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Journal articles on the topic 'Orthostatic stress'

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Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Kawai, Mio, Nobuyuki Miyai, and Mikio Arita. "The prevalence of orthostatic dysregulation among newly graduated female nurses after employment and its associations with autonomic nervous function, stress, and depressive symptoms." SAGE Open Medicine 9 (January 2021): 205031212110121. http://dx.doi.org/10.1177/20503121211012180.

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Objectives: We aimed to examine the prevalence of orthostatic dysregulation among newly graduated female nurses after employment and its associations with autonomic nervous function, stress, and depressive symptoms. Methods: This follow-up study included 48 newly graduated female nurses (aged 22 ± 3 years) employed in acute care hospitals. The orthostatic dysregulation symptoms were evaluated using a screening checklist. A sit-to-stand test was conducted to assess the autonomic nervous function. Subjective stress and depressive symptoms were determined using a self-administered questionnaire. The data were collected at baseline on the first month and on the seventh month of employment. Statistical differences within groups were analyzed using paired t-test and McNemar’s test. The independent associations of orthostatic dysregulation status with stress and depressive symptoms were analyzed using a multivariate logistic regression model. Results: The percentage of individuals who were diagnosed with orthostatic dysregulation increased from 25.0% at baseline to 35.4% at follow-up. Logistic regression analyses revealed that stress and depressive symptoms were closely associated with orthostatic dysregulation status at follow-up, despite a weak association reported at baseline. The participants were categorized according to their orthostatic dysregulation status: among individuals without orthostatic dysregulation at baseline but with orthostatic dysregulation at follow-up, the increase in autonomic nervous activity, as assessed by the coefficient of variation of the R-R intervals, in response to the postural changes was significantly attenuated at follow-up. Furthermore, this group exhibited a significant increase in stress and depressive symptoms. Conclusions: At 7 months after employment, newly graduated nurses showed a higher prevalence of orthostatic dysregulation in combination with autonomic nervous system modulation, which was accompanied by an increase in stress and depressive symptoms. These observations suggest that the orthostatic dysregulation is associated with poor mental and physical health among newly graduated nurses in the early phase of employment.
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12

Wilson, Thad E., Jian Cui, Rong Zhang, and Craig G. Crandall. "Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (November 2006): R1443—R1448. http://dx.doi.org/10.1152/ajpregu.00712.2005.

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Orthostatic tolerance is reduced in the heat-stressed human. This study tested the following hypotheses: 1) whole body heat stress reduces cerebral blood velocity (CBV) and increases cerebral vascular resistance (CVR); and 2) reductions in CBV and increases in CVR in response to an orthostatic challenge will be greater while subjects are heat stressed. Fifteen subjects were instrumented for measurements of CBV (transcranial ultrasonography), mean arterial blood pressure (MAP), heart rate, and internal temperature. Whole body heating increased both internal temperature (36.4 ± 0.1 to 37.3 ± 0.1° C) and heart rate (59 ± 3 to 90 ± 3 beats/min); P < 0.001. Whole body heating also reduced CBV (62 ± 3 to 53 ± 2 cm/s) primarily via an elevation in CVR (1.35 ± 0.06 to 1.63 ± 0.07 mmHg · cm−1 · s); P < 0.001. A subset of subjects ( n = 8) were exposed to lower-body negative pressure (LBNP 10, 20, 30, 40 mmHg) in both normothermic and heat-stressed conditions. During normothermia, LBNP of 30 mmHg (highest level of LBNP achieved by the majority of subjects in both thermal conditions) did not significantly alter CBV, CVR, or MAP. During whole body heating, this LBNP decreased MAP (81 ± 2 to 75 ± 3 mmHg), decreased CBV (50 ± 4 to 39 ± 1 cm/s), and increased CVR (1.67 ± 0.17 to 1.92 ± 0.12 mmHg · cm−1 · s); P < 0.05. These data indicate that heat stress decreases CBV, and the reduction in CBV for a given orthostatic challenge is greater during heat stress. These outcomes reduce the reserve to buffer further decreases in cerebral perfusion before presyncope. Increases in CVR during whole body heating, coupled with even greater increases in CVR during orthostasis and heat stress, likely contribute to orthostatic intolerance.
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13

Harteveld, Lisette M., Nico A. Blom, J. Gert van Dijk, Robert H. Reijntjes, Paul J. van Someren, Fabian I. Kerkhof, Irene M. Kuipers, Lukas A. J. Rammeloo, Eco J. C. de Geus, and Arend D. J. ten Harkel. "Orthostatic stress response in pediatric Fontan patients and the effect of ACE inhibition." PLOS ONE 17, no. 9 (September 1, 2022): e0273940. http://dx.doi.org/10.1371/journal.pone.0273940.

