing induces altered levels of metabolites for endothelial nitric oxide production that mostly normalizes within one week following racing. The clinical relevance of these transient changes has yet to be elucidated in the athletic population. [ABSTRACT FROM AUTHOR]

Large‐volume therapeutic phlebotomy is the mainstay of hemochromatosis treatment and offers an opportunity to investigate the hemodynamic changes during acute hypovolemia. An otherwise healthy 64‐year‐old male with hemochromatosis participated. On nine separate visits, 1000 mL therapeutic phlebotomy was performed. On one occasion, pre‐ and post‐phlebotomy orthostatic challenge with 27° reverse Trendelenburg position was administered. Mean arterial pressure, heart rate, and stroke volume were measured continuously during the procedures. The patient's tolerance to the interventions was continuously evaluated. The procedures were well tolerated by the patient. Mean arterial pressure was maintained during hemorrhage and following phlebotomy in both supine and reverse Trendelenburg positions, primarily through an increase in heart rate and systemic vascular resistance. The present study found that 1000 mL therapeutic phlebotomy in a patient with hemochromatosis may be acceptably and safely used to model hemorrhage. The approach demonstrates high clinical applicability and ethically robustness in comparison with volunteer studies. [ABSTRACT FROM AUTHOR]

Background: Stroke volume can be estimated beat-to-beat and non-invasively by pulse wave analysis (PWA). However, its reliability has been questioned during marked alterations in systemic vascular resistance (SVR). We studied the effect of SVR on the agreement between stroke volume by PWA and Doppler ultrasound during reductions in stroke volume in healthy volunteers. Methods: In a previous study we simultaneously measured stroke volume by PWA (SVPWA) and suprasternal Doppler ultrasound (SVUS). We exposed 16 healthy volunteers to lower body negative pressure (LBNP) to reduce stroke volume in combination with isometric hand grip to elevate SVR. LBNP was increased by 20 mmHg every 6 minutes from 0 to 80 mmHg, or until hemodynamic decompensation. The agreement between SVPWA and SVUS was examined using Bland-Altman analysis with mixed regression. Within-subject limits of agreement (LOA) was calculated from the residual standard deviation. SVRUS was calculated from SVUS. We allowed for a sloped bias line by introducing the mean of the methods and SVRUS as explanatory variables to examine whether the agreement was dependent on the magnitude of stroke volume and SVRUS. Results: Bias ± limits of agreement (LOA) was 27.0 ± 30.1 mL. The within-subject LOA was ±11.1 mL. The within-subject percentage error was 14.6%. The difference between methods decreased with higher means of the methods (-0.15 mL/mL, confidence interval (CI): -0.19 to -0.11, P<0.001). The difference between methods increased with higher SVRUS (0.60 mL/mmHg × min × L-1, 95% CI: 0.48 to 0.72, P<0.001). Conclusion: PWA overestimated stroke volume compared to Doppler ultrasound during reductions in stroke volume and elevated SVR in healthy volunteers. The agreement between SVPWA and SVUS decreased during increases in SVR. This is relevant in settings where a high level of reliability is required. [ABSTRACT FROM AUTHOR]

Background: Trauma patients frequently receive supplemental oxygen, but its hemodynamic effects in blood loss are poorly understood. We studied the effects of oxygen on the hemodynamic response and tolerance to simulated blood loss in healthy volunteers. Methods: Fifteen healthy volunteers were exposed to simulated blood loss by lower body negative pressure (LBNP) on two separate visits at least 24 h apart. They were randomized to inhale 100% oxygen or medical air on visit 1, while inhaling the other on visit 2. To simulate progressive blood loss LBNP was increased every 3 min in levels of 10 mmHg from 0 to 80 mmHg or until hemodynamic decompensation. Oxygen and air were delivered on a reservoired face mask at 15 L/min. The effect of oxygen compared to air on the changes in cardiac output, stroke volume and middle cerebral artery blood velocity (MCAV) was examined with mixed regression to account for repeated measurements within subjects. The effect of oxygen compared to air on the tolerance to blood loss was measured as the time to hemodynamic decompensation in a shared frailty model. Cardiac output was the primary outcome variable. Results: Oxygen had no statistically significant effect on the changes in cardiac output (0.031 L/min/LBNP level, 95% confidence interval (CI): − 0.015 to 0.077, P = 0.188), stroke volume (0.39 mL/LBNP level, 95% CI: − 0.39 to 1.2, P = 0.383), or MCAV (0.25 cm/s/LBNP level, 95% CI: − 0.11 to 0.61, P = 0.176). Four subjects exhibited hemodynamic decompensation when inhaling oxygen compared to 10 when inhaling air (proportional hazard ratio 0.24, 95% CI: 0.065 to 0.85, P = 0.027). Conclusions: We found no effect of oxygen compared to air on the changes in cardiac output, stroke volume or MCAV during simulated blood loss in healthy volunteers. However, oxygen had a favorable effect on the tolerance to simulated blood loss with fewer hemodynamic decompensations. Our findings suggest that supplemental oxygen does not adversely affect the hemodynamic response to simulated blood loss. Trial registration This trial was registered in ClinicalTrials.gov (NCT05150418) December 9, 2021 [ABSTRACT FROM AUTHOR]

Cardiorespiratory fitness (CRF) is an excellent marker of overall health. This study aimed to assess criterion validity and responsiveness of estimated CRF models (eCRF) in patients with inflammatory joint disease (IJD). CRF was measured directly as peak oxygen uptake (VO2peak) by a Cardiopulmonary Exercise Test (CPET), while one generic eCRF model (eCRFGEN) and two disease-specific eCRF models (eCRFALT and eCRFPGA) were used to estimate CRF at baseline and after 3 months in 55 Norwegian patients with IJD. Moderate correlations were observed between eCRFGEN, eCRFALT, eCRFPGA, and VO2peak at baseline (ICC 0.60, 0.64 and 0.62, respectively) and 3 months (ICC 0.62, 0.65 and 0.57, respectively). All eCRF models overestimated measured VO2peak, and there was large variability in agreement of individual measurements at baseline and at 3 months. Weak correlations were observed for responsiveness of eCRFGEN (ICC 0.39), eCRFALT (ICC 0.40) and eCRFPGA (ICC 0.39). Mean differences between change in eCRF models and change in VO2peak were small, but the wide limits of agreement exceeded the pre-defined clinically acceptable margins. The eCRF models possessed adequate ability to detect ≥3.5 mL/kg/min improvement in VO2peak. eCRF may suffice for group-level assessment, but caution is advised when applying eCRF to individual patients with IJD. [ABSTRACT FROM AUTHOR]

