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Dynamic cerebral autoregulation (CA) is challenged by exercise and may become less effective when exercise is exhaustive. Exercise may increase arterial glucose concentration, and we evaluated whether the cerebrovascular response to exercise is affected by hyperglycemia. The effects of a hyperinsulinemic euglycemic clamp (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRI) and systemic vascular resistance index (SVRI) responses were evaluated in seven healthy subjects at rest and during rhythmic handgrip exercise. Transfer function analysis of the dynamic relationship between beat-to-beat changes in mean arterial pressure and middle cerebral artery (MCA) mean blood flow velocity ([V.sub.mean]) was used to assess dynamic CA. At rest, SVRI decreased with HY and EU (P < 0.01). CVRI was maintained with EU but became reduced with HY [11% (SD 3); P < 0.01], and MCA [V.sub.mean] increased (P < 0.05), whereas brain catecholamine uptake and arterial [PCO.sub.2] did not change significantly. HY did not affect the normalized low-frequency gain between mean arterial pressure and MCA [V.sub.mean] or the phase shift, indicating maintained dynamic CA. With HY, the increase in CVRI associated with exercise was enhanced (19 [+ or -] 7% vs. 9 [+ or -] 7%; P < 0.05), concomitant with a larger increase in heart rate and cardiac output and a larger reduction in SVRI (22 [+ or -] 4% vs. 14 [+ or -] 2%; P < 0.05). Thus hyperglycemia lowered cerebral vascular tone independently of CA capacity at rest, whereas dynamic CA remained able to modulate cerebral blood flow around the exercise-induced increase in MCA [V.sub.mean]. These findings suggest that elevated blood glucose does not explain that dynamic CA is affected during intense exercise. cerebral autoregulation; cardiac output; human; vascular tone doi:10.1152/ajpheart.00045.2007

Postural stress requires immediate autonomic nervous action to maintain blood pressure. We determined time-domain cardiac baroreflex sensitivity (BRS) and time delay ([tau]) between systolic blood pressure and interbeat interval variations during stepwise changes in the angle of vertical body axis ([alpha]). The assumption was that with increasing postural stress, BRS becomes attenuated, accompanied by a shift in -r toward higher values. In 10 healthy young volunteers, [alpha] included 20 degrees head-down tilt (-20[degrees]), supine (0[degrees]), 30 and 70 degrees head-up tilt (30[degrees], 70[degrees]), and free standing (90[degrees]). Noninvasive blood pressures were analyzed over 6-min periods before and after each change in [alpha]. The BRS was determined by frequency-domain analysis and with xBRS, a cross-correlation time-domain method. On average, between 28 (-20[degrees]) to 45 (90[degrees]) xBRS estimates per minute became available. Following a change in [alpha], xBRS reached a different mean level in the first minute in 78% of the cases and in 93% after 6 min. With increasing [alpha], BRS decreased: BRS = -10.1-sin([alpha]) + 18.7 ([r.sup.2] = 0.99) with tight correlation between xBRS and cross-spectral gain ([r.sup.2] ~ 0.97). Delay [tau] shifted toward higher values. In conclusion, in healthy subjects the sensitivity of the cardiac baroreflex obtained from time domain decreases linearly with sin([tau]), and the start of baroreflex adaptation to a physiological perturbation like postural stress occurs rapidly. The decreases of BRS and reduction of short [tau] may be the result of reduced vagal activity with increasing [alpha]. blood pressure regulation; tilt; sequential and spectral analysis; vagal and sympathetic tone