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Background Many cardiocirculatory mechanisms are involved in the adaptation to orthostatic stress. While these mechanisms may be impaired in Fontan patients. However, it is yet unclear how Fontan patients, who exhibit a critical fluid balance, respond to orthostatic stress. Angiotensin converting enzyme inhibitors are often prescribed to Fontan patients, but they may negatively influence orthostatic tolerance. Therefore, we evaluated the response to orthostatic stress in pediatric Fontan patients before and after treatment with enalapril. Methods Thirty-five Fontan patients (aged 14 years) with moderate-good systolic ventricular function without pre-existent enalapril treatment were included. Before and after a three-month enalapril treatment period, the hemodynamic response to head-up tilt test was evaluated by various parameters including cardiac index, blood pressure, cerebral blood flow, aortic stiffness and cardiac autonomous nervous activity. Thirty-four healthy subjects (aged 13 years) served as controls. Results Fontan patients had a decreased cerebral blood flow and increased aortic stiffness in the supine position compared to controls, while all other factors did not differ. Patients and controls showed a comparable response to head-up tilt test for most parameters. Twenty-seven patients completed the enalapril study with a mean dosage of 0.3±0.1mg/kg/day. Most parameters were unaffected by enalapril, only the percent decrease in cardiac index to tilt was higher after treatment, but the cardiac index during tilt was not lower (3.0L/min/m2 pre-enalapril versus 2.8L/min/m2 after treatment; P = 0.15). Conclusion Pediatric Fontan patients adequately respond to orthostasis with maintenance of blood pressure and cerebral blood flow and sufficient autonomic response. Enalapril treatment did not alter the response. Clinical trial information Scientific title: ACE inhibition in Fontan patients: its effect on body fluid regulation (sAFE-study). The Netherlands National Trial Register: Trail NL6415. Registered 2017-07-20. Trial information: https://www.trialregister.nl/trial/6415
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14

Nagata, Katsutaro, Takuya Hasegawa, Yasumasa Hirokado, Katsuhiko Kiyama, Kazuo Honda, and Yukio Aoyama. "Endocrinological stress and oxidative stress of orthostatic hypotension." Autonomic Neuroscience 135, no. 1-2 (September 2007): 44–45. http://dx.doi.org/10.1016/j.autneu.2007.06.060.

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15

Meendering, Jessica R., Britta N. Torgrimson, Belinda L. Houghton, John R. Halliwill, and Christopher T. Minson. "Menstrual cycle and sex affect hemodynamic responses to combined orthostatic and heat stress." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 2 (August 2005): H631—H642. http://dx.doi.org/10.1152/ajpheart.00029.2005.

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Women have decreased orthostatic tolerance compared with men, and anecdotal evidence suggests women are more susceptible to orthostatic intolerance in warm environments. Because estrogen and progesterone affect numerous physiological variables that may alter orthostatic tolerance, the purpose of our study was to compare orthostatic tolerance across the menstrual cycle phases in women during combined orthostatic and heat stress and to compare these data with those of men. Eight normally menstruating women and eight males (22 ± 4.0 and 23 ± 3.5 yr, respectively) completed the protocol. Women were studied during their early follicular (EF), ovulatory (OV), and midluteal (ML) phases. Men were studied twice within 2–4 wk. Heart rate, cardiac output, blood pressure, core temperature (Tc), and cutaneous vascular conductance (CVC) were measured during three head-up tilt tests, consisting of two tilts in the thermoneutral condition and one tilt after a 0.5°C rise in Tc. There was no difference in orthostatic tolerance across the menstrual cycle phases, despite higher CVC in the ML phase after heating (EF, 42.3 ± 4.8; OV, 40.1 ± 3.7; ML, 57.5 ± 4.5; P < 0.05). Orthostatic tolerance in the heat was greater in men than women ( P < 0.05). These data suggest that although many physiological variables associated with blood pressure regulation fluctuate during the menstrual cycle, orthostatic tolerance in the heat remains unchanged. Additionally, our data support a clear sex difference in orthostatic tolerance and extend upon previous data to show that the sex difference in the heat is not attributable to fluctuating hormone profiles during the menstrual cycle.
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16