Since 2011, the Department of Vascular Surgery at Oslo University Hospital has offered screening for abdominal aortic aneurysm (AAA) to 65-year-old men living in Oslo, Norway. The aim of this study was to evaluate the effect of the screening project on AAA-related mortality and rupture and repair rates in the screened population.Methods: This cohort study included men that participated in AAA screening at the Department of Vascular Surgery at Oslo University Hospital in the period May 2011 to September 2019. All men with screen-detected AAA (aortic diameter ≥ 30 mm) and subaneurysmal aortic dilatation (aortic diameter 25– 29 mm) were included. A stratified (1:1 with the subaneurysm group), randomized selection of men with normal aortic diameter (< 25 mm) upon screening was also included. The follow-up data on events (ruptures, repairs, and deaths) after screening were collected retrospectively from patient electronic medical records at Oslo University Hospital, the National Population Register and the Norwegian Cause of Death Registry (CoDR).Results: In total, 2048 men were included, with a median follow-up time of 7.1 years (IQR 3.8). Among men with screen-detected AAA, 0.6% died of AAA-related causes (0.9 AAA-related deaths per 1000 person-years). The rupture rate was 0.3% among men with screen-detected AAA or subaneurysmal aortic dilatation, giving an incidence of 0.5 ruptures per 1000 person-years. The overall repair rate in the AAA group was 20.6% (36.1 repairs per 1000 person-years) and 0.6% (0.9 repairs per 1000 person-years) in the subaneurysm group.Conclusion: In a population screened for AAA, the incidence of rupture and the AAA-related mortality was very low. Almost one-fifth of the participants with screen-detected AAA underwent elective repair, representing a group that might have presented with rupture if untreated. These results indicate that screening is valuable in preventing AAA rupture and AAA-related mortality. [ABSTRACT FROM AUTHOR]

Background: Inflammatory joint diseases (IJD) are accompanied by an increased risk of cardiovascular disease (CVD). Cardiorespiratory fitness (CRF) is a modifiable CVD risk factor and low levels of CRF associate with an elevated CVD risk. This study aimed to investigate the associations between CVD risk factors, disease activity and CRF in patients with IJD and to explore differences between patients with normal versus low levels of CRF. Methods: CRF was measured as peak oxygen uptake (VO2peak) with a cardiopulmonary exercise test. Participants were also evaluated for: Body composition, blood pressure, blood lipids, inflammatory markers and disease activity. Patient-reported use of cigarettes/snuff, medication, disease duration, pain, fatigue, CVD history, habitual physical activity and exercise beliefs and self-efficacy were collected by questionnaire. Cross-sectional associations between CVD risk factors, disease-related factors and CRF were analyzed by multiple linear regression. CRF was categorized to normal CRF (VO2peak ≥ 80%) or low CRF (VO2peak < 80%) according to age- and gender-stratified reference data. Differences in demographic, CVD and disease-related factors between patients with normal versus low CRF were explored. Results: In 60 Norwegian patients with IJD [34 females, age 59 years (IQR: 52–63)], mean VO2peak was 30.2 (± 6.9) mL/kg/min, corresponding to 83% (± 18) of normative reference values. Age (coefficient: − 0.18 years, p = 0.01) and fat mass (coefficient: − 0.67 %, p < 0.001) were inversely associated with CRF, while physical activity index (coefficient: 0.13 points, p = 0.05) was positively associated with CRF (R2 = 0.66). There were no significant associations between CRF, classical CVD risk factors and disease-related variables. Compared to patients with low CRF (n = 30), patients with normal CRF (n = 30) had higher peak oxygen uptake (+ 9.4 mL/kg/min, p < 0.001), high-density lipoprotein cholesterol (+ 0.5 mmol L−1, p < 0.001), and exercise self-efficacy (+ 6.9, p < 0.01) as well as lower fat mass (− 8.7%, p < 0.001), resting heart rate (− 8.0 beats/min, p < 0.01) and triglycerides (− 0.5 mmol L−1, p < 0.01). Conclusions: In this sample of IJD-patients, age, fatmass and physical activity level were associated with CRF. CRF was lower than reference values and patients with normal CRF presented with a more favorable health profile. There is a continued need for exercise interventions to improve CRF in patients with IJD. Trial registration: NCT04922840. [ABSTRACT FROM AUTHOR]

In young patients referred for exercise-induced pain in the legs, false positive tests are a potential problem for the post-exercise ankle–brachial index (ABI) test when using the current American Heart Association guidelines for diagnosing peripheral artery disease (PAD). The present study aimed to investigate post-exercise ABI in healthy young people, and to explore whether the current diagnostic criteria for pathological ABI should be revised. Forty-eight volunteers (18–30 years) were included. Resting examinations included ABI and ultrasound of the external iliac artery. Post-exercise examinations after a treadmill load included ABI and ultrasound of the external iliac artery; after 0 min and after 3 min. A total of 60.5% of the participants had a post-exercise decrease in ABI > 20%. A total of 6.5% showed a decrease in ankle systolic blood pressure >30 mmHg. No significant association was observed between a change in blood flow in the external iliac artery and a reduction in ABI post-exercise. Analyses of the ultrasound recordings showed no turbulence in the external iliac artery. According to the results, a 20% decrease in ABI post-exercise seems to be a physiological condition present in young people. We support the need for a reassessment of the criteria for diagnosing PAD. [ABSTRACT FROM AUTHOR]

Background: Chronic mesenteric ischemia (CMI) due to either atherosclerosis of the mesenteric arteries or median arcuate ligament syndrome (MALS) is an underdiagnosed entity. The etiology of MALS and its existence have been debated and questioned. We aimed to identify plasma biomarkers indicating mesenteric ischemia in patients with CMI and MALS. Methods: Plasma α-glutathione S-transferase (α-GST), intestinal fatty acid-binding protein (I-FABP), citrulline, and ischemia modified albumin (IMA) were analyzed in fifty-eight patients with CMI (Group A, n=44) and MALS (Group B, n=14) before and after revascularization. The plasma levels of these potential biomarkers were compared with those of healthy individuals (Group C, n=16). Group comparison was performed with the Mann–Whitney U-test. Cross-tabulation and its derivatives were obtained. Receiver operating characteristic (ROC) curves and area under the curve (AUC) were calculated. Results: Plasma levels of α-GST were significantly raised in the patients with CMI (7.8 ng/mL, p< 0.001) and MALS (8.4 ng/mL, p< 0.001), as compared with the control Group C (3.3 ng/mL). The threshold for normal median plasma α-GST levels of 4 ng/mL yielded a sensitivity of 93% and 86%, specificity of 86% and 88%, respectively, for the diagnosis of CMI due to atherosclerosis and MALS. AUC of ROC curves was 0.96 (p< 0.0001) for CMI and 0.85 (p< 0.002) for MALS. The patient groups did not differ from the healthy controls in any other biomarkers. Conclusion: Plasma α-GST levels are elevated in CMI and MALS patients. Elevated plasma levels of α-GST suggest ischemia as the etiology of MALS. [ABSTRACT FROM AUTHOR]

Supplemental oxygen is widely administered in trauma patients, often leading to hyperoxia. However, the clinical evidence for providing supplemental oxygen in all trauma patients is scarce, and hyperoxia has been found to increase mortality in some patient populations. Hypovolemia is a common finding in trauma patients, which affects many hemodynamic parameters, but little is known about how supplemental oxygen affects systemic and cerebral hemodynamics during hypovolemia. We therefore plan to conduct an experimental, randomized, double blinded crossover study to investigate the effect of 100% oxygen compared to room air delivered by a face mask with reservoir on systemic and cerebral hemodynamics during simulated hypovolemia in the lower body negative pressure model in 15 healthy volunteers. We will measure cardiac output, stroke volume, blood pressure, middle cerebral artery velocity and tolerance to hypovolemia continuously in all subjects at two visits to investigate whether oxygen affects the cardiovascular response to simulated hypovolemia. The effect of oxygen on the outcome variables will be analyzed with mixed linear regression. Trial registration: The study is registered in the European Union Drug Regulating Authorities Clinical Trials Database (EudraCT, registration number 2021-003238-35). [ABSTRACT FROM AUTHOR]

