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Relevant bibliographies by topics / Orthostatic stress

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Academic literature on the topic 'Orthostatic stress'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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Journal articles on the topic "Orthostatic stress"

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Watenpaugh, Donald E., Deborah D. O'Leary, Suzanne M. Schneider, Stuart M. C. Lee, Brandon R. Macias, Kunihiko Tanaka, Richard L. Hughson, and Alan R. Hargens. "Lower body negative pressure exercise plus brief postexercise lower body negative pressure improve post-bed rest orthostatic tolerance." Journal of Applied Physiology 103, no. 6 (December 2007): 1964–72. http://dx.doi.org/10.1152/japplphysiol.00132.2007.

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Orthostatic intolerance follows actual weightlessness and weightlessness simulated by bed rest. Orthostasis immediately after acute exercise imposes greater cardiovascular stress than orthostasis without prior exercise. We hypothesized that 5 min/day of simulated orthostasis [supine lower body negative pressure (LBNP)] immediately following LBNP exercise maintains orthostatic tolerance during bed rest. Identical twins (14 women, 16 men) underwent 30 days of 6° head-down tilt bed rest. One of each pair was randomly selected as a control, and their sibling performed 40 min/day of treadmill exercise while supine in 53 mmHg (SD 4) [7.05 kPa (SD 0.50)] LBNP. LBNP continued for 5 min after exercise stopped. Head-up tilt at 60° plus graded LBNP assessed orthostatic tolerance before and after bed rest. Hemodynamic measurements accompanied these tests. Bed rest decreased orthostatic tolerance time to a greater extent in control [34% (SD 10)] than in countermeasure subjects [13% (SD 20); P < 0.004]. Controls exhibited cardiac stroke volume reduction and relative cardioacceleration typically seen after bed rest, yet no such changes occurred in the countermeasure group. These findings demonstrate that 40 min/day of supine LBNP treadmill exercise followed immediately by 5 min of resting LBNP attenuates, but does not fully prevent, the orthostatic intolerance associated with 30 days of bed rest. We speculate that longer postexercise LBNP may improve results. Together with our earlier related studies, these ground-based results support spaceflight evaluation of postexercise orthostatic stress as a time-efficient countermeasure against postflight orthostatic intolerance.

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Bronzwaer, Anne-Sophie G. T., Jasper Verbree, Wim J. Stok, Mat J. A. P. Daemen, Mark A. van Buchem, Matthias J. P. van Osch, and Johannes J. van Lieshout. "The cerebrovascular response to lower-body negative pressure vs. head-up tilt." Journal of Applied Physiology 122, no. 4 (April 1, 2017): 877–83. http://dx.doi.org/10.1152/japplphysiol.00797.2016.

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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 (CBF v) 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 CBF v 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 CBF v 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. NEW & NOTEWORTHY Lower-body negative pressure (LBNP) has the potential to serve as a MRI-compatible surrogate of orthostatic stress but a comparison with actual orthostasis was lacking. This study showed that the pronounced reduction in end-tidal Pco2 together with gravitational effects on the brain circulation lead to a larger decline in cerebral blood flow velocity in response to head-up tilt than during lower-body negative pressure. This should be taken into account when employing lower-body negative pressure as MRI-compatible alternative to orthostatic stress.

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Taylor, J. A., G. A. Hand, D. G. Johnson, and D. R. Seals. "Sympathoadrenal-circulatory regulation of arterial pressure during orthostatic stress in young and older men." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 5 (November 1, 1992): R1147—R1155. http://dx.doi.org/10.1152/ajpregu.1992.263.5.r1147.