Fedorova, D. N., A. E. Soloveva, M. Fudim, V. L. Galenko, A. V. Kozlenok, A. V. Berezina, and S. V. Villevalde. "Frequency of hemodynamic response to orthostatic stress in heart failure with reduced ejection fraction, associations with clinical blood pressure." Russian Journal of Cardiology 27, no. 2S (May 20, 2022): 5005. http://dx.doi.org/10.15829/1560-4071-2022-5005.

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Aim. To assess hemodynamic response to active standing test (AST) with beat-to-beat blood pressure (BP) monitoring, their association with office BP and symptoms of orthostatic intolerance in patients with heart failure (HF).Material and methods. Outpatient HF patients with documented left ventricular ejection fraction <40%, followed up in a HF center and receiving optimal medical therapy, underwent AST with beat-to-beat non-invasive BP monitoring.Hemodynamic response was assessed according to the European Federation of Autonomic Societies criteria.Results. The study included 87 patients (mean age, 57±10 years; men, 76%). Normal hemodynamic response to orthostatic stress was observed in 36 (41,4%) patients. Pathological response prevailed during the first minute of orthostatic stress — initial orthostatic hypotension (OH) (n=29, 33,3%) and delayed BP recovery (n=18, 20,7%). Classical OH was detected in 4 (4,6%) patients. There was no orthostatic hypertension, defined as an increase in systolic BP (SBP) ≥20 mm Hg. According to office BP, hypotension was observed in 19 (21,8%) patients (SBP <90 mm Hg in 4 patients and 90-100 mm Hg in 15), hypertension (SBP >140 mm Hg) in 11 (12,6%) patients. Pathological response to orthostatic stress were more often observed in office SBP >140 mm Hg compared to SBP ≤140 mmHg (90,9% and 53,9%, p=0,020).Orthostatic intolerance was noted in 43 (49,4%) patients and were not associated with the level of office SBP (p=0,398) or pathological responses to orthostatic stress (p=0,758 for initial OH and p=0,248 for delayed BP recovery).Conclusion. The pathological hemodynamic response in AST with beat-to-beat BP monitoring in ambulatory patients with HF is most often represented by initial OH and delayed BP recovery associated with office SBP >140 mmHg. The frequency of symptoms of orthostatic intolerance did not differ between groups depending on the presence of an inadequate response to orthostatic stress.
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17

Privett, Sheena E., Greg P. Whyte, Keith P. George, John M. Mulcahy, and N. Tim Cable. "Pre- and Post-Exercise Orthostatic Stress." Medicine & Science in Sports & Exercise 38, Supplement (May 2006): S194. http://dx.doi.org/10.1249/00005768-200605001-01747.

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18

Schroeder, Christoph, Sandor Batkai, Stefan Engeli, Jens Tank, André Diedrich, Friedrich C. Luft, and Jens Jordan. "Circulating endocannabinoid concentrations during orthostatic stress." Clinical Autonomic Research 19, no. 6 (September 15, 2009): 343–46. http://dx.doi.org/10.1007/s10286-009-0026-1.

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19

Conboy, Erin E., Amy E. Fogelman, Charity L. Sauder, and Chester A. Ray. "Endurance training reduces renal vasoconstriction to orthostatic stress." American Journal of Physiology-Renal Physiology 298, no. 2 (February 2010): F279—F284. http://dx.doi.org/10.1152/ajprenal.00447.2009.