Trauma patients may suffer significant blood loss, and noninvasive methods to diagnose hypovolemia in these patients are needed. Physiologic effects of hypovolemia, aiming to maintain blood pressure, are largely mediated by increased sympathetic nervous activity. Trauma patients may however experience pain, which also increases sympathetic nervous activity, potentially confounding measures of hypovolemia. Elucidating the common and separate effects of the two stimuli on diagnostic methods is therefore important. Lower body negative pressure (LBNP) and cold pressor test (CPT) are experimental models of central hypovolemia and pain, respectively. In the present analysis, we explored the effects of LBNP and CPT on pre‐ejection period and pulse transit time, aiming to further elucidate the potential use of these variables in diagnosing hypovolemia in trauma patients. We exposed healthy volunteers to four experimental sequences with hypovolemia (LBNP 60 mmHg) or normovolemia (LBNP 0 mmHg) and pain (CPT) or no pain (sham) in a 2 × 2 fashion. We calculated pre‐ejection period and pulse transit time from ECG and ascending aortic blood velocity (suprasternal Doppler) and continuous noninvasive arterial pressure waveform (volume‐clamp method). Fourteen subjects were available for the current analyses. This experimental study found that pre‐ejection period increased with hypovolemia and remained unaltered with pain. Pulse transit time was reduced by pain and increased with hypovolemia. Thus, the direction of change in pulse transit time has the potential to distinguish hypovolemia and pain. [ABSTRACT FROM AUTHOR]

Introduction: Due to diagnostic delay, chronic mesenteric ischemia (CMI) is underdiagnosed. We assumed that the patients suspected of CMI of the atherosclerotic origin or median arcuate ligament syndrome (MALS) could be identified earlier with endoscopic duplex ultrasound (E-DUS). Patients and Methods: Fifty CMI patients with CTA-verified stenosis of either ≥ 50% and ≥ 70% of celiac artery (CA) and superior mesenteric artery (SMA) were examined with E-DUS and transabdominal duplex ultrasound (TA-DUS). Peak systolic velocities (PSV) of ≥ 200cm/s and ≥ 275cm/s for CA and SMA, respectively, were compared with CTA. Subgroup analysis was performed for the patients with (n=21) and without (n=29) prior revascularization treatment of CMI. The diagnostic ability of E-DUS and TA-DUS was tested with crosstabulation analysis. Receiver operating characteristics (ROC) curve analysis was performed, and the area under the curve (AUC) was calculated to investigate the test accuracy. Results: In the patients with ≥ 70% stenosis, E-DUS had higher sensitivity than TA-DUS (91% vs 81% for CA and 100% vs 92% for SMA). AUC for SMA ≥ 70% in E-DUS was 0.75 and with TA-DUS 0.68. The sensitivity of E-DUS for CTA-verified stenosis ≥ 70% for CA was 100% in the patients without prior treatment. E-DUS demonstrated higher sensitivity than TA-DUS for both arteries with stenosis ≥ 50% and ≥ 70% in the treatment-naive patients. Conclusion: E-DUS is equally valid as TA-DUS for the investigation of CMI patients and should be used as an initial diagnostic tool for patients suspected of CMI. [ABSTRACT FROM AUTHOR]

In general, aerobic exercise has a positive impact on the vascular system, but the syndrome of relative energy-deficiency in sports (RED-S) makes this impact less clear for the athlete. The present cross-sectional controlled study aimed to investigate the vascular function in female elite long-distance runners, compared to inactive women. Sixteen female elite long-distance runners and seventeen healthy controls were recruited. Assessments of vascular function and morphology included endothelial function, evaluated by flow-mediated dilatation (FMD), vascular stiffness, evaluated with pulse wave velocity (PWV), carotid artery reactivity (CAR %), and carotid intima-media thickness (cIMT). Blood samples included hormone analyses, metabolic parameters, lipids, and biomarkers reflecting endothelial activation. RED-S risk was assessed through the low energy availability in female questionnaire (LEAF-Q), and body composition was measured by dual-energy X-ray absorptiometry (DXA). We found no significant differences in brachial FMD, PWV, CAR %, cIMT, or biomarkers reflecting endothelial activation between the two groups. Forty-four percent of the runners had a LEAF-Q score consistent with being at risk of RED-S. Runners showed significantly higher HDL-cholesterol and insulin sensitivity compared to controls. In conclusion, Norwegian female elite runners had an as good vascular function and morphology as inactive women of the same age. [ABSTRACT FROM AUTHOR]

Background: The selection of patients with MALS for surgical treatment depends upon the reliability of the symptom interpretation and the diagnostic work-up. We aimed to follow up the results of the laparoscopic decompression of the patients with MALS.Patients and Methods: In a single-center, 52 consecutive MALS patients were followed-up, prospectively, after transperitoneal laparoscopic decompression. MALS was diagnosed with a computed tomography angiography (CTA) verified stenosis, ≥50% of the celiac artery (CA), and with duplex ultrasound, a peak systolic velocity (PSV) ≥2.0 m/s. Postoperative, CTA, and duplex ultrasound were performed, and the patients were followed-up at 3, 6, 12 months, and yearly after that.Results: Mean age of the patients was 47 ±21 years, and 65% were females. The patients had a mean weight loss of 8.4 ±7.2 kg. Fifty-one patients had the laparoscopic operation with a mean operation time of 102 ± 28 minutes. Forty-seven patients (90%) achieved relief from the symptoms either completely (67%) or partially (23%) at 3-6 months of follow-up. Significant improvement in postoperative PSV was found compared to the preoperative values, p<0.001. Five patients (10%) with no immediate effect of the operation, but two of them became free from symptoms during the mean study follow-up of 2.4 ± 2 years. Five patients (10%) had operative complications, including one trocar injury to the liver, one pneumothorax, and three cases of bleeding from the branches of CA. Two patients died of cancer disease during the study period. Only two patients (4%) had symptoms relapse, both later treated successfully.Conclusion: Laparoscopic transperitoneal decompression provides most of the patients a persistent relief from MALS symptoms. [ABSTRACT FROM AUTHOR]

Diabetic peripheral neuropathy (DPN) leads to several changes in the skin, and some of these may influence the skin impedance spectrum. In the present study we have developed a prototype solution for skin impedance spectroscopy at selected skin sites (big toe pulp, heel and toe ball) that was tested in a pilot study on five patients with DPN and five healthy controls. At the big toe, most of the controls had markedly lower impedance than the DPN group, especially in the range of 1-100 kHz. The separation between the groups seemed to be weaker at the heel and weakest at the toeball. The results may indicate that monitoring of the skin impedance spectrum may be a method for detection of skin changes associated with DPN, encouraging further studies with the big toe sensor in particular. [ABSTRACT FROM AUTHOR]