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Our purpose was to test the hypothesis that human aging alters sympathoadrenal-circulatory control of arterial blood pressure during orthostasis. Plasma catecholamine and hemodynamic adjustments to two different forms of orthostatic stress, lower body suction (-10 to -50 mmHg) and standing, were determined in 14 young (26 +/- 1 yr) and 13 older (64 +/- 1) healthy, normally active men. During quiet supine rest, cardiac output tended to be lower and systemic vascular resistance higher in the older men, but no other differences were observed. On average, arterial blood pressure was well maintained during both forms of orthostasis in the two groups; the older men actually demonstrated better maintenance of pressure (P < 0.05) and a lesser incidence of orthostatic hypotension than the young men during lower body suction. Despite a blunted reflex tachycardia during orthostatic stress (P < 0.05), cardiac output tended to decrease less in the older men because of a smaller decline in stroke volume (P < 0.05, suction only), whereas the reflex increases in systemic vascular resistance were not different in the two groups. The whole forearm vasoconstrictor response tended to be attenuated in the older men during lower body suction, but was identical in the two groups with standing. Forearm skin vascular resistance was unaltered during lower body suction in both groups. Orthostasis-evoked increases in antecubital venous plasma norepinephrine concentrations were similar in the young and older men, whereas little or no increases in plasma epinephrine concentrations were observed in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

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Fu, Qi, Sarah Witkowski, Kazunobu Okazaki, and Benjamin D. Levine. "Effects of gender and hypovolemia on sympathetic neural responses to orthostatic stress." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 1 (July 2005): R109—R116. http://dx.doi.org/10.1152/ajpregu.00013.2005.

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We tested the hypothesis that women have blunted sympathetic neural responses to orthostatic stress compared with men, which may be elicited under hypovolemic conditions. Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in eight healthy young women and seven men in supine position and during 6 min of 60° head-up tilt (HUT) under normovolemic and hypovolemic conditions (randomly), with ∼4-wk interval. Acute hypovolemia was produced by diuretic (furosemide) administration ∼2 h before testing. Orthostatic tolerance was determined by progressive lower body negative pressure to presyncope. We found that furosemide produced an ∼13% reduction in plasma volume, causing a similar increase in supine MSNA in men and women (mean ± SD of 5 ± 7 vs. 6 ± 5 bursts/min; P = 0.895). MSNA increased during HUT and was greater in the hypovolemic than in the normovolemic condition (32 ± 6 bursts/min in normovolemia vs. 44 ± 15 bursts/min in hypovolemia in men, P = 0.055; 35 ± 9 vs. 45 ± 8 bursts/min in women, P < 0.001); these responses were not different between the genders (gender effect: P = 0.832 and 0.814 in normovolemia and hypovolemia, respectively). Total peripheral resistance increased proportionately with increases in MSNA during HUT; these responses were similar between the genders. However, systolic blood pressure was lower, whereas diastolic blood pressure was similar in women compared with men during HUT, which was associated with a smaller stroke volume or stroke index. Orthostatic tolerance was lower in women, especially under hypovolemic conditions. These results indicate that men and women have comparable sympathetic neural responses during orthostatic stress under normovolemic and hypovolemic conditions. The lower orthostatic tolerance in women is predominantly because of a smaller stroke volume, presumably due to less cardiac filling during orthostasis, especially under hypovolemic conditions, which may overwhelm the vasomotor reserve available for vasoconstriction or precipitate neurally mediated sympathetic withdrawal and syncope.

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Kimmerly, Derek S., and J. Kevin Shoemaker. "Hypovolemia and neurovascular control during orthostatic stress." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 2 (February 1, 2002): H645—H655. http://dx.doi.org/10.1152/ajpheart.00535.2001.

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Humans exposed to real or simulated microgravity experience decrements in blood pressure regulation during orthostatic stress that may be related to autonomic dysregulation and/or hypovolemia. We examined the hypothesis that hypovolemia, without the deconditioning effects of bed rest or spaceflight, would augment the sympathoneural and vasomotor response to graded orthostatic stress. Radial artery blood pressure (tonometry), stroke volume (SV), brachial blood flow (Doppler ultrasound), heart rate (electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA; microneurography), and estimated central venous pressure (CVP) were recorded during five levels (−5, −10, −15, −20 and −40 mmHg) of randomly assigned lower body negative pressure (LBNP) ( n = 8). Forearm (FVR) and total peripheral vascular resistance (TPR) were calculated. The test was repeated under randomly assigned placebo (normovolemia) or diuretic (spironolactone: 100 mg/day, 3 days) (hypovolemia) conditions. The diuretic produced an ∼16% reduction in plasma volume. Compared with normovolemia, SV and cardiac output were reduced by ∼12% and ∼10% at baseline and during LBNP after the diuretic. During hypovolemia, there was an upward shift in the %ΔMSNA/ΔCVP, ΔFVR/ΔCVP, and ΔTPR/ΔCVP relationships during 0 to −20 mmHg LBNP. In contrast to normovolemia, blood pressure increased at −40 mmHg LBNP during hypovolemia due to larger gains in the %ΔMSNA/ΔCVP and ΔTPR/ΔCVP relationships. It was concluded that acute hypovolemia augmented the neurovascular component of blood pressure control during moderate orthostasis, effectively compensating for decrements in SV and cardiac output.