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Endurance training has been associated with increased orthostatic intolerance. The purpose of the present study was to test the hypothesis that endurance training reduces renal vasoconstriction to orthostatic stress. Blood pressure, heart rate, and renal blood flow velocity were measured during a 25-min 60° head-up tilt (HUT) test before and after 8 wk of endurance training in eight healthy sedentary subjects (26 ± 1 yrs). Training elicited a 21 ± 3% increase in peak oxygen uptake (V̇o2peak) and a reduction in heart rate at rest of 8 ± 2 beats/min. During HUT, heart rate progressively increased (∼20 beats/min) over the 25-min HUT trial both before and after training. Systolic arterial blood pressure during HUT was unchanged with training, whereas diastolic arterial blood pressure was lower at the end of HUT after training. Before training renal blood flow velocity (Δ14 ± 5 cm/s) and renal vascular conductance (Δ22 ± 7%) decreased during HUT, whereas after training renal blood flow velocity (Δ2 ± 5 cm/s) and renal vascular conductance (Δ1 ± 12%) did not change significantly during HUT. Renal blood flow velocity and vascular conductance responses to HUT did not change in control subjects during the 8-wk period. These results demonstrate that endurance training reduces renal vasoconstriction during an orthostatic challenge and may contribute to training-induced orthostatic intolerance.
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20

Zhang, Rong, Julie H. Zuckerman, James A. Pawelczyk, and Benjamin D. Levine. "Effects of head-down-tilt bed rest on cerebral hemodynamics during orthostatic stress." Journal of Applied Physiology 83, no. 6 (December 1, 1997): 2139–45. http://dx.doi.org/10.1152/jappl.1997.83.6.2139.

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Zhang, Rong, Julie H. Zuckerman, James A. Pawelczyk, and Benjamin D. Levine. Effects of head-down-tilt bed rest on cerebral hemodynamics during orthostatic stress. J. Appl. Physiol. 83(6): 2139–2145, 1997.—Our aim was to determine whether the adaptation to simulated microgravity (μG) impairs regulation of cerebral blood flow (CBF) during orthostatic stress and contributes to orthostatic intolerance. Twelve healthy subjects (aged 24 ± 5 yr) underwent 2 wk of −6° head-down-tilt (HDT) bed rest to simulate hemodynamic changes that occur when humans are exposed to μG. CBF velocity in the middle cerebral artery (transcranial Doppler), blood pressure, cardiac output (acetylene rebreathing), and forearm blood flow were measured at each level of a ramped protocol of lower body negative pressure (LBNP; −15, −30, and −40 mmHg × 5 min, −50 mmHg × 3 min, then −10 mmHg every 3 min to presyncope) before and after bed rest. Orthostatic tolerance was assessed by using the cumulative stress index (CSI; mmHg × minutes) for the LBNP protocol. After bed rest, each individual’s orthostatic tolerance was reduced, with the group CSI decreased by 24% associated with greater decreases in cardiac output and greater increases in systemic vascular resistance at each level of LBNP. Before bed rest, mean CBF velocity decreased by 14, 10, and 45% at −40 mmHg, −50 mmHg, and maximal LBNP, respectively. After bed rest, mean velocity decreased by 16% at −30 mmHg and by 21, 35, and 39% at −40 mmHg, −50 mmHg, and maximal LBNP, respectively. Compared with pre-bed rest, post-bed-rest mean velocity was less by 11, 10, and 21% at −30, −40, and −50 mmHg, respectively. However, there was no significant difference at maximal LBNP. We conclude that cerebral autoregulation during orthostatic stress is impaired by adaptation to simulated μG as evidenced by an earlier and greater fall in CBF velocity during LBNP. We speculate that impairment of cerebral autoregulation may contribute to the reduced orthostatic tolerance after bed rest.
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Steinback, Craig D., Deborah D. O’Leary, Jason Bakker, Angela D. Cechetto, Hanif M. Ladak, and J. Kevin Shoemaker. "Carotid distensibility, baroreflex sensitivity, and orthostatic stress." Journal of Applied Physiology 99, no. 1 (July 2005): 64–70. http://dx.doi.org/10.1152/japplphysiol.01248.2004.

