Reductions in baroreflex responsiveness have been thought to increase the prevalence of orthostatic hypotension in endurance trained athletes. To test this hypothesis, cardiovascular responses to orthostatic stress, cardiopulmonary and carotid baroreflex responsiveness, and the effect of cardiopulmonary receptor deactivation on carotid baroreflex responses were examined in 24 men categorized by maximal aerobic power (V02max) into one of three groups: high fit (HF, V0-2max=67.0±1.9 ml•kg^-1•min^-1), moderately fit (MF, V0-2max=50.9±1.4 ml•kg^-1•min^-1), and low fit (LF, V0-2max=38.9±1.5 ml•kg^-1•min^-1). Orthostatic stress was induced using lower body negative pressure (LBNP) at -5, -10, -15, -20, -35, and -50 torr. Cardiopulmonary baroreflex responsiveness was assessed as the slope of the relationship between forearm vascular resistance (FVR, strain gauge plethysmography) and central venous pressure (CVP, dependent arm technigue) during LBNP<-35 torr. Carotid baroreflex responsiveness was assessed as the change in heart rate (HR, electrocardiography) or mean arterial pressure (MAP, radial artery catheter) elicited by 600 msec pulses of neck pressure and neck suction (NP/NS) from +40 to -70 torr. Pressures were applied using a lead collar wrapped about the subjects' necks during held expiration. Stimulus response data were fit to a logistic model and the parameters describing the curve were compared using two-factor ANOVA. The reductions CVP, mean (MAP), systolic, and pulse pressures during LBNP were similar between groups (P<0.05). However, diastolic blood pressure increased during LBNP m all but the HF group. (P<0.05). The slope of the FVR/CVP relationship did not differ between groups, nor did the form of the carotid-cardiac baroreflex stimulus response curve change during LBNP. changes in HR elicited with NP/NS were not different between groups (£>0.05). The range of the MAP stimulus response curve, however, was significantly less in the HP group compared to either the MP or LF group (£<0.05). These data imply that carotid baroreflex control of HR is unaltered by endurance exercise training, but carotid baroreflex control of blood pressure is impaired significantly, predisposing athletes to faintness.

A research report submitted to the Faculty of Medicine, University of the Witwatersrand, in partial fulfilment of the requirements for the degree of Master of Science in Medicine in Applied Physiology. Johannesburg, 1997. / A post-exercise reduction in blood pressure (BP) may be the primary reason that athletes suffer from exerclse-assoclated collapse (EAC) at the end ot ultra-endurance running ever.s. Plasma volume decreases, possibly caused by dehydration, may be the cause of the decrease til blood pressure, In order to determine whether there is a correlation between plasma volume changes and the post-exercise BP drop, this study evaluated alterations in pre- and post-race blood pressures and changes in blood and plasma volumes, It found that compared to resting values, systolic, dlastollc and mean arterial blood pressures (mmHg) fell significantly from 119 ± 4, mean ± standard deviation, 74 ± 8, and 88 ± 5 respectively to '106 ± 14, 62 ± 12 and 77 ± 10 (ps 0,05), whereas pulse pressure failed to change, Compared to pre-race values, plasma and blood volume were found not to have changed significantly, During the race plasma urea (U) and creatinine (C) concentrations increased significantly, whereas body mass and body mass index both fell significantly. Haernatocrlt, haemoglobin, mean cell volume, red blood cell number, mean cell haemoglobin concentration, the mean cell haemoglobin, plasma sodium, potassium, chloride and protein concentrations, the U:C ratio and osmolality remained constant. There were no significClnt correlations between changes in plasma or blood volume and changes in blood pressure, These data support the Idea that a post-race decrease in blood pressure does not result primarily from an intravascular fluid loss, It is likely therefore that athletes who collapse at the end of ultraendurance races due to EAC do so as a result of 'post-exercise hypotension' secondary to venous pooling, and not as a result of a reduction in plasma volume, / MT2017

The response of the circulatory system to gravity and hydrostatic forces has been well studied, for example the hydrostatic indifferent point (the location at which pressure does not change with posture) of the venous system has been established to be an important determinant of orthostatic responses and it has been found to be located near the diaphragm. However, the role of the abdomen has been less researched; for example, it appears that the concept that the abdominal compartment may have its own hydrostatic indifferent point has been overlooked. The goal of the present study was to establish the location of the abdominal hydrostatic indifferent point (HIPab) and to test the hypothesis that binding of the lower abdomen would shift the location of the HIPab cranially. Intra-abdominal pressure was measured using a modified wick needle technique in the supine and upright posture before and after binding of the lower abdomen in 7 anesthetized rats. In the unbound condition, the HIPab was located 5.2 ± 0.3 cm caudal to the xyphoid, meaning the hepatic veins were exposed to relatively large negative interstitial pressures during head-up tilt. Binding of the lower abdomen significantly (p <0.05) shifted the HIPab cranially by 1.7 cm. Thus, the relatively caudal location of the HIPab causes a relatively large hepatic transmural pressure owing to the fall in interstitial pressure during upright posture. The cranial shift of the HIPab by binding of the lower abdomen lessens the fall in hepatic extramural pressure and thereby protects the hepatic veins from distension.