Background: Chronic mesenteric ischemia (CMI) due to either atherosclerosis of the mesenteric arteries or median arcuate ligament syndrome (MALS) is an underdiagnosed entity. The etiology of MALS and its existence have been debated and questioned. We aimed to identify plasma biomarkers indicating mesenteric ischemia in patients with CMI and MALS.Methods: Plasma α-glutathione S-transferase (α-GST), intestinal fatty acid-binding protein (I-FABP), citrulline, and ischemia modified albumin (IMA) were analyzed in fifty-eight patients with CMI (Group A, n=44) and MALS (Group B, n=14) before and after revascularization. The plasma levels of these potential biomarkers were compared with those of healthy individuals (Group C, n=16). Group comparison was performed with the Mann-Whitney U-test. Cross-tabulation and its derivatives were obtained. Receiver operating characteristic (ROC) curves and area under the curve (AUC) were calculated.Results: Plasma levels of α-GST were significantly raised in the patients with CMI (7.8 ng/mL, p<0.001) and MALS (8.4 ng/mL, p<0.001), as compared with the control Group C (3.3 ng/mL). The threshold for normal median plasma α-GST levels of 4 ng/mL yielded a sensitivity of 93% and 86%, specificity of 86% and 88%, respectively, for the diagnosis of CMI due to atherosclerosis and MALS. AUC of ROC curves was 0.96 (p<0.0001) for CMI and 0.85 (p<0.002) for MALS. The patient groups did not differ from the healthy controls in any other biomarkers.Conclusion: Plasma α-GST levels are elevated in CMI and MALS patients. Elevated plasma levels of α-GST suggest ischemia as the etiology of MALS. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of lower extremity intermittent negative pressure (INP) treatment for 1 hour twice daily for 12 weeks, on circulating vascular biomarkers in patients with intermittent claudication. Patients were randomized to treatment with –40 mmHg INP (treatment group), or –10 mmHg INP (sham control group). Venous blood samples were collected at baseline and after 12 weeks, and concentrations of vascular adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin, P-selectin, von Willebrand factor (vWF), l -arginine, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) were analyzed. A larger proportion of the patients in the treatment group (25/31) had a reduction in vWF levels after 12 weeks, compared to the sham control group (17/30) (p = 0.043). Within the treatment group there was a significant mean (SEM) reduction in the concentration of vWF of –11% (4) (p = 0.019), whereas there was no significant change in the levels of vWF in the sham control group (1% (6); p = 0.85). There were no significant differences in the change of any of the biomarker levels between the groups after 12 weeks of treatment. In conclusion, there were no differences in the change of the circulating levels of the measured biomarkers between the treatment group and the sham control group after 12 weeks of INP treatment. However, the observed changes in vWF might indicate a beneficial effect of INP treatment on endothelial activation and endothelial injury. Clinicaltrials.gov Identifier: NCT03640676 [ABSTRACT FROM AUTHOR]

One year of training data from 8 elite orienteers were divided into a transition phase (TP), general preparatory phase (GPP), specific preparatory phase (SPP), and competition phase (CP). Average weekly training volume and frequency, hours at different intensities (zones 1–3), cross-training, running, orienteering, interval training, continuous training, and competition were calculated. Training volume was higher in GPP than TP, SPP, and CP (14.9 vs 9.7, 11.5, and 10.6 h/wk, P < .05). Training frequency was higher in GPP than TP (10 vs 7.5 sessions/wk, P < .05). Zone 1 training was higher in GPP than TP, SPP, and CP (11.3 vs 7.1, 8.3, and 7.7 h/wk, P < .05). Zone 3 training was higher in SPP and CP than in TP and GPP (0.9 and 1.1 vs 1.6 and 1.5 h/ wk, P < .05). Cross-training was higher in GPP than SPP and CP (4.3 vs 0.8 h/wk, P < .05). Interval training was higher in GPP than TP, SPP, and CP (0.7 vs 0.3 h/wk, P < .05). High-intensity continuous training was higher in GPP than CP (0.9 vs 0.4 h/ wk, P < .05), while competition was higher in SPP and CP than in TP and GPP (1.3 and 1.5 vs 0.6 and 0.3 h/wk, P < .01). In conclusion, these champion endurance athletes achieved a progressive reduction in total training volume from GPP to CP via a shortening of each individual session while the number of training sessions remained unchanged. This decrease in training volume was primarily due to a reduction in the number of hours of low-intensity, non-sport-specific cross-training. [ABSTRACT FROM AUTHOR]

Purpose: Cerebral blood flow (CBF) needs to be precisely controlled to maintain brain functions. While previously believed to be autoregulated and near constant over a wide blood pressure range, CBF is now understood as more pressure passive. However, there are still questions regarding the integrated nature of CBF regulation and more specifically the role of cardiac output. Our aim was, therefore, to explore the effects of MAP and cardiac output on CBF in a combined model of reduced preload and increased afterload. Method: 16 healthy volunteers were exposed to combinations of different levels of simultaneous lower body negative pressure and isometric hand grip. We measured blood velocity in the middle cerebral artery (MCAV) and internal carotid artery (ICAV) by Doppler ultrasound, and cerebral oxygen saturation (ScO2) by near-infrared spectroscopy, as surrogates for CBF. The effect of changes in MAP and cardiac output on CBF was estimated with mixed multiple regression. Result: Both MAP and cardiac output had independent effects on MCAV, ICAV and ScO2. For ICAV and ScO2 there was also a statistically significant interaction effect between MAP and cardiac output. The estimated effect of a change of 10 mmHg in MAP on MCAV was 3.11 cm/s (95% CI 2.51–3.71, P < 0.001), and the effect of a change of 1 L/min in cardiac output was 3.41 cm/s (95% CI 2.82–4.00, P < 0.001). Conclusion: The present study indicates that during reductions in cardiac output, both MAP and cardiac output have independent effects on CBF. [ABSTRACT FROM AUTHOR]

Whether the beneficial effects observed in patients with intermittent claudication are generalizable to patients with more severe stages of PAD should be investigated in a larger trial, however, observational data indicate a positive effect in selected patients with critical limb ischemia not amenable for revascularization. Keywords: Peripheral artery disease; intermittent claudication; intermittent negative pressure treatment EN Peripheral artery disease intermittent claudication intermittent negative pressure treatment 217 220 4 05/04/21 20210301 NES 210301 1. This was the first double-blind, randomized sham-controlled trial to show that INP treatment increases walking capacity in patients with intermittent claudication, and the first randomized controlled trial that documented the clinical effects of FlowOx treatment. However, more recently, two randomized controlled trials did not find additional effects of INP treatment in patients with intermittent claudication, hence the effect of INP treatment in patients with PAD has been debated [[14]]. [Extracted from the article]