Vasovagal syncope is the most common cause of transient loss of consciousness, and recurrent vasovagal fainting has a profound impact on quality of life. Physical countermaneuvers are applied as a means of tertiary prevention but have so far only proven useful at the onset of a faint. This placebo-controlled crossover study tested the hypothesis that leg crossing increases orthostatic tolerance. Nine naive healthy subjects [6 females, median age 25 yr (range 20-41 yr), mean body mass index 23 (SD 2)] were subjected to passive head-up tilt combined with a graded lower body negative pressure challenge (20, 40, and 60 mmHg) determining orthostatic tolerance thrice, in randomized order: 1) control, 2) with leg crossing, and 3) with oral placebo. Blood pressure (Finometer), heart rate, and changes in thoracic blood volume (impedance), stroke volume, and cardiac output (Modelflow) were followed during orthostatic stress. Primary outcome was time to presyncope (systolic blood pressure [less than or equal to] 85 mmHg, heart rate [greater than or equal to] 140 beats/min). With leg crossing, orthostatic tolerance increased from 26 [+ or -] 2 to 34 [+ ro -] 2 min (placebo 23 [+ or -] 3 min, P < 0.001). During leg crossing, mean arterial pressure (81 vs. 81 mmHg) and cardiac output (95 vs. 94% supine) remained unchanged; heart rate increase was lower (13 vs. 18 beats/min, P < 0.05); stroke volume was higher (79 vs. 74% supine, P < 0.05); and there was a trend toward lower thoracic impedance. Leg crossing increases orthostatic tolerance in healthy human subjects. As a measure of prevention, it is a worthwhile addition to the management of vasovagal syncope. blood pressure; lower body negative pressure; prevention; syncope

The first step to exercise is preceded by the required assumption of the upright body position, which itself involves physical activity. The gravitational displacement of blood from the chest to the lower parts of the body elicits a fall in central blood volume (CBV), which corresponds to the fraction of thoracic blood volume directly available to the left ventricle. The reduction in CBV and stroke volume (SV) in response to postural stress, post-exercise, or to blood loss results in reduced left ventricular filling, which may manifest as orthostatic intolerance. When termination of exercise removes the leg muscle pump function, CBV is no longer maintained. The resulting imbalance between a reduced cardiac output (CO) and a still enhanced peripheral vascular conductance may provoke post-exercise hypotension (PEH). Instruments that quantify CBV are not readily available and to express which magnitude of the CBV in a healthy subject should remains difficult. In the physiological laboratory, the CBV can be modified by making use of postural stressors, such as lower body "negative" or sub-atmospheric pressure (LBNP) or passive head-up tilt (HUT), while quantifying relevant biomedical parameters of blood flow and oxygenation. Several approaches, such as wearable sensors and advanced machine-learning techniques, have been followed in an attempt to improve methodologies for better prediction of outcomes and to guide treatment in civil patients and on the battlefield. In the recent decade, efforts have been made to develop algorithms and apply artificial intelligence (AI) in the field of hemodynamic monitoring. Advances in quantifying and monitoring CBV during environmental stress from exercise to hemorrhage and understanding the analogy between postural stress and central hypovolemia during anesthesia offer great relevance for healthy subjects and clinical populations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Transcatheter aortic valve implantation (TAVI) is a minimally invasive, life‐saving treatment for patients with severe aortic valve stenosis that improves quality of life. We examined cardiac output and cerebral blood flow in patients undergoing TAVI to test the hypothesis that improved cardiac output after TAVI is associated with an increase in cerebral blood flow. DESIGN: Prospective cohort study. SETTING: European high‐volume tertiary multidisciplinary cardiac care. PARTICIPANTS: Thirty‐one patients (78.3 ± 4.6 years; 61% female) with severe symptomatic aortic valve stenosis. MEASUREMENTS: Noninvasive prospective assessment of cardiac output (L/min) by inert gas rebreathing and cerebral blood flow of the total gray matter (mL/100 g per min) using arterial spin labeling magnetic resonance imaging in resting state less than 24 hours before TAVI and at 3‐month follow‐up. Cerebral blood flow change was defined as the difference relative to baseline. RESULTS: On average, cardiac output in patients with severe aortic valve stenosis increased from 4.0 ± 1.1 to 5.4 ± 2.4 L/min after TAVI (P =.003). The increase in cerebral blood flow after TAVI strongly varied between patients (7% ± 24%; P =.41) and related to the increase in cardiac output, with an 8.2% (standard error = 2.3%; P =.003) increase in cerebral blood flow per every additional liter of cardiac output following the TAVI procedure. CONCLUSION: Following TAVI, there was an association of increase in cardiac output with increase in cerebral blood flow. These findings encourage future larger studies to determine the influence of TAVI on cerebral blood flow and cognitive function. [ABSTRACT FROM AUTHOR]