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Javorka, Michal, Fatima El-Hamad, Barbora Czippelova, Zuzana Turianikova, Jana Krohova, Zuzana Lazarova, and Mathias Baumert. "Role of respiration in the cardiovascular response to orthostatic and mental stress." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 6 (June 1, 2018): R761—R769. http://dx.doi.org/10.1152/ajpregu.00430.2017.

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The objective of this study was to determine the response of heart rate and blood pressure variability (respiratory sinus arrhythmia, baroreflex sensitivity) to orthostatic and mental stress, focusing on causality and the mediating effect of respiration. Seventy-seven healthy young volunteers (46 women, 31 men) aged 18.4 ± 2.7 yr underwent an experimental protocol comprising supine rest, 45° head-up tilt, recovery, and a mental arithmetic task. Heart rate variability and blood pressure variability were analyzed in the time and frequency domain and modeled as a multivariate autoregressive process where the respiratory volume signal acted as an external driver. During head-up tilt, tidal volume increased while respiratory rate decreased. During mental stress, breathing rate increased and tidal volume was elevated slightly. Respiratory sinus arrhythmia decreased during both interventions. Baroreflex function was preserved during orthostasis but was decreased during mental stress. While sex differences were not observed during baseline conditions, cardiovascular response to orthostatic stress and respiratory response to mental stress was more prominent in men compared with women. The respiratory response to the mental arithmetic tasks was more prominent in men despite a significantly higher subjectively perceived stress level in women. In conclusion, respiration shows a distinct response to orthostatic versus mental stress, mediating cardiovascular variability; it needs to be considered for correct interpretation of heart rate and blood pressure phenomena.

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Yamazaki, Fumio. "Heat stress and orthostatic tolerance." Journal of Physical Fitness and Sports Medicine 1, no. 2 (2012): 271–80. http://dx.doi.org/10.7600/jpfsm.1.271.

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Krabbendam, Ineke, Loes C. A. Jacobs, Fred K. Lotgering, and Marc E. A. Spaanderman. "Venous response to orthostatic stress." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1587—H1593. http://dx.doi.org/10.1152/ajpheart.00571.2008.

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Head-up tilt (HUT) induces a reduction in preload, which is thought to be restored through sympathetic venoconstriction, reducing unstressed volume (Vu) and venous compliance (VeC). In this study, we assessed venous inflow and outflow responses and their reproducibility and determined the relation with autonomic function during HUT. Eight healthy non-pregnant women were subjected to 20° head-down tilt to 60° HUT at 20° intervals. At each rotational step, we randomly assessed forearm pressure-volume (P-V) curves (venous occlusion plethysmography) during inflow (VeCIN) and outflow [venous emptying rate (VEROUT)]. VeCIN was defined as the ratio of the slope of the volume-time curve and pressure-time curve, with direct intravenous pressure measurement. VEROUT was determined using the derivate of a quadratic regression model using cuff pressure. We defined Vu as the y-intercept of the P-V curve. We calculated, for both methods, the coefficients of reproducibility (CR) and variation (CV). Vascular sympathetic activity was determined by spectral analysis. VeCIN decreased at each rotational step compared with the supine position ( P < 0.05), whereas VEROUT increased. CR of VeCIN was higher in the supine position than VEROUT but lower during HUT. CV varied between 19% and 25% (VeCIN) and between 12% and 21% (VEROUT). HUT decreased Vu. The change in VeCIN and VEROUT correlated with the change in vascular sympathetic activity ( r = −0.36, P < 0.01, and r = 0.48, P < 0.01). This is the first study in which a reproducible reduction in VeCIN and Vu and a rise in VEROUT during HUT are documented. The alterations in venous characteristics relate to changes in vascular sympathetic activity.