The overall objective of this review was to investigate the role and development of sprinting speed in soccer. Time-motion analyses show that short sprints occur frequently during soccer games. Straight sprinting is the most frequent action before goals, both for the scoring and assisting player. Straight-line sprinting velocity (both acceleration and maximal sprinting speed), certain agility skills, and repeated-sprint ability are shown to distinguish groups from different performance levels. Professional players have become faster over time, indicating that sprinting skills are becoming more and more important in modern soccer. In research literature, the majority of soccer-related training interventions have provided positive effects on sprinting capabilities, leading to the assumption that all kinds of training can be performed with success. However, most successful intervention studies are time consuming and challenging to incorporate into the overall soccer training program. Even though the principle of specificity is clearly present, several questions remain regarding the optimal training methods within the larger context of the team-sport setting. Considering time-efficiency effects, soccer players may benefit more by performing sprint-training regimens similar to the progression model used in strength training and by world-leading athletics practitioners, compared with the majority of guidelines that traditionally have been presented in research literature. [ABSTRACT FROM AUTHOR]

Whilst both cardiac output (CO) and total peripheral resistance (TPR) determine mean arterial blood pressure (MAP), their relative importance in the pressor response to isometric exercise remains unclear. This study aimed to elucidate the relative importance of these two different factors by examining pressor responses during cardiopulmonary unloading leading to step-wise reductions in CO. Hemodynamics were investigated in 11 healthy individuals before, during and after two-minute isometric exercise during lower body negative pressure (LBNP; -20mmHg and -40mmHg). The blood pressure response to isometric exercise was similar during normal and reduced preload, despite a step-wise reduction in CO during LBNP (-20mmHg and -40mmHg). During -20mmHg LBNP, the decreased stroke volume, and consequently CO, was counteracted by an increased TPR, while heart rate (HR) was unaffected. HR was increased during -40 mmHg LBNP, although insufficient to maintain CO; the drop in CO was perfectly compensated by an increased TPR to maintain MAP. Likewise, transient application of LBNP (-20mmHg and -40mmHg) resulted in a short transient drop in MAP, caused by a decrease in CO, which was compensated by an increase in TPR. This study suggests that, in case of reductions of CO, changes in TPR are primarily responsible for maintaining the pressor response during isometric exercise. This highlights the relative importance of TPR compared to CO in mediating the pressor response during isometric exercise. [ABSTRACT FROM AUTHOR]

Universities around the world are facing an epidemic of mental distress among their students. The problem is truly a public health issue, affecting many and with serious consequences. The global burden of disease-agenda calls for effective interventions with lasting effects that have the potential to improve the mental health of young adults. In this study we aimed to determine whether yoga, a popular and widely available mind-body practice, can improve student mental health. We performed a randomised controlled trial with 202 healthy university students in the Oslo area. The participants were assigned to a yoga group or waitlist control group in a 1:1 ratio by a simple online randomisation program. The intervention group was offered 24 yoga sessions over 12 weeks. Measurements were taken at week 0 (baseline), week 12 (post-intervention), and week 24 (follow-up). The primary outcome was psychological distress assessed by the HSCL-25 questionnaire. Analysis was performed based on the intention to treat-principle. Between 24 January 2017, and 27 August 2017, we randomly assigned 202 students to a yoga intervention group (n = 100), or waitlist control group (n = 102). Compared with the control group, the yoga participants demonstrated a significant reduction in distress symptoms both at post-intervention (adjusted difference in the mean change −0.15, 95% CI −0.26 to −0.03, p = 0.0110) and follow-up (adjusted difference in the mean change −0.18, 95% CI −0.29 to −0.06, p = 0.0025). Sleep quality also improved at post-intervention and follow-up. No adverse events were reported. Our findings suggest that yoga has a moderately large and lasting effect, at least for some months, reducing symptoms of distress and improving sleep quality among students. Further research should seek ways to enhance the effect, assess an even longer follow-up period, include active control groups, and consider performing similar studies in other cultural settings. Trial registration: ClinicalTrials.gov identifier: NCT04258540. [ABSTRACT FROM AUTHOR]

Prolonged exercise is known to cause changes in common biomarkers. Occasionally, competition athletes need medical assistance and hospitalisation during prolonged exercise events. To aid clinicians treating patients and medical teams in such events we have studied common biomarkers after at The Norseman Xtreme Triathlon (Norseman), an Ironman distance triathlon with an accumulated climb of 5200 m, and an Olympic triathlon for comparison. Blood samples were collected before, immediately after, and the day following the Norseman Xtreme Triatlon (n = 98) and Oslo Olympic Triathlon (n = 15). Increased levels of clinical significance were seen at the finish line of the Norseman in white blood cells count (WBC) (14.2 [13.5–14.9] 109/L, p < 0.001), creatinine kinase (CK) (2450 [1620–3950] U/L, p < 0.001) and NT-proBNP (576 [331–856] ng/L, p < 0.001). The following day there were clinically significant changes in CRP (39 [27–56] mg/L, p < 0.001) and Aspartate Aminotransferase (AST) (142 [99–191] U/L, p < 0.001). In comparison, after the Olympic triathlon distance, there were statistically significant, but less clinically important, changes in WBC (7.8 [6.7–9.6] 109/L, p < 0.001), CK (303 [182–393] U/L, p < 0.001) and NT-proBNP (77 [49–88] ng/L, p < 0.01) immediately after the race, and in CRP (2 [1–3] mg/L, p < 0.001) and AST (31 [26–41] U/L, p < 0.01) the following day. Subclinical changes were also observed in Hemoglobin, Thrombocytes, K+, Ca2+, Mg2+, Creatinine, Alanine Aminotransferase and Thyroxine after the Norseman. In conclusion, there were significant changes in biomarkers used in a clinical setting after the Norseman. Of largest clinical importance were clinically significant increased WBC, CRP, AST, CK and NT-proBNP after the Norseman. This is important to be aware of when athletes engaging in prolonged exercise events receive medical assistance or are hospitalised. [ABSTRACT FROM AUTHOR]