Keywords: oxygen consumption; regulation of skeletal muscle mass; Parkinson's disease and autonomic function; artificial intelligence & hemodynamic monitoring; arterial thrombosis & exercise; atrial fibrillation & cognitive decline; breath-hold diving; T2DM & cerebral perfusion/sympathetic control EN oxygen consumption regulation of skeletal muscle mass Parkinson's disease and autonomic function artificial intelligence & hemodynamic monitoring arterial thrombosis & exercise atrial fibrillation & cognitive decline breath-hold diving T2DM & cerebral perfusion/sympathetic control 1 3 3 02/10/22 20220208 NES 220208 In 1993 the Swedish physiologist Björn Folkow (1921-2012) wrote " I .. in humans, it is particularly difficult to differentiate between manifestations of aging per se and symptoms of morbidity, especially at higher ages when morbidity is common i " (Folkow and Svanborg, [2]). Exercise training is a well-recognized tool in the management of T2D due to its many cardiometabolic benefits, however T2D may negatively affect cardiovascular responses to exercise. Oxygen consumption, regulation of skeletal muscle mass, Parkinson's disease and autonomic function, artificial intelligence & hemodynamic monitoring, arterial thrombosis & exercise, atrial fibrillation & cognitive decline, T2DM & cerebral perfusion/sympathetic control, breath-hold diving. [Extracted from the article]

The human brain is constantly active and even small limitations to cerebral blood flow (CBF) may be critical for preserving oxygen and substrate supply, e.g., during exercise and hypoxia. Exhaustive exercise evokes a competition for the supply of oxygenated blood between the brain and the working muscles, and inability to increase cardiac output sufficiently during exercise may jeopardize cerebral perfusion of relevance for diabetic patients. The challenge in diabetes care is to optimize metabolic control to slow progression of vascular disease, but likely because of a limited ability to increase cardiac output, these patients perceive aerobic exercise to be more strenuous than healthy subjects and that limits the possibility to apply physical activity as a preventive lifestyle intervention. In this review, we consider the effects of functional activation by exercise on the brain and how it contributes to understanding the control of CBF with the limited exercise tolerance experienced by type 2 diabetic patients. Whether a decline in cerebral oxygenation and thereby reduced neural drive to working muscles plays a role for "central" fatigue during exhaustive exercise is addressed in relation to brain's attenuated vascular response to exercise in type 2 diabetic subjects. [ABSTRACT FROM AUTHOR]

Heart rate (HR) has an impact on the central blood pressure (BP) wave shape and is related to pulse wave velocity and therefore to timing and duration of systole and diastole. This study tested the hypothesis that in healthy subjects both in rest and during sympathetic stimulation the relation between HR and pulse pressure (PP) is described by a linear effect model. Forty-four healthy volunteers were subjected to sympathetic stimulation by continuous lower body negative pressure (LBNP) until the onset of pre-syncopal symptoms. Changes in PP and HR were tracked non-invasively and modeled by linear mixed effect (LME) models. The dataset was split into two groups: the first was used for creating a model and the second for its evaluation. Models were created on the data obtained during LBNP. Model performance was expressed as absolute median error (1st; 3rd quantiles) and bias with limits of agreement (LOA) between modeled and measured PP. From rest to sympathetic stimulation, mean BP was maintained while HR increased (∼30%) and PP decreased gradually (∼20%). During baseline, PP could be modeled with an absolute error of 6 (4; 10) mm Hg and geometric mean ratio of the bias was 0.97 (LOA: 0.8-1.1). During LBNP, absolute median model error was 5 (4; 8) mmHg with geometric mean ratio 1.02 (LOA: 0.8-1.3). In conclusion, both during rest and during sustained sympathetic outflow induced by progressive central hypovolemia, a LME model of HR provides for an estimate of PP in healthy young adults. [ABSTRACT FROM AUTHOR]