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Hainsworth, Roger. "Heart rate and orthostatic stress." Clinical Autonomic Research 10, no. 6 (December 2000): 323–25. http://dx.doi.org/10.1007/bf02322255.

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Raj, Satish R. "What is the optimal orthostatic stress to diagnose orthostatic hypotension?" Clinical Autonomic Research 15, no. 2 (April 2005): 67–68. http://dx.doi.org/10.1007/s10286-005-0265-8.

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Dissertations / Theses on the topic "Orthostatic stress"

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Serrador, Jorge M. "Cerebral autoregulation during orthostatic stress." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/NQ58188.pdf.

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Howden, Reuben. "Tolerance to orthostatic stress and human cardiovascular control." Thesis, De Montfort University, 2002. http://hdl.handle.net/2086/4812.

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Heldt, Thomas 1972. "Computational models of cardiovascular response to orthostatic stress." Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/28761.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2004.
Includes bibliographical references (p. 163-185).
The cardiovascular response to changes in posture has been the focus of numerous investigations in the past. Yet despite considerable, targeted experimental effort, the mechanisms underlying orthostatic intolerance (OI) following spaceflight remain elusive. The number of hypotheses still under consideration and the lack of a single unifying theory of the pathophysiology of spaceflight-induced OI testify to the difficulty of the problem. In this investigation, we developed and validated a comprehensives lumped-parameter model of the cardiovascular system and its short-term homeostatic control mechanisms with the particular aim of simulating the short-term, transient hemodynamic response to gravitational stress. Our effort to combine model building with model analysis led us to conduct extensive sensitivity analyses and investigate inverse modeling methods to estimate physiological parameters from transient hemodynamic data. Based on current hypotheses, we simulated the system-level hemodynamic effects of changes in parameters that have been implicated in the orthostatic intolerance phenomenon. Our simulations indicate that changes in total blood volume have the biggest detrimental impact on blood pressure homeostasis in the head-up posture. If the baseline volume status is borderline hypovolemic, changes in other parameters can significantly impact the cardiovascular system's ability to maintain mean arterial pressure constant. In particular, any deleterious changes in the venous tone feedback impairs blood pressure homeostasis significantly. This result has important implications as it suggests that al-adrenergic agonists might help alleviate the orthostatic syndrome seen post-spaceflight.
by Thomas Heldt.
Ph.D.

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Ramsey, Michael W., Bradley J. Behnke, Rhonda D. Prisby, and Michael D. Delp. "Aging Alters Regional Vascular Conductance and Arterial Pressure During Orthostatic Stress." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/4098.

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Berry, Narelle Margaret, and narelle berry@unisa edu au. "Acute and long term interventions to assess the adaptability of the cardiovascular responses to orthostatic stress." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070228.123618.