Purpose: Physiological tests may aid in diagnosing median arcuate ligament syndrome (MALS). MALS is a symptomatic compression of the celiac artery causing symptoms similar to chronic mesenteric ischemia (CMI) of atherosclerotic etiology. Simultaneous use of visible light spectroscopy (VLS) and laser doppler flowmetry (LDF) during upper endoscopy may detect microcirculatory changes in these patients.Patients and Methods: In a single-center, prospective comparative cohort, 25 patients were evaluated for MALS. Patients with a consensus diagnosis of MALS (n=15) underwent a gastroscopy assisted, transmucosal microcirculatory assessment with LDF and VLS. Results were compared to individuals with normal intestinal circulation (n=38) evaluated with duplex ultrasonography, and to patients with chronic mesenteric ischemia (n=32). Treatment response was evaluated clinically at 1, 3, 6, and 12 months, and with ultrasound, VLS and LDF at three months. Health-related quality of life (QoL) was assessed with Euroqol (EQ-5D-5L), preoperatively, and 12 months postoperatively.Results: Preoperative mean transmucosal oxygen saturation was significantly lower in patients with MALS (SO2 76±6), as compared to healthy individuals (SO2 81±4), p=0.02. An overall significant improvement in SO2 after surgical decompression of the celiac artery was found (SO2 81±3.7, p=0.05). Eleven (92%) patients with clinical improvement after laparoscopic decompression had a definitive diagnosis of MALS. Median follow-up was 18 months (4-24 months). Four of the five dimensions investigated with EQ-5D-5L improved.Conclusion: VLS detected a significantly lower baseline transmucosal SO2 in patients with MALS as compared to control subjects with normal intestinal circulation. An improvement in SO2 after laparoscopic decompression was found, supporting a possible ischemic etiology in our patient population. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to assess prevalence of left ventricular (LV) systolic and diastolic function in stable cohort of COPD patients, where LV disease had been thoroughly excluded in advance. Methods: 100 COPD outpatients in GOLD II-IV and 34 controls were included. Patients were divided by invasive mean pulmonary artery pressure (mPAP) in COPD-PH (≥25 mmHg) and COPD-non-PH (<25 mmHg), which was subdivided in mPAP ≤20 mmHg and 21–24 mmHg. LV myocardial performance index (LV MPI) and strain by tissue Doppler imaging (TDI) were used for evaluation of LV global and systolic function, respectively. LV MPI ≥0.51 and strain ≤-15.8% were considered abnormal. LV diastolic function was assessed by the ratio between peak early (E) and late (A) velocity, early TDI E´, E/E´, isovolumic relaxation time, and left atrium volume. Results: LV MPI ≥0.51 was found in 64.9% and 88.5% and LV strain ≤-15.8% in 62.2.% and 76.9% in the COPD-non-PH and COPD-PH patients, respectively. Similarly, LV MPI and LV strain were impaired even in patients with mPAP <20 mmHg. In multiple regression analyses, residual volume and stroke volume were best associated to LV MPI and LV strain, respectively. Except for isovolumic relaxation time, standard diastolic echo indices as E/A, E´, E/E´ and left atrium volume did not change from normal individuals to COPD-non-PH. Conclusions: Subclinical LV systolic dysfunction was a frequent finding in this cohort of COPD patients, even in those with normal pulmonary artery pressure. Evidence of LV diastolic dysfunction was hardly present as measured by conventional echo indices. [ABSTRACT FROM AUTHOR]

Objectives: To examine evidence of exercise‐induced bronchoconstriction (EIB) defined as ≥10% reduction in forced expiratory volume in one second (FEV1) and exercise‐induced arterial hypoxemia (EIAH) defined as ≥4% reduction in oxygen saturation (SpO2) from before to after participation in the Norseman Xtreme Triathlon. Secondarily, to assess whether changes in FEV1 and SpO2 are related to respiratory symptoms, training volume, and race time. Methods: In this quasi‐experimental non‐controlled study, we included 63 triathletes (50♂/13♀) aged 40.3 (±9.0) years (mean ± SD). Fifty‐seven (46♂/11♀) measured lung function and 54 (44♂/10♀) measured SpO2 before the race, 8‐10 minutes after the race (post‐test 1) and the day after the race (post‐test 2). Respiratory symptoms and training volume were recorded with modified AQUA questionnaire. ANOVA for repeated measures was used to detect differences in lung function and SpO2. Statistical significance was accepted at 0.05 level. Results: Twenty‐six participants (46%) presented with EIB at post‐test 1 and 16 (28%) at post‐test 2. Lung function variables were significantly reduced from baseline to post‐test 1 and 2. Thirty‐five participants (65%) showed evidence of mild to moderate EIAH. No significant correlations were observed except a weak correlation between maximal reduction in FEV1 and respiratory symptoms (r = 0.35, P =.016). Conclusion: Our results demonstrated that 46% of the participants presented with EIB and 65% showed evidence of EIAH after the Norseman Xtreme Triathlon. Changes in FEV1 and SpO2 were not correlated to weekly training hours or race time. We observed a weak correlation between maximal reduction in FEV1 and respiratory symptoms. [ABSTRACT FROM AUTHOR]

Low-carbohydrate-high-fat (LCHF) diets are efficient for weight loss, and are also used by healthy people to maintain bodyweight. The main aim of this study was to investigate the effect of 3-week energy-balanced LCHF-diet, with >75 percentage energy (E%) from fat, on glucose tolerance and lipid profile in normal weight, young, healthy women. The second aim of the study was to investigate if a bout of exercise would prevent any negative effect of LCHF-diet on glucose tolerance. Seventeen females participated, age 23.5 ± 0.5 years; body mass index 21.0 ± 0.4 kg/m2, with a mean dietary intake of 78 ± 1 E% fat, 19 ± 1 E% protein and 3 ± 0 E% carbohydrates. Measurements were performed at baseline and post-intervention. Fasting glucose decreased from 4.7 ± 0.1 to 4.4 mmol/L (p < 0.001) during the dietary intervention whereas fasting insulin was unaffected. Glucose area under the curve (AUC) and insulin AUC did not change during an OGTT after the intervention. Before the intervention, a bout of aerobic exercise reduced fasting glucose (4.4 ± 0.1 mmol/L, p < 0.001) and glucose AUC (739 ± 41 to 661 ± 25, p = 0.008) during OGTT the following morning. After the intervention, exercise did not reduce fasting glucose the following morning, and glucose AUC during an OGTT increased compared to the day before (789 ± 43 to 889 ± 40 mmol/L∙120min–1, p = 0.001). AUC for insulin was unaffected. The dietary intervention increased total cholesterol (p < 0.001), low-density lipoprotein (p ≤ 0.001), high-density lipoprotein (p = 0.011), triglycerides (p = 0.035), and free fatty acids (p = 0.021). In conclusion, 3-week LCHF-diet reduced fasting glucose, while glucose tolerance was unaffected. A bout of exercise post-intervention did not decrease AUC glucose as it did at baseline. Total cholesterol increased, mainly due to increments in low-density lipoprotein. LCHF-diets should be further evaluated and carefully considered for healthy individuals. [ABSTRACT FROM AUTHOR]

Background: The effect of statins over time on coronary atherosclerosis in patients with inflammatory joint diseases (IJD) is unknown. Our aim was to evaluate the change in coronary plaque morphology and volume in long-term statin-treated patients with IJD. Methods: Sixty-eight patients with IJD and carotid artery plaque(s) underwent coronary computed tomography angiography before and after a mean of 4.7 (range 4.0–6.0) years of statin treatment. The treatment target for low density lipoprotein cholesterol (LDL-c) was ≤1.8 mmol/L. Changes in plaque volume (calcified, mixed/soft and total) and coronary artery calcification (CAC) from baseline to follow-up were assessed using the 17-segment American Heart Association-model. Results: Median (IQR) increase in CAC after statin treatment was 38 (5–236) Agatston units (p<0.001). Calcified and total plaque volume increased with 5.6 (0.0–49.1) and 2.9 (0.0–23.5) mm3, respectively (p<0.001 for both). The median (IQR) change in soft/mixed plaque volume was -10 (-7.1–0.0), p = <0.001. Patients who had obtained the LDL-c treatment target at follow-up, experienced reduced progression of both CAC and total plaque volume compared to patients with LDL-c >1.8mmol/L (21 [2–143] vs. 69 [16–423], p = 0.006 and 0.65 [-1.0–13.9] vs. 13.0 [0.0–60.8] mm3, p = 0.019, respectively). Conclusions: A progression of total atherosclerotic plaque volume in statin-treated patients with IJD was observed. However, soft/mixed plaque volume was reduced, suggesting an alteration in plaque composition. Patients with recommended LDL-c levels at follow-up had reduced atherosclerotic progression compared to patients with LDL-c levels above the treatment target, suggesting a beneficial effect of treatment to guideline-recommended lipid targets in IJD patients. [ABSTRACT FROM AUTHOR]