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In this study, we tested the hypothesis that carotid arteries undergo rapid changes in distensibility on moving from the supine to head-up tilt (HUT) postures and, subsequently, that this change in carotid distensibility (cDa) might be associated with concurrent reductions in cardiovagal baroreflex sensitivity (BRS). Thus the effect of posture on carotid vascular mechanics and cardiovagal BRS with consideration for altered central hemodynamics (i.e., stroke volume; Doppler ultrasound) was examined. Carotid pulse pressure (cPP; Millar transducer) and contralateral B-mode ultrasound images were assessed at the carotid artery during supine and 60° HUT postures. From these measures, cDa was calculated at 5-mmHg pressure increments experienced during the cardiac cycle ( n = 6). cPP ( n = 9) was not different in the two postures. A smaller stroke volume being ejected into a smaller carotid artery in HUT explained the maintenance of cPP in HUT. Also, compared with supine, cDa was reset to a lower level in HUT (main effect of posture; P < 0.05). Cardiovagal BRS (sequence method) was diminished in HUT vs. supine ( P < 0.05). A positive correlation was observed between the tilt-induced changes in maximal cDa (in early systole) and cardiovagal BRS ( r2 = 0.75; P < 0.05), but there was little predictive relationship between changes in cPP, systolic vessel dimensions, or average cDa and the corresponding change in BRS. The present results indicate that HUT elicits rapid changes in carotid artery mechanics and further suggest that reductions in the maximal cDa measured in early systole contribute to reduced cardiovagal BRS with HUT.
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Schlader, Zachary J., Thad E. Wilson, and Craig G. Crandall. "Mechanisms of orthostatic intolerance during heat stress." Autonomic Neuroscience 196 (April 2016): 37–46. http://dx.doi.org/10.1016/j.autneu.2015.12.005.

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23

Heldt, Thomas, Eun B. Shim, Roger D. Kamm, and Roger G. Mark. "Computational modeling of cardiovascular response to orthostatic stress." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1239–54. http://dx.doi.org/10.1152/japplphysiol.00241.2001.

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The objective of this study is to develop a model of the cardiovascular system capable of simulating the short-term (≤5 min) transient and steady-state hemodynamic responses to head-up tilt and lower body negative pressure. The model consists of a closed-loop lumped-parameter representation of the circulation connected to set-point models of the arterial and cardiopulmonary baroreflexes. Model parameters are largely based on literature values. Model verification was performed by comparing the simulation output under baseline conditions and at different levels of orthostatic stress to sets of population-averaged hemodynamic data reported in the literature. On the basis of experimental evidence, we adjusted some model parameters to simulate experimental data. Orthostatic stress simulations are not statistically different from experimental data (two-sided test of significance with Bonferroni adjustment for multiple comparisons). Transient response characteristics of heart rate to tilt also compare well with reported data. A case study is presented on how the model is intended to be used in the future to investigate the effects of postspaceflight orthostatic intolerance.
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COOPER, V. L., and R. HAINSWORTH. "Effects of head-up tilting on baroreceptor control in subjects with different tolerances to orthostatic stress." Clinical Science 103, no. 3 (August 5, 2002): 221–26. http://dx.doi.org/10.1042/cs1030221.

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During orthostatic stress, an increase in peripheral vascular resistance normally results in arterial blood pressure being well maintained, despite a decrease in cardiac output. The present study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was increased during orthostatic stress and whether failure to develop this increase was associated with poor orthostatic tolerance. Three groups of subjects were studied: asymptomatic controls; patients investigated for suspected posturally related syncope but who had normal responses to an orthostatic stress test (normal patients); and patients who were shown to have low orthostatic tolerance (early fainters). We determined responses of R–R interval and forearm vascular resistance (mean arterial pressure/brachial artery velocity by Doppler ultrasonography) to the loading and unloading of carotid baroreceptors by application of pressures of -30 and +30mmHg to a chamber fitted over the neck. Responses were determined after 20min of supine rest and after 10min of head-up tilt at 60°. Responses of cardiac interval were not significantly different between the three groups, and they were not altered by the postural change. Vascular responses also did not differ between the groups during supine rest. However, in healthy volunteers and in normal patients, responses to both neck suction and pressure were significantly enhanced during head-up tilt. In controls, responses to suction were increased by tilt from 0.04±0.1 to -1.01±0.2%·mmHg-1 (means±S.E.M.; P<0.001) and those to neck pressure from -0.6±0.3 to -3.1±1.1%·mmHg-1 (P<0.05). In the normal patients, the corresponding changes were: during suction, from -0.2±0.1 to -0.7±0.1%·mmHg-1 (P<0.05); during pressure, from -0.7±0.1 to -1.5±0.3%·mmHg-1 (P<0.05). In contrast, in patients with low orthostatic tolerance, posture had no effect on the reflex (neck suction, from -0.3±0.1 to -0.3±0.1%·mmHg-1; neck pressure, from -1.0±0.3 to -0.9±0.2%·mmHg-1). We suggest that an increase in the sensitivity of the carotid baroreceptor/vascular resistance reflex may be important in the maintenance of blood pressure during orthostatic stress, and that failure of this to occur in patients with posturally related syncope may go some way towards explaining their poor orthostatic tolerance.
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O'Leary, D. D., R. L. Hughson, J. K. Shoemaker, D. K. Greaves, D. E. Watenpaugh, B. R. Macias, and A. R. Hargens. "Heterogeneity of responses to orthostatic stress in homozygous twins." Journal of Applied Physiology 102, no. 1 (January 2007): 249–54. http://dx.doi.org/10.1152/japplphysiol.00240.2006.