Orthostatic vasovagal syncope is the sudden loss of consciousness resulting from a temporary impairment of cerebral blood flow, within approximately an hour of standing. Patients who suffer from this problem have "vasovagal syndrome". The purpose of this thesis was to devise a method to detect the syndrome following the assumption of upright position. Data from 106 syncopal patients undergoing head-up tilt table testing (HUT) were acquired, including electrical activity of the heart (electrocardiogram), blood pressure, oxygen saturation, and cerebral perfusion parameters from near-infrared spectroscopy (NIRS). The data set was examined with the aim of generating automatic diagnoses. Comparison of the rate-pressure product (blood pressure multiplied by heart rate) during the time of syncope with a recommended threshold, in addition to comparison with monitoring the fall of systolic blood pressure during prolonged tilt, yielded an 84% accuracy rate for vasovagal syndrome. The thesis reviewed the techniques used on the aforementioned time series by previous researchers, emphasising the concepts underlying "time-frequency analysis", a method for analysing nonstationary signals. Since even healthy patients experience time-varying frequency information in their haemodynamics, a transform known as the Smoothed Pseudo-Wigner Ville Distribution (SPWVD) is well suited to their analysis. This distribution was applied to RR tachograms, plots of heart period against time. After the smoothing parameters of the SPWVD were chosen based on artificial data, the optimised transform was then applied to a second artificial tachogram to calculate the LF/HF (low- to high-frequency) ratio, an indicator of heart rate variability. The computed LF/HF ratio tracked the expected value within an error margin of 3.6%. Finally, by applying the same transform to clinical data, it was proved to offer better resolution than an alternative known as the Lomb periodogram. Classical techniques from the literature predicting vasovagal syncope were found to fail on the current data set: out of 29 tests, only two yielded statistically significant differences between the two patient groups. These were compared with the author's time-frequency analysis of RR tachograms, linear regression of heart rate, and examination of NIRS oscillations and changes on tilt. Of these, the ICFV during time period P3 was found to perform best (negative predictive value: 0.86). A linear classifier was used to combine the best four predictors; it achieved an overall accuracy of 0.88. Following the data-driven approach, an analytical modelling approach was undertaken. In order to define an appropriate model that traded off simplicity with comprehensiveness, the mechanisms of vasovagal syncope were reviewed. A model of orthostasis was developed, validated, and used toward parameter estimation from patient data. Three parameters (baroreceptor operating point, cardiac effectiveness, and baroreflex gain) were gleaned from the supine baseline recording to "normalise" the model for a given patient, before four new parameters (sympathetic and parasympathetic gains at the sino-atrial node, peripheral vasoconstriction gain, and total blood volume) were estimated from the data collected in the upright position. The expectation was that this approach would improve feature extraction (and hence prediction accuracy) as well as the clinical interpretation of the results. However, the modelling approach was found to offer no significant improvement upon the data-driven signal processing results: a linear classifier on the four post-tilt parameters yielded a negative predictive value of just 0.69. This result may have been due to inaccuracies in the time series data owing to instrumentation error. It is also possible that the modelling approach was not able to provide the quality of feature extraction necessary for predicting vasovagal syncope in the elderly. Finally, methods to predict syncope during mid- to late HUT were examined. Using information derived from heart rate and baroreflex sensitivity, a technique was developed to ease patient comfort by terminating the test approximately 2 minutes before syncope was expected to occur.

Cardiovascular and hormonal responses to +700 head-up tilt (HUT: orthostatic challenge) were compared between six endurance exercise trained (ET) and six untrained (UT) subjects prior to and immediately following 4 hours of -60 head-down rest (HDR). The ET subjects showed a significant (P < 0.05) decrease in orthostatic tolerance time (pre syncopal symptoms) during post-HDR HUT, while no difference was observed between ET and UT groups in pre-HDR HUT. The volume regulatory hormonal responses were similar between ET and UT groups whether during HUT or HDR. The pre-syncopal subjects had a greater increase in plasma arginine vasopressin and less increase in plasma renin activity and plasma aldosterone during HUT than was observed in non syncopal subjects. These data suggest that HDR deconditioning was more effective in the ET subjects.