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This thesis comprises of four experiments from which related but independent analyses were undertaken. The interventions employed were designed to investigate the effect of cardiovascular adaptation, both in the short and long term on the cardiovascular responses to orthostatic stress. The first study, described in Chapter 3, tested the hypothesis that the cardiovascular system (CVS) could adapt to repeated orthostatic challenges in a single session. 14 subjects were exposed to ten +75° head-up tilts (HUT) over 70 mins. Each tilt involved a 5 min supine period (SUPINE) followed by 2 min HUT (TILT). Various indices of cardiovascular function were determined non-invasively. Cardiovascular responses to HUT10 for the final 30s of SUPINE and the first 30s of TILT were compared with those of HUT1. Integrated cardiac baroreflex sensitivity (BRS) was assessed using the Valsalva Manoeuvre (VM). Results showed MAP and DBP increased in both SUPINE (MAP p=0.009, DBP p=0.002) and TILT (MAP p=0.003, DBP p=0.009) for HUT10 compared with HUT1. TPR increased during TILT only (p=0.001) during HUT10 compared with HUT1. CO and SV were decreased during SUPINE at HUT10 relative to HUT1, however, there were no differences in TILT at HUT10 for either CO or SV. There was no change in the response of BRS, HR or SBP from HUT1 to HUT10. This study indicated that 10 repetitive HUTs can elicit changes in the cardiovascular responses to orthostasis, reflected by an increased TPR. The second study, described in Chapter 4, investigated the effect of the repeated HUT protocol outlined above on the cardiovascular responses to the squat-stand test (SST). 16 subjects were randomly allocated into either a tilting group that underwent ten +75° HUTs in 70 min (TILTING) or a control group that underwent 70 min of rest (CONTROL). Before and after the 70 min of either HUT or rest, subjects performed a SST (SST1 and SST2 respectively). The same cardiovascular parameters as those used in Chapter 3 were determined during both SSTs. The final 30s of SQUAT and the first 30s of STAND (divided into three 10-sec blocks termed STAND10, STAND20 and STAND30) were compared between SST1 and SST2, results were as follows. TILTING: during the SQUAT phase of SST2, SBP, MAP, DBP and TPR were significantly elevated (p less than 0.05) and HR was significantly decreased (p=0.032) compared with SST1; at STAND10, DBP and MAP were significantly increased (p less than 0.05); at STAND20, SBP was increased (p=0.03); and, at STAND30, DBP, SBP and MAP (p less than 0.05) were increased. There were no differences observed between SST1 and SST2 in the CONTROL group. Results indicated that ten consecutive +75° HUTs can improve the CVS responses to the SST. This is predominantly due to an increase in DBP, indicative of a change in vascular resistance. The third study, outlined in Chapter 5, investigated the effect of lower limb unilateral and bilateral resistance exercise on the blood pressure (BP) and HR responses in young males. 12 normotensive, sedentary young males were divided into 2 groups; one group exercised unilaterally and the other bilaterally. Thirty seconds of resting data were collected before subjects performed 4 SETs of 10-12 reps on a seated leg press. SET 1 was performed at 50% of 10-12RM, SET 2 was performed at 75% and SET 3 and SET 4 were performed at 10- 12RM. Bilateral resistance exercise elicited greater increases in SBP than unilateral exercise at SETs 2, 3 and 4 (p less than 0.05). DBP was only greater with bilateral exercise relative to unilateral exercise at SET 2 (p=0.036). There were no differences between the groups for the HR response. This study demonstrated that the BP response to bilateral lower limb resistance exercise was significantly greater than that of unilateral exercise in young sedentary males. This information could be beneficial to many populations for whom lower BP responses to exercise would be an advantage. Following on from this, to investigate long term improvements in cardiovascular responses to orthostasis the study outlined in Chapter 6, investigated the effect of acute (10 weeks) and chronic (more than 4 years) resistance training (RT) on the cardiovascular responses to both HUT and SST. 22 young males were allocated into three groups. The UNILATERAL (N=7) and the BILATERAL (N=7) groups performed baseline testing followed by 10 weeks of lower limb RT (performed unilaterally or bilaterally), followed by repeats of the tests performed at baseline. The CONTROL group (N=8) followed the same protocol except they were asked to perform no resistance training during the 10 weeks between testing sessions. An additional 7 subjects were allocated to a CHRONIC group consisting of individuals who had been training for more than 4 years. These subjects only performed the baseline testing. Baseline testing consisted of a number of cardiovascular tests, ultrasound for vein diameter, BRS via VM, and tests for calf ejection fraction and venous elasticity. Results demonstrated that neither unilateral nor bilateral RT caused an alteration in the cardiovascular response to the HUT or SST. There were no changes in any cardiovascular variable in response to acute RT relative to the control group. The CHRONIC group had a decreased cardiovascular response to both orthostatic challenges, with a decrease in SV in response to HUT being greater in the chronic group relative to the other groups (p less than 0.05) and the TPR response to SST being significantly less than the control group (p less than 0.05). The CHRONIC group also had a smaller elastic modulus for the right leg in comparison to the other groups (p less than 0.05). Results indicate that heavy resistance exercise may cause a decreased cardiovascular response to orthostatic stress and that these decreases may be controlled by a decreased venous elasticity. Collectively, these results demonstrate that the CVS is highly adaptable to repeated orthostatic stress and the dominant underlying feature of this protective adaptation is increased vascular resistance. Following the repeated HUT the CVS is in a more protected state and has become better able to defend itself against the adverse consequences of rapidly applied hydrostatic force. However lower limb RT performed bilaterally (with large increases in BP) or unilaterally (with lower increases in BP) does not improve CVS response to orthostatic stress, in fact chronic RT (more than 4 yrs) appears to impair the CVS response to orthostasis, potentially due to decreased venous elasticity.