Mucosal pathology due to chronic mesenteric ischemia (CMI) is rarely seen during upper endoscopy. Combining Laser Doppler Flowmetry (LDF) and Visible Light Spectroscopy (VLS) may aid in detection of CMI at an early stage. We aimed to investigate the utility of LDF and VLS in detecting microcirculatory changes in patients with CMI during upper endoscopy. In a single center, prospective study, 104 patients were evaluated for mesenteric ischemia during a 24 months period. Patients with a consensus diagnosis of CMI (n = 40) were examined with LDF and VLS. Thirty-two were successfully treated and had a definitive diagnosis of CMI. Results were compared with controls (n = 38) with normal intestinal circulation evaluated with duplex ultrasonography (DUS). Treatment response was evaluated clinically and with DUS at 1 month and with VLS and LDF at 3 months. A significant reduction in mucosal capillary hemoglobin oxygen saturation (SO2) was found in CMI patients compared to controls before treatment: mean ± SD: 67 ± 9%, 81 ± 4%, respectively (p < .001). A significant reduction was also seen for the relative hemoglobin (rHb) amount, flow and velocity (p < .001). The sensitivity of SO2 measured by VLS for diagnosing CMI was 94% and the specificity 72% (cut-off 78%), calculated with ROC curve analysis. A combination of SO2 and rHb increased the test sensitivity and specificity to 97% and 79%, respectively. Conclusion: CMI patients have significantly reduced microcirculation in the stomach and duodenum compared to controls. The results suggest that VLS should be included when performing an upper endoscopy in patients with suspected CMI. [ABSTRACT FROM AUTHOR]

Purpose: Respiratory variations in pulse pressure (dPP) and photoplethysmographic waveform amplitude (dPOP) are used for evaluation of volume status in mechanically ventilated patients. Amplification of intrathoracic pressure changes may enable their use also during spontaneous breathing. We investigated the association between the degree of hypovolemia and dPP and dPOP at different levels of two commonly applied clinical interventions; positive expiratory pressure (PEP) and continuous positive airway pressure (CPAP). Methods: 20 healthy volunteers were exposed to progressive hypovolemia by lower body negative pressure (LBNP). PEP of 0 (baseline), 5 and 10 cmH2O was applied by an expiratory resistor and CPAP of 0 (baseline), 5 and 10 cmH2O by a facemask. dPP was obtained non-invasively with the volume clamp method and dPOP from a pulse oximeter. Central venous pressure was measured in 10 subjects. Associations between changes were examined using linear mixed-effects regression models. Results: dPP increased with progressive LBNP at all levels of PEP and CPAP. The LBNP-induced increase in dPP was amplified by PEP 10 cmH20. dPOP increased with progressive LBNP during PEP 5 and PEP 10, and during all levels of CPAP. There was no additional effect of the level of PEP or CPAP on dPOP. Progressive hypovolemia and increasing levels of PEP were reflected by increasing respiratory variations in CVP. Conclusion: dPP and dPOP reflected progressive hypovolemia in spontaneously breathing healthy volunteers during PEP and CPAP. An increase in PEP from baseline to 10 cmH2O augmented the increase in dPP, but not in dPOP. [ABSTRACT FROM AUTHOR]

Objective: To investigate the association between sympathetic activity, reactive hyperemia and brachial artery flow-mediated dilation (FMD). Background: It is claimed that major surgery has an impact on endothelial function, as observed by post-operative reduced brachial artery FMD response. However, another explanation for the observed reduced FMD response post-operatively may be sympathetic stress-induced reduction in blood flow. Methods: Seventeen healthy volunteers with a median age (25th-75th percentiles) of 23.5 (23–24.8) years were recruited. Participants’ brachial blood flow and FMD response were measured (i) during normal non-stress conditions (Normal1); (ii) during exposure to ice water; and (iii) afterwards, under normal non-stress conditions (Normal2). We continuously measured arterial blood pressure (Finometer), heart rate (ECG), skin blood flow of the index finger (laser Doppler), and brachial artery blood flow and diameter (Ultrasound Doppler). Measurements were taken at baseline; before a 5-min suprasystolic forearm occlusion; and following a 3-min post-occlusion, to measure reactive hyperemia and FMD. Results: Median (25th-75th percentiles) FMD response after exposure to ice water was reduced compared to non-stress conditions [4.9 (2.9–8.4) % during ice water vs. 9.7 (7.6–12.2) % Normal1 and 9.7 (6.4–10.3) % Normal2, P < 0.001]. Blood flow 60 s after cuff-deflation during ice water exposure was significantly reduced to 328 (289–421) mL compared to non-stress conditions (both P < 0.05). No differences were observed between Normal1 [446 (359–506) mL] and Normal2 [455 (365–515) mL] (both P > 0.05). Heart rate significantly increased during ice water exposure [67 (59–69) beats/min)] compared to 55 (49–60) beats/min during Normal1 and 54 (47–60) beats/min during Normal2 (both P < 0.05). MAP did not change during Normal1 [72 (64–84)] or during Normal2 [71 (65–81) mm Hg] (both P > 0.05), but increased to 86 (75–98) mm Hg during ice water exposure (P < 0.05). Conclusions: Increased sympathetic activity resulted in decreased blood flow and brachial artery FMD response in healthy volunteers, independent of endothelial dysfunction. Future studies should adjust for blood flow when interpreting the FMD response. [ABSTRACT FROM AUTHOR]

Reductions in cerebral oxygen saturation (ScO2) measured by near infra-red spectroscopy have been found during compensated hypovolemia in the lower body negative pressure (LBNP)-model, which may reflect reduced cerebral blood flow. However, ScO2 may also be contaminated from extracranial (scalp) tissues, mainly supplied by the external carotid artery (ECA), and it is possible that a ScO2 reduction during hypovolemia is caused by reduced scalp, and not cerebral, blood flow. The aim of the present study was to explore the associations between blood flow in precerebral arteries and ScO2 during LBNP-induced hypovolemia. Twenty healthy volunteers were exposed to LBNP 20, 40, 60 and 80 mmHg. Blood flow in the internal carotid artery (ICA), ECA and vertebral artery (VA) was measured by Doppler ultrasound. Stroke volume for calculating cardiac output was measured by suprasternal Doppler. Associations of changes within subjects were examined using linear mixed-effects regression models. LBNP reduced cardiac output, ScO2 and ICA and ECA blood flow. Changes in flow in both ICA and ECA were associated with changes in ScO2 and cardiac output. Flow in the VA did not change during LBNP and changes in VA flow were not associated with changes in ScO2 or cardiac output. During experimental compensated hypovolemia in healthy, conscious subjects, a reduced ScO2 may thus reflect a reduction in both cerebral and extracranial blood flow. [ABSTRACT FROM AUTHOR]