A descriptive study was conducted comparing the blood pressure and heart rate responses to position change among hypovolemic and normovolemic subjects. A convenience sample of 32 men and women from an emergency room with complaints of diarrhea, vomiting, vaginal or rectal bleeding for $\ge$12 hours duration were recruited. The normovolemic group consisted of a convenience sample of 30 men and women from the community. Data analysis included a mixed design analysis of variance. Compared to supine baseline measurements, between group changes in the systolic, diastolic, and mean arterial blood pressure were not statistically significant (p $>$.05). Once the subject stood, heart rate increased statistically significant in both groups (p $<$.05). The data suggest orthostatic hypotension can be considered when the supine resting heart rate is $\ge$87 beats per minute, and if upon standing, heart rate increases by $\ge$19.33 or is $\ge$110 beats per minute. Heart rate measurements should be taken at one minute after standing.

Persons with chronic fatigue syndrome (CFS) often complain of an inability to maintain activity levels and experience a variety of orthostatic symptoms such as dizziness, trembling, nausea, postural hypotension with bradycardia or tachycardia, sweating, palpitations, paleness, and syncope. Orthostatic intolerance (OI) may be defined as an inability to maintain systolic blood pressure (SBP) within 20 mmHg of resting level upon moving from a supine to upright posture. The primary objective of this study is to determine whether men and women with CFS are more susceptible to OI during a 3-stage head-up tilt (HUT) than non CFS, sedentary subjects matched by age, sex, and ethnicity. The secondary objective is to examine whether possible underlying mechanisms may be predictively associated with OI susceptibility in CFS. Possible causes of OI include autonomic nervous system (ANS) dysfunction and altered hematological profile. Thus, specific aims included within this objective are: 1) to determine whether there are differences in resting cardiovascular function {i.e., blood pressure [BP], heart rate [HR], stroke volume [SV], cardiac output [CO], total peripheral resistance [TPR], and contractility [i.e., ejection fraction (EF), fractional shortening (FS), and the velocity of circumferential shortening corrected by HR (VCFc)]}, ANS function {i.e., beta1-, beta2-, and alpha-receptor sensitivities, baroreceptor sensitivity [BRS], and vagal function [i.e., respiratory sinus arrhythmia (RSA), RSA envelope (RSAE), high frequency (HF) spectral component, and HR range]}, and hematological profile [i.e., red blood cell volume (RBCV), plasma volume (PBV), and total blood volume (TBV)] between CFS and non-CFS groups; and 2) to determine whether cardiovascular, ANS, and hematological measures differentially predicted OI during HUT. The results indicate that OI susceptibility does not occur with greater prevalence in persons with CFS than non-CFS sedentary persons. However, power analyses revealed that with a much larger sample size group differences in OI susceptibility would be found. The CFS group was distinguished from the control group only by differences in blood volume measures. There appears to be no substantive group differences in a range of cardiovascular and ANS measures; moreover, none of these measures, including the blood volume measures, accounted for differences in OI susceptibility. Compensatory mechanisms may be present in CFS for the diminished blood volume that could explain the lack of group differences in OI susceptibility. In addition, future research may find some clues relevant to CFS pathophysiology in the assessment of hemodynamic responses during orthostatic challenge in the present subjects.