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Diehl, Ursula Anne. "The role of the hydrostatic indifferent point in governing splachnic blood pooling during orthostatic stress." Thesis, University of Iowa, 2011. https://ir.uiowa.edu/etd/948.

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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.

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Pawelczyk, James A. (James Anthony). "Interactions between Carotid and Cardiopulmonary Baroreceptor Populations in Men with Varied Levels of Maximal Aerobic Power." Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc331205/.

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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.

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Stevens, Glen Harold John. "Blood Pressure Regulation During Simulated Orthostatism Prior to and Following Endurance Exercise Training." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc277914/.

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Cardiovascular responses and tolerance to an orthostatic stress were examined in eight men before and after eight months of endurance exercise training. Following training, maximal oxygen consumption and blood volume were increased, and resting heart rate reduced. Orthostatic tolerance was reduced following training in all eight subjects. It was concluded that prolonged endurance training decreased orthostatic tolerance and this decrease in tolerance appeared associated with attenuated baroreflex sensitivity and alterations in autonomic balance secondary to an increased parasympathetic tone noted with training.

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Zhang, Qingguang. "HUMAN CARDIOVASCULAR RESPONSES TO SIMULATED PARTIAL GRAVITY AND A SHORT HYPERGRAVITY EXPOSURE." UKnowledge, 2015. http://uknowledge.uky.edu/cbme_etds/30.

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Orthostatic intolerance (OI), i.e., the inability to maintain stable arterial pressure during upright posture, is a major problem for astronauts after spaceflight. Therefore, one important goal of spaceflight-related research is the development of countermeasures to prevent post flight OI. Given the rarity and expense of spaceflight, countermeasure development requires ground-based simulations of partial gravity to induce appropriate orthostatic effects on the human body, and to test the efficacy of potential countermeasures. To test the efficacy of upright lower body positive pressure (LBPP) as a model for simulating cardiovascular responses to lunar and Martian gravities on Earth, cardiovascular responses to upright LBPP were compared with those of head-up tilt (HUT), a well-accepted simulation of partial gravity, in both ambulatory and cardiovascularly deconditioned subjects. Results indicate that upright LBPP and HUT induced similar changes in cardiovascular regulation, supporting the use of upright LBPP as a potential model for simulating cardiovascular responses to standing and moving in lunar and Martian gravities. To test the efficacy of a short exposure to artificial gravity (AG) as a countermeasure to spaceflight-induced OI, orthostatic tolerance limits (OTL) and cardiovascular responses to orthostatic stress were tested in cardiovascularly deconditioned subjects, using combined 70º head-up tilt and progressively increased lower body negative pressure, once following 90 minutes AG exposure and once following 90 minutes of -6º head-down bed rest (HDBR). Results indicate that a short AG exposure increased OTL of cardiovascularly deconditioned subjects, with increased baroreflex and sympathetic responsiveness, compared to those measured after HDBR exposure. To gain more insight into mechanisms of causal connectivity in cardiovascular and cardiorespiratory oscillations during orthostatic challenge in both ambulatory and cardiovascularly deconditioned subjects, couplings among R-R intervals (RRI), systolic blood pressure (SBP) and respiratory oscillations in response to graded HUT and dehydration were studied using a phase synchronization approach. Results indicate that increasing orthostatic stress disassociated interactions among RRI, SBP and respiration, and that dehydration exacerbated the disconnection. The loss of causality from SBP to RRI following dehydration suggests that dehydration also reduced involvement of baroreflex regulation, which may contribute to the increased occurrence of OI.

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Samin, Azfar. "Neuronal modelling of baroreflex response to orthostatic stress." 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=232699&T=F.

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Books on the topic "Orthostatic stress"

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Urquhart, Nathan Alexander. The cardiovascular response to acute, repeated orthostatic stress. Ottawa: National Library of Canada, 2003.

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Livingstone, Kristina. The cardiovascular hemodynamic responses to various levels of orthostatic stress in children. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2007.

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Samin, Azfar. Neuronal modelling of baroreflex response to orthostatic stress. 2005.