Introduction: In the initial phase of hypovolemic shock, mean blood pressure (BP) is maintained by sympathetically mediated vasoconstriction rendering BP monitoring insensitive to detect blood loss early. Late detection can result in reduced tissue oxygenation and eventually cellular death. We hypothesized that a machine learning algorithm that interprets currently used and new hemodynamic parameters could facilitate in the detection of impending hypovolemic shock. Method: In 42 (27 female) young [mean (sd): 24 (4) years], healthy subjects central blood volume (CBV) was progressively reduced by application of -50 mmHg lower body negative pressure until the onset of pre-syncope. A support vector machine was trained to classify samples into normovolemia (class 0), initial phase of CBV reduction (class 1) or advanced CBV reduction (class 2). Nine models making use of different features were computed to compare sensitivity and specificity of different non-invasive hemodynamic derived signals. Model features included: volumetric hemodynamic parameters (stroke volume and cardiac output), BP curve dynamics, near-infrared spectroscopy determined cortical brain oxygenation, end-tidal carbon dioxide pressure, thoracic bio-impedance, and middle cerebral artery transcranial Doppler (TCD) blood flow velocity. Model performance was tested by quantifying the predictions with three methods: sensitivity and specificity, absolute error, and quantification of the log odds ratio of class 2 vs. class 0 probability estimates. Results: The combination with maximal sensitivity and specificity for classes 1 and 2 was found for the model comprising volumetric features (class 1: 0.73-0.98 and class 2: 0.56-0.96). Overall lowest model error was found for the models comprising TCD curve hemodynamics. Using probability estimates the best combination of sensitivity for class 1 (0.67) and specificity (0.87) was found for the model that contained the TCD cerebral blood flow velocity derived pulse height. The highest combination for class 2 was found for the model with the volumetric features (0.72 and 0.91). Conclusion: The most sensitive models for the detection of advanced CBV reduction comprised data that describe features from volumetric parameters and from cerebral blood flow velocity hemodynamics. In a validated model of hemorrhage in humans these parameters provide the best indication of the progression of central hypovolemia. [ABSTRACT FROM AUTHOR]

An association between cerebral blood flow ( CBF) and cardiac output ( CO) has been established in young healthy subjects. As of yet it is unclear how this association evolves over the life span. To that purpose, we continuously recorded mean arterial pressure ( MAP; finger plethysmography), CO (pulse contour; CO-trek), mean blood flow velocity in the middle cerebral artery ( MCAV; transcranial Doppler ultrasonography), and end-tidal CO2 partial pressure (Pet CO2) in healthy young (19-27 years), middle-aged (51-61 years), and elderly subjects (70-79 years). Decreases and increases in CO were accomplished using lower body negative pressure and dynamic handgrip exercise, respectively. Aging in itself did not alter dynamic cerebral autoregulation or cerebrovascular CO2 reactivity. A linear relation between changes in CO and MCAVmean was observed in middle-aged ( P < 0.01) and elderly ( P = 0.04) subjects but not in young ( P = 0.45) subjects, taking concurrent changes in MAP and Pet CO2 into account. These data imply that with aging, brain perfusion becomes increasingly dependent on CO. [ABSTRACT FROM AUTHOR]

Lower-body negative pressure (LBNP) has been proposed as a MRI-compatible surrogate for orthostatic stress. Although the effects of LBNP on cerebral hemodynamic behavior have been considered to reflect those of orthostatic stress, a direct comparison with actual orthostasis is lacking. We assessed the effects of LBNP (≤50 mmHg) vs. head-up tilt (HUT; at 70°) in 10 healthy subjects (5 female) on transcranial Doppler-determined cerebral blood flow velocity (CBFv) in the middle cerebral artery and cerebral perfusion pressure (CPP) as estimated from the blood pressure signal (finger plethysmography). CPP was maintained during LBNP but decreased after 2 min in response to HUT, leading to an ~15% difference in CPP between LBNP and HUT (P ≤ 0.020). Mean CBFv initially decreased similarly in response to LBNP and for HUT, but, from minute 3 on, the decline became ~50% smaller (P ≤ 0.029) during LBNP. The reduction in end-tidal PCO2 partial pressure (PETCO2) was comparable but with an earlier return toward baseline values in response to LBNP but not during HUT (P = 0.008). We consider the larger decrease in CBFv during HUT vs. LBNP attributable to the pronounced reduction in PETCO2 and to gravitational influences on CPP, and this should be taken into account when applying LBNP as an MRI-compatible orthostatic stress modality. [ABSTRACT FROM AUTHOR]