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Early analysis into the role of genetics on cardiovascular regulation has been accomplished by comparing blood pressure and heart rate in homozygous twins during unstressed, resting physiological conditions. However, many variables, including cognitive and environmental factors, contribute to the regulation of cardiovascular hemodynamics. Therefore, the purpose of this study was to determine the hemodynamic response of identical twins to an orthostatic stress, ranging from supine rest to presyncope. Heart rate, arterial blood pressure, middle cerebral artery blood velocity, an index of cerebrovascular resistance, cardiac output, total peripheral resistance, and end-tidal carbon dioxide were measured in 16 healthy monozygotic twin pairs. Five minutes of supine resting baseline data were collected, followed by 5 min of 60° head-up tilt. After 5 min of head-up tilt, lower body negative pressure was applied in increments of 10 mmHg every 3 min until the onset of presyncope, at which time the subject was returned to the supine position for a 5-min recovery period. The data indicate that cardiovascular regulation under orthostatic stress demonstrates a significant degree of variance between identical twins, despite similar orthostatic tolerance. As the level of stress increases, so does the difference in the cardiovascular response within a twin pair. The elevated variance with increasing stress may be due to an increase in the role of environmental factors, as the influential role of genetics nears a functional limit. Therefore, although orthostatic tolerance times were very similar between identical twins, the mechanism involved in sustaining cardiovascular function during increasing stress was different.
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Tobaldini, Eleonora, Edgar Toschi-Dias, Liliane Appratto de Souza, Karina Rabello Casali, Marco Vicenzi, Giulia Sandrone, Chiara Cogliati, Maria Teresa La Rovere, Gian Domenico Pinna, and Nicola Montano. "Cardiac and Peripheral Autonomic Responses to Orthostatic Stress During Transcutaneous Vagus Nerve Stimulation in Healthy Subjects." Journal of Clinical Medicine 8, no. 4 (April 11, 2019): 496. http://dx.doi.org/10.3390/jcm8040496.

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Previous studies showed that transcutaneous vagus nerve stimulation (tVNS) modulates the autonomic nervous system (ANS) in resting condition. However, the autonomic regulation in response to an orthostatic challenge during tVNS in healthy subjects remains unknown. We tested the hypothesis that tVNS reduces heart rate (HR) and alters the responsivity of ANS to orthostatic stress in healthy subjects. In a randomized and cross-over trial, thirteen healthy subjects underwent two experimental sessions on different days: (1) tVNS and (2) control. Using a tVNS device, an auricular electrode was placed on the left cymba conchae of the external ear; an electric current with a pulse frequency of 25 Hz and amplitude between 1 and 6 mA was applied. For the assessment of ANS, the beat-to-beat HR and systolic arterial pressure (SAP) were analyzed using linear and nonlinear approaches during clinostatic and orthostatic conditions. In clinostatic conditions, tVNS reduced HR (p < 0.01), SAP variability (p < 0.01), and cardiac and peripheral sympathetic modulation (p < 0.01). The responsivity of the peripheral sympathetic modulation to orthostatic stress during tVNS was significantly higher when compared to the control session (p = 0.03). In conclusion, tVNS reduces the HR and affects cardiac and peripheral autonomic control and increases the responses of peripheral autonomic control to orthostatic stress in healthy subjects.
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Buharin, Vasiliy E., Andrew J. Butler, and Minoru Shinohara. "Motor cortical disinhibition with baroreceptor unloading induced by orthostatic stress." Journal of Neurophysiology 111, no. 12 (June 15, 2014): 2656–64. http://dx.doi.org/10.1152/jn.00778.2013.