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TWAM, S. M. R. Pot Journal: Postural Orthostatic Tachycardia Syndrome , 120 Pages Beautiful Journal for Postural Orthostatic Tachycardia Syndrome Management with Stress and Energy Trackers, POTS Symptom and More. Independently Published, 2020.

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Book chapters on the topic "Orthostatic stress"

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Nobuaki, Yutaka, Akira Amano, Takao Shimayoshi, Jianyin Lu, Eun B. Shim, and Tetsuya Matsuda. "A Model for Simulation of Infant Cardiovascular Response to Orthostatic Stress." In Functional Imaging and Modeling of the Heart, 190–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-72907-5_20.

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Kaňa, M., M. Jiřina, and J. Holčík. "Estimation of Sympathetic and Parasympathetic Level during Orthostatic Stress Using Artificial Neural Networks." In Recent Advances in Mechatronics, 431–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-05022-0_73.

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Ottesen, Johnny T., Vera Novak, and Mette S. Olufsen. "Development of Patient Specific Cardiovascular Models Predicting Dynamics in Response to Orthostatic Stress Challenges." In Lecture Notes in Mathematics, 177–213. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32882-4_10.

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Novak, Peter. "Autonomic Tests." In Autonomic Testing, edited by Peter Novak, 13–43. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190889227.003.0004.

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Autonomic tests are focused on the cardiovascular and sudomotor systems. Established cardiovascular reflex function tests are heart rate variability during paced deep breathing, Valsalva maneuver, and tilt test. Transcranial Doppler is essential to assess cerebral vasculature and blood flow regulation to orthostatic stress. Skin biopsy also assesses small sensory and sudomotor fibers. The test results can be graded by a quantitative scale for grading of cardiovascular reflex tests, transcranial Doppler, quantitative sudomotor axon reflex test, and small fiber (epidermal sensory and sweat gland) densities from skin biopsies (QASAT). The QASAT is the validated objective instrument for grading of dysautonomia, related small fiber neuropathy, and cerebral blood flow.

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Deharo, Jean-Claude. "Reflex syncope." In ESC CardioMed, 2024–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0470.

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Reflex syncope, also called neurally mediated syncope, accounts for 56–73% of the aetiologies of syncope, with a balanced incidence over the various age categories. The most common form is ‘vasovagal syncope’ where the trigger is pain, fever, instrumentation, emotion, or orthostatic stress; ‘situational syncope’ refers to syncope triggered by a specific situation, that is, micturition, defecation, swallowing, cough; and ‘carotid sinus syncope’, which may be triggered by carotid sinus manipulation or diagnosed in patients with syncope and positive carotid sinus massage. The term ‘atypical reflex syncope’ is used to describe reflex syncope occurring without an apparent trigger: the diagnosis is mainly based on history, exclusion of other causes of syncope, and a positive head-up tilt test. Although recent developments have prompted new pathophysiological hypotheses, including the adenosine pathway, the diagnostic strategy for reflex syncope remains mainly based on clinical evaluation and very few ancillary diagnostic tests. The pharmacological armament is still very limited while new perspectives have been opened for specific subgroup of patients. Regarding the very rare patients who are candidates for permanent cardiac pacing, a new pragmatic approach may help their selection and the prediction of the effect of pacing.

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Campen, C. (Linda) MC Van, Peter C. Rowe, and Frans C. Visser. "Cerebral Blood Flow is reduced in Severe Myalgic EncephalomyelitisChronic Fatigue Syndrome Patients during Mild Orthostatic Stress Testing An Exploratory Study at 20 Degrees of Head-Up Tilt Testing." In Prime Archives in Medicine. Vide Leaf, Hyderabad, 2021. http://dx.doi.org/10.37247/pamed2ed.3.2021.2.

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Conference papers on the topic "Orthostatic stress"

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Borovik, Anatoly S., Vladimir O. Negulyaev, Olga S. Tarasova, and Olga L. Vinogradova. "Estimation of Time Characteristics of Baroreflex Resetting During Orthostatic Stress." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158012.

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Reulecke, S., S. Charleston-Villalobos, T. Aljama-Corrales, S. Charleston-Villalobos, A. Voss, R. Gonzalez-Camarena, M. Gaitan-Gonzalez, et al. "Temporal cardiovascular causality during orthostatic stress by extended partial directed coherence." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857021.