Increase in mean shear stress represents an important and potent hemodynamic stimulus to improve conduit artery endothelial function in humans. No previous study has examined whether fluctuations in shear rate patterns, without altering mean shear stress, impacts conduit artery endothelial function. This study examined the hypothesis that 30-min exposure to fluctuations in shear rate patterns, in the presence of unaltered mean shear rate, improves brachial artery flow-mediated dilation. Fifteen healthy men (27.3 ± 5.0 yr) completed the study. Bilateral brachial artery flow-mediated dilation was assessed before and after unilateral exposure to 30 min of intermittent negative pressure (10 s, -40mmHg; 7 s, 0 mmHg) to induce fluctuation in shear rate, while the contralateral arm was exposed to a resting period. Negative pressure significantly increased shear rate, followed by a decrease in shear rate upon pressure release (both P < 0.001). Across the 30-min intervention, mean shear rate was not different compared with baseline (P = 0.458). A linear mixed model revealed a significant effect of time observed for flow-mediated dilation (P = 0.029), with exploratory post hoc analysis showing an increase in the intervention arm (ΔFMD +2.0%, P = 0.008), but not in the contralateral control arm (ΔFMD +0.5%, P = 0.664). However, there was no effect for arm (P = 0.619) or interaction effect (P = 0.096). In conclusion, we found that fluctuations in shear patterns, with unaltered mean shear, improves brachial artery flow-mediated dilation. These novel data suggest that fluctuations in shear pattern, even in the absence of altered mean shear, represent a stimulus to acute change in endothelial function in healthy individuals. NEW & NOTEWORTHY Intermittent negative pressure applied to the forearm induced significant fluctuations in antegrade and retrograde shear rate, while mean shear was preserved relative to baseline. Our exploratory study revealed that brachial artery flow-mediated dilation was significantly improved following 30-min exposure to intermittent negative pressure. Fluctuations in blood flow or shear rate, with unaltered mean shear, may have important implications for vascular health; however, further research is required to identify the underlying mechanisms and potential long-term health benefits. [ABSTRACT FROM AUTHOR]

The purpose of the present study was to investigate muscle hypertrophy, strength, and myonuclear and satellite cell (SC) responses to high-frequency blood flow-restricted resistance exercise (BFRRE). Thirteen individuals [24 ± 2 yr (mean ± SD), 9 men] completed two 5-day blocks of 7 BFRRE sessions, separated by a 10-day rest period. Four sets of unilateral knee extensions to voluntary failure at 20% of one repetition maximum (1RM) were conducted with partial blood flow restriction (90-100 mmHg). Muscle samples obtained before, during, 3 days, and 10 days after training were analyzed for muscle fiber area (MFA), myonuclei, SC, and mRNA and miRNA expression. Muscle size was measured by ultrasonography and magnetic resonance imaging and strength with 1RM knee extension. With the first block of BFRRE, SC number increased in both fiber types (70%-80%, P < 0.05), whereas type I and II MFA decreased by 6 ± 7% and 15 ± 11% (P < 0.05), respectively. With the second block of training, muscle size increased by 6%-8%, whereas the number of SCs (type I: 80 ± 63%, type II: 147 ± 95%), myonuclei (type I: 30 ± 24%, type II: 31 ± 28%), and MFA (type I: 19 ± 19%, type II: 11 ± 19%) peaked 10 days after the second block of BFRRE, whereas strength peaked after 20 days of detraining (6 ± 6%, P < 0.05). Pax7- and p21 mRNA expression were elevated during the intervention, whereas myostatin, IGF1R, MyoD, myogenin, cyclinD1 and -D2 mRNA did not change until 3-10 days postintervention. High-frequency lowload BFRRE induced robust increases in SC, myonuclei, and muscle size but modest strength gains. Intriguingly, the responses were delayed and peaked 10-20 days after the training intervention, indicating overreaching. [ABSTRACT FROM AUTHOR]

Background: Intermittent negative pressure (INP) applied to the lower leg and foot increases foot perfusion in healthy volunteers. The aim of the present study was to describe the effects of INP to the lower leg and foot on foot macro- and microcirculation in patients with lower extremity peripheral arterial disease (PAD). Methods: In this experimental study, we analyzed foot circulation during INP in 20 patients [median (range): 75 (63-84yrs)] with PAD. One leg was placed inside an air-tight vacuum chamber connected to an INP-generator. During application of INP (alternating 10s of -40mmHg/7s of atmospheric pressure), we continuously recorded blood flow velocity in a distal foot artery (ultrasound Doppler), skin blood flow on the pulp of the first toes (laser Doppler), heart rate (ECG), and systemic blood pressure (Finometer). After a 5-min baseline sequence (no pressure), a 10-min INP sequence was applied, followed by 5-min post-INP (no pressure). To compare and quantify blood flow fluctuations between sequences, we calculated cumulative up-and-down fluctuations in arterial blood flow velocity per minute. Results: Onset of INP induced an increase in arterial flow velocity and skin blood flow. Peak blood flow velocity was reached 3s after the onset of negative pressure, and increased 46% [(95% CI 36–57), P<0.001] above baseline. Peak skin blood flow was reached 2s after the onset of negative pressure, and increased 89% (95% CI 48–130), P<0.001) above baseline. Cumulative fluctuations per minute were significantly higher during INP-sequences compared to baseline [21 (95% CI 12–30)cm/s/min to 41 (95% CI 32–51)cm/s/min, P<0.001]. Mean INP blood flow velocity increased significantly ~12% above mean baseline blood flow velocity [(6.7 (95% CI 5.2–8.3)cm/s to 7.5 (95% CI 5.9–9.1)cm/s, P = 0.03)]. Conclusion: INP increases foot macro- and microcirculatory flow pulsatility in patients with PAD. Additionally, application of INP resulted in increased mean arterial blood flow velocity. [ABSTRACT FROM AUTHOR]

In previous studies, Flow Mediated Dilation ( FMD) was used to study the effect of cardiac surgery on endothelial function. This study investigated the effect of on-pump cardiac surgery on FMD and reactive hyperemia. The FMD-response and reactive hyperemia were measured in 25 patients the morning before- and the first morning after cardiac surgery. Brachial artery diameter and blood flow were measured with ultrasound at baseline before 5 min occlusion of the blood flow to the forearm, and continuously for 3 min after release of the occlusion. An exponential wash-out model was fitted to the blood flow over time. Nineteen patients remained for final data analysis. Data are mean ± SEM. The FMD response was reduced after surgery from 3.3 ± 0.5% to 1.4 ± 0.6% ( P = 0.02). Max blood flow after cuff release was reduced from 342 ± 30 mL preoperatively to 305 ± 30 mL postoperatively ( P < 0.00) and fell toward baseline significantly quicker; preoperative half-life was 36 ± 2.4 sec. versus 29 ± 1.9 sec postoperatively ( P < 0.00). Resting blood flow was reduced from 84 ± 9 mL/min to 66 ± 9 mL/min, ( P < 0.00). Brachial artery baseline diameter was unaffected by coronary artery bypass surgery ( P = 0.3). The observed reduction in brachial artery FMD after surgery, by previous authors taken to represent endothelial dysfunction, may at least partly be due to reduced hyperemic flow postoperatively. In studies where FMD is measured on multiple occasions, flow data should also be included. Reduced postoperative blood flow to the arm may indicate regional differences in vascular resistance after cardiac surgery. [ABSTRACT FROM AUTHOR]