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Unloading of the baroreceptors due to orthostatic stress increases corticospinal excitability. The purpose of this study was to examine the effects of baroreceptor unloading due to orthostatic stress on intracortical excitatory and inhibitory pathways in the motor cortex. With transcranial magnetic stimulation, measures of intracortical excitability for a hand muscle were tested on 2 days in healthy young adults. Lower body negative pressure (LBNP) of 40 mmHg was applied during one of the days and not during the Control day. During application of LBNP heart rate and the low-frequency component of heart rate variability increased, while mean arterial blood pressure was maintained. In the resting state, LBNP decreased short-interval intracortical inhibition (SICI) and had no effect on intracortical facilitation (ICF) or short-interval intracortical facilitation (SICF) compared with the Control day. During isometric contraction, no effects of LBNP were observed on tested measures of intracortical excitability including SICI, SICF, and cortical silent period. It was concluded that baroreceptor unloading due to orthostatic stress results in diminished intracortical inhibition, at least in the resting muscle.
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Cui, Jian, Cheryl Blaha, Michael D. Herr, and Lawrence I. Sinoway. "Lower-limb venous distension reflex and orthostatic tolerance in young healthy humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 319, no. 2 (August 1, 2020): R142—R147. http://dx.doi.org/10.1152/ajpregu.00269.2019.

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Earlier reports suggest that limb venous distension evokes reflex increases in muscle sympathetic nerve activity (MSNA) and blood pressure (BP) (i.e., venous distension reflex). Our recent report also shows that suction of arterially occluded limb evokes venous distension reflex. We postulate that the venous distension reflex contributes to autonomic responses to orthostatic stress. In this study, we hypothesized that orthostatic tolerance would be linked to the MSNA response seen with lower limb suction. Fifteen healthy subjects were tested in the supine position. Negative pressure (−100 mmHg) was applied on an arterially occluded lower limb for 2 min. MSNA from the peroneal nerve in the limb not exposed to suction, ECG, and BP (Finometer) was recorded throughout the study. Limb occlusion without suction was used as a control trial. In a separate visit, the individual’s orthostatic tolerance was assessed using a graded lower body negative pressure (LBNP) tolerance test. Mean arterial BP and MSNA (18.6 ± 1.9 to 23.6 ± 2.0 bursts/min) significantly (both P < 0.05) increased during limb suction. Orthostatic tolerance index positively correlated ( R = 0.636, P = 0.011) with the MSNA response seen with suction during occlusion. Since the venous distension reflex strength correlates with the level of orthostatic tolerance, we speculate that lower-limb venous distension reflex engagement increases the sympathetic responses during orthostatic challenge and serves to maintain BP with postural stress.
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29

Ocon, Anthony J., Zachary R. Messer, Marvin S. Medow, and Julian M. Stewart. "Increasing orthostatic stress impairs neurocognitive functioning in chronic fatigue syndrome with postural tachycardia syndrome." Clinical Science 122, no. 5 (November 8, 2011): 227–38. http://dx.doi.org/10.1042/cs20110241.