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Javorka, Michal, Barbora Czippelova, Lenka Chladekova, Zuzana Turianikova, Zuzana Visnovcova, Zuzana Lazarova, and Ingrid Tonhajzerova. "Cardiovascular control during orthostatic and mental stress: Conditional entropy based analysis." In 2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2014. http://dx.doi.org/10.1109/esgco.2014.6847495.

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MITSIS, GEORGIOS D., RONG ZHANG, BENJAMIN D. LEVINE, and VASILIS Z. MARMARELIS. "NONLINEAR PHYSIOLOGICAL SYSTEMS IDENTIFICATION: APPLICATION TO CEREBRAL HEMODYNAMICS UNDER ORTHOSTATIC STRESS." In Proceedings of the Seventh International Workshop. WORLD SCIENTIFIC, 2006. http://dx.doi.org/10.1142/9789812773197_0035.

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Alvarado-Alvarez, N., S. Charleston-Villalobos, S. Reulecke, G. Dorantes-Mendez, A. Voss, R. Gonzalez-Camarena, and T. Aljama-Corrales. "Time-Frequency Analysis of Cardiovascular Variability during an Orthostatic Stress by Complete EMD." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176709.

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Verma, Ajay K., Amanmeet Garg, Andrew Blaber, Reza Fazel-Rezai, and Kouhyar Tavakolian. "Analysis of causal cardio-postural interaction under orthostatic stress using convergent cross mapping." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7591194.

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Etter, Karen E., and M. Keith Sharp. "Modeling of Orthostatic Intolerance During Lower Body Negative Pressure." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19053.

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Postflight orthostatic intolerance (POI) afflicts a significant fraction of male astronauts and nearly all female astronauts when they first stand on Earth after spaceflight. Symptoms include dizziness and fainting, which can impact their abilities to perform critical tasks during the post-landing period. On the Moon or Mars, poor performance or accidents resulting from POI may have potentially catastrophic consequences due to the more hazardous conditions and lack of medical facilities. In addition, the long duration flights necessary to reach Mars may elicit adaptations that increase the risk of POI. Of the many factors that may influence POI, one of the few that may explain the gradual decline in arterial blood pressure experienced by many subjects during stand tests is the loss of blood volume by capillary filtration. Previous simulations suggest that elevated capillary filtration rates distinguish nonfinishers from finishers of stand tests [1, 2]. In this investigation, further computer modeling was undertaken to compare modeled orthostatic response to that of volunteers during graded orthostatic stress (GOS) involving head up tilt (HUT) and lower body negative pressure (LBNP), which reliably produces presyncope and is a candidate training countermeasure for preventing POI.

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Valente, Martina, Michal Javorka, Zuzana Turianikova, Barbora Czippelova, Jana Krohova, Giandomenico Nollo, and Luca Faes. "Cardiovascular and respiratory variability during orthostatic and mental stress: A comparison of entropy estimators." In 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2017. http://dx.doi.org/10.1109/embc.2017.8037606.

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Johnny, Ottesen,. "On the Track of Syncope Induced by Orthostatic Stress - Feedback Mechanisms Regulating the Cardiovascular System." In Modeling and Control in Biomedical Systems, edited by Rees, Stephen, chair Andreassen, Steen and Andreassen, Steen. Elsevier, 2009. http://dx.doi.org/10.3182/20090812-3-dk-2006.00032.

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Blanco, Igor, Peyman Zirak, Ana Fortuna, Gianluca Cotta, Mercedes Mayos, Anna Mola, and Turgut Durduran. "The effect of obstructive sleep apnea on the cerebral blood flow response to orthostatic stress." In Biomedical Optics. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/biomed.2014.bm3a.10.

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Reports on the topic "Orthostatic stress"

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Self, David A., Curtis D. White, Robert M. Shaffstall, Benjamin L. Mtinangi, and Jennifer S. Croft. Differences in Mechanism Between Syncope Resulting from Rapid Onset Acceleration and Orthostatic Stress. Fort Belvoir, VA: Defense Technical Information Center, April 1996. http://dx.doi.org/10.21236/ada333371.

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