Sensations of dizziness or fainting (pre-syncope or syncope) on standing up from a lying or a seated position are usually associated with impaired blood pressure regulation leading to inadequate perfusion of the brain. The purpose of this project was to develop a simple method to provide scientists and doctors a convenient way to monitor cardiovascular control during orthostatic stress with the non-invasive FinometerTM device. This apparatus provides a continuous estimate of arterial blood pressure (BP) contour from the finger and computes brachial blood pressure contours (systolic (SBP) and diastolic (DBP) blood pressure), heart rate (HR), stroke volume and cardiac output (Q) from the Modelflow equation. In this thesis, a method was implemented to obtain an estimate of central venous pressure (CVP) to provide greater insight into cardiovascular control. The accuracy and potential errors resulting from measurement of finger arterial pressure were also evaluated. The thesis first examined whether key variables essential to monitor cardiovascular control can be reliably measured by the FinometerTM in comparison to independent methods. HR was accurate and precise at rest and during stress (difference between methods: 0.05± 0.18 beats/min). According to standards established by the American Association for the Advancement of Medical Instrumentation (AAMI); at rest, DBP was accurate but not precise (1.6± 8.8 mmHg) and SBP was not accurate but precise (14.2± 8.0 mmHg). These errors could be due to an improper use of our reference method. The post-test correction for individual characteristics proposed by the FinometerTM developers did improve overall Q estimation (0.255± 0.441 L/min (6.9%) instead of 0.797± 0.441 L/min (22.4%)) when compared with Doppler ultrasound but did not account for the increasing error with a greater orthostatic stress induced by lower body negative pressure. Using finger BP instead of aortic BP to calculate Q did not explain this error as revealed by a new approach that compared the simultaneous pulse contours from different methods. Indeed, there was no significant difference between the error of the estimation of Q from the finger arterial pulse compared to the estimation of Q from the independent measurement by tonometry on the brachial artery at rest (-1.13± 14.67%) and at the maximum orthostatic stress used (-0.61± 9.33%) (p>0.05). Using brachial BP to calculate Q did not improve the result found with finger BP. The first hypothesis of this thesis that CVP could be estimated from outputs of the FinometerTM compared to direct venous pressure measurement was supported for the individual (0.2± 1.7 mmHg) and test specific (0.1± 1.2 mmHg) equations. The general equations derived from group data were accurate but not precise enough (0.4± 2.8 mmHg) to be used in clinical and research setting. The success of the individual equations suggests that it might be possible to derive a personal equation that will be useful over a long period for similar tests by using a catheter only once. The second and third hypotheses related to the cause of discrepancy between Q from FinometerTM and Q from Doppler, were not supported by the data. However, a new contour analysis method introduced here in a graphical format might provide an opportunity for systematic analyses of the deviation between methods. It could reveal sources of error allowing future improvements in the accuracy and precision of Q from FinometerTM during orthostatic or physical stress.

Sensations of dizziness or fainting (pre-syncope or syncope) on standing up from a lying or a seated position are usually associated with impaired blood pressure regulation leading to inadequate perfusion of the brain. The purpose of this project was to develop a simple method to provide scientists and doctors a convenient way to monitor cardiovascular control during orthostatic stress with the non-invasive FinometerTM device. This apparatus provides a continuous estimate of arterial blood pressure (BP) contour from the finger and computes brachial blood pressure contours (systolic (SBP) and diastolic (DBP) blood pressure), heart rate (HR), stroke volume and cardiac output (Q) from the Modelflow equation. In this thesis, a method was implemented to obtain an estimate of central venous pressure (CVP) to provide greater insight into cardiovascular control. The accuracy and potential errors resulting from measurement of finger arterial pressure were also evaluated. The thesis first examined whether key variables essential to monitor cardiovascular control can be reliably measured by the FinometerTM in comparison to independent methods. HR was accurate and precise at rest and during stress (difference between methods: 0.05± 0.18 beats/min). According to standards established by the American Association for the Advancement of Medical Instrumentation (AAMI); at rest, DBP was accurate but not precise (1.6± 8.8 mmHg) and SBP was not accurate but precise (14.2± 8.0 mmHg). These errors could be due to an improper use of our reference method. The post-test correction for individual characteristics proposed by the FinometerTM developers did improve overall Q estimation (0.255± 0.441 L/min (6.9%) instead of 0.797± 0.441 L/min (22.4%)) when compared with Doppler ultrasound but did not account for the increasing error with a greater orthostatic stress induced by lower body negative pressure. Using finger BP instead of aortic BP to calculate Q did not explain this error as revealed by a new approach that compared the simultaneous pulse contours from different methods. Indeed, there was no significant difference between the error of the estimation of Q from the finger arterial pulse compared to the estimation of Q from the independent measurement by tonometry on the brachial artery at rest (-1.13± 14.67%) and at the maximum orthostatic stress used (-0.61± 9.33%) (p>0.05). Using brachial BP to calculate Q did not improve the result found with finger BP. The first hypothesis of this thesis that CVP could be estimated from outputs of the FinometerTM compared to direct venous pressure measurement was supported for the individual (0.2± 1.7 mmHg) and test specific (0.1± 1.2 mmHg) equations. The general equations derived from group data were accurate but not precise enough (0.4± 2.8 mmHg) to be used in clinical and research setting. The success of the individual equations suggests that it might be possible to derive a personal equation that will be useful over a long period for similar tests by using a catheter only once. The second and third hypotheses related to the cause of discrepancy between Q from FinometerTM and Q from Doppler, were not supported by the data. However, a new contour analysis method introduced here in a graphical format might provide an opportunity for systematic analyses of the deviation between methods. It could reveal sources of error allowing future improvements in the accuracy and precision of Q from FinometerTM during orthostatic or physical stress.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1940. / Typescript. Includes abstract and vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves [27]-[28]).