Renal hypoxia is thought to be an important pathophysiological factor in the progression of chronic kidney disease (CKD) and the associated hypertension. In a previous study among CKD patients, supplementation with 100% oxygen reduced sympathetic nerve activity (SNA) and lowered blood pressure (BP). We aimed to assess the underlying haemodynamic modulation and hypothesized a decreased systemic vascular resistance (SVR). To that end, 19 CKD patients were studied during 15-min intervals of increasing partial oxygen pressure (ppO2) from room air (0.21 ATA) to 1.0 ATA and further up to 2.4 ATA, while continuously measuring finger arterial blood pressure (Finapres). Off-line, we derived indexes of SVR, cardiac output (CO) and baroreflex sensitivity from the continuous BP recordings (Modelflow). During oxygen supplementation, systolic, and diastolic BP both increased dose-dependently from 128 ± 24 and 72 ± 19 mmHg respectively at baseline to 141 ± 23 (p < 0.001) and 80 ± 21 mmHg (p < 0.001) at 1.0 ATA oxygen. Comparing baseline and 1.0 ATA oxygen, SVR increased from 1440 ± 546 to 1745 ± 710 dyns/cm5 (p = 0.009), heart rate decreased from 60 ± 8 to 58 ± 6 bpm (p < 0.001) and CO from 5.0 ± 1.3 to 4.6 ± 1.1 L/min (p = 0.02). Baroreflex sensitivity remained unchanged (13ş13 to 15±12ms/mmHg). These blood pressure effects were absent in a negative control group of eight young healthy subjects. We conclude that oxygen supplementation in CKD patients causes a non-baroreflex mediated increased in SVR and blood pressure. [ABSTRACT FROM AUTHOR]

Blood pressure (BP) decreases in the first weeks after Roux-and-Y gastric bypass surgery. Yet the pathophysiology of the BP-lowering effects observed after gastric bypass surgery is incompletely understood. We evaluated BP, systemic hemodynamics, and baroreflex sensitivity in 15 obese women[mean age 42 ± 7 standard deviation (SD) yr, body mass index 45 ± 6 kg/m2] 2 wk before and 6 wk following Rouxand-Y gastric bypass surgery. Six weeks after gastric bypass surgery, mean body weight decreased by 13 ± 5 kg (10%, P < 0.001). Office BP decreased from 137 ± 10/86 ± 6 to 128± 12/81 ± 9 mmHg (P < 0.001, P < 0.01), while daytime ambulatory BP decreased from 128 ± 14/80 ± 9 to 114 ± 10/73 ± 6 mmHg (P = 0.01, P = 0.05), whereas nighttime BP decreased from 111 ± 13/66 ± 7 to 102 ± 9/ 62 ± 7 mmHg (P = 0.04, P < 0.01). The decrease in BP was associated with a 1.6 ± 1.2 l/min (20%, P < 0.01) decrease in cardiac output (CO), while systemic vascular resistance increased (153 ± 189 dyn·s·cm-5, 15%, P < 0.01). The maximal ascending slope in systolic blood pressure decreased (192 mmHg/s, 19%, P = 0.01), suggesting a reduction in left ventricular contractility. Baroreflex sensitivity increased from 9.0 [6.4-14.3] to 13.8 [8.5-19.0] ms/mmHg (median [interquartile range]; P < 0.01) and was inversely correlated with the reductions in heart rate (R=-0.64, P = 0.02) and CO (R=-0.61, P = 0.03). In contrast, changes in body weight were not correlated with changes in either BP or CO. The BP reduction following Roux-and-Y gastric bypass surgery is correlated with a decrease in CO independent of changes in body weight. The contribution of heart rate to the reduction in CO together with enhanced baroreflex sensitivity suggests a shift toward increased parasympathetic cardiovascular control. NEW & NOTEWORTHY The reason for the decrease in blood pressure (BP) in the first weeks after gastric bypass surgery remains to be elucidated. We show that the reduction in BP following surgery is caused by a decrease in cardiac output. In addition, the maximal ascending slope in systolic blood pressure decreased suggesting a reduction in left ventricular contractility and cardiac workload. These findings help to understand the physiological changes following gastric bypass surgery and are relevant in light of the increased risk of heart failure in these patients. [ABSTRACT FROM AUTHOR]