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CFS (chronic fatigue syndrome) is commonly co-morbid with POTS (postural tachycardia syndrome). Individuals with CFS/POTS experience unrelenting fatigue, tachycardia during orthostatic stress and ill-defined neurocognitive impairment, often described as ‘mental fog’. We hypothesized that orthostatic stress causes neurocognitive impairment in CFS/POTS related to decreased CBFV (cerebral blood flow velocity). A total of 16 CFS/POTS and 20 control subjects underwent graded tilt table testing (at 0, 15, 30, 45, 60 and 75°) with continuous cardiovascular, cerebrovascular, and respiratory monitoring and neurocognitive testing using an n-back task at each angle. The n-back task tests working memory, concentration, attention and information processing. The n-back task imposes increasing cognitive challenge with escalating (0-, 1-, 2-, 3- and 4-back) difficulty levels. Subject dropout due to orthostatic presyncope at each angle was similar between groups. There were no n-back accuracy or RT (reaction time) differences between groups while supine. CFS/POTS subjects responded less correctly during the n-back task test and had greater nRT (normalized RT) at 45, 60 and 75°. Furthermore, at 75° CFS/POTS subjects responded less correctly and had greater nRT than controls during the 2-, 3- and 4-back tests. Changes in CBFV were not different between the groups and were not associated with n-back task test scores. Thus we conclude that increasing orthostatic stress combined with a cognitive challenge impairs the neurocognitive abilities of working memory, accuracy and information processing in CFS/POTS, but that this is not related to changes in CBFV. Individuals with CFS/POTS should be aware that orthostatic stress may impair their neurocognitive abilities.
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30

Masuki, Shizue, John H. Eisenach, Christopher P. Johnson, Niki M. Dietz, Lisa M. Benrud-Larson, William G. Schrage, Timothy B. Curry, Paola Sandroni, Phillip A. Low, and Michael J. Joyner. "Excessive heart rate response to orthostatic stress in postural tachycardia syndrome is not caused by anxiety." Journal of Applied Physiology 102, no. 3 (March 2007): 896–903. http://dx.doi.org/10.1152/japplphysiol.00927.2006.

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Postural tachycardia syndrome (POTS) is characterized by excessive increases in heart rate (HR) without hypotension during orthostasis. The relationship between the tachycardia and anxiety is uncertain. Therefore, we tested whether the HR response to orthostatic stress in POTS is primarily related to psychological factors. POTS patients ( n = 14) and healthy controls ( n = 10) underwent graded venous pooling with lower body negative pressure (LBNP) to −40 mmHg while wearing deflated antishock trousers. “Sham” venous pooling was performed by 1) trouser inflation to 5 mmHg during LBNP and 2) vacuum pump activation without LBNP. HR responses to mental stress were also measured in both groups, and a questionnaire was used to measure psychological parameters. During LBNP, HR in POTS patients increased 39 ± 5 beats/min vs. 19 ± 3 beats/min in control subjects at −40 mmHg ( P < 0.01). LBNP with trouser inflation markedly blunted the HR responses in the patients (9 ± 2 beats/min) and controls (2 ± 1 beats/min), and there was no HR increase during vacuum application without LBNP in either group. HR responses during mental stress were not different in the patients and controls (18 ± 2 vs. 19 ± 1 beats/min; P > 0.6). Anxiety, somatic vigilance, and catastrophic cognitions were significantly higher in the patients ( P < 0.05), but they were not related to the HR responses during LBNP or mental stress ( P > 0.1). These results suggest that the HR response to orthostatic stress in POTS patients is not caused by anxiety but that it is a physiological response that maintains arterial pressure during venous pooling.
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31

Hinghofer-Szalkay, Helmut G., Andreas Rössler, Joyce M. Evans, Michael B. Stenger, Fritz B. Moore, and Charles F. Knapp. "Circulatory galanin levels increase severalfold with intense orthostatic challenge in healthy humans." Journal of Applied Physiology 100, no. 3 (March 2006): 844–49. http://dx.doi.org/10.1152/japplphysiol.01039.2005.

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The purpose of this study was to test the hypothesis that plasma galanin concentration (pGal) is regularly increased in healthy humans with extensive orthostatic stress. Twenty-six test persons (14 men, 12 women) were brought to an orthostatic end point via a progressive cardiovascular stress (PCS) protocol consisting of 70° head-up tilt plus increasing levels of lower body negative pressure until either hemodynamically defined presyncope or other signs of orthostatic intolerance occurred (nausea, clammy skin, excessive sweating, pallor of the skin). We further tested for possible gender, gravitational, and muscular training influences on plasma pGal responses: PCS was applied before and after 3 wk of daily vertical acceleration exposure training on a Human Powered Centrifuge. Test persons were randomly assigned to active (with bicycle work) or passive (without work) groups (seven men, six women in each group). Resting pGal was 26 ± 3 pg/ml in men and 39 ± 15 pg/ml in women (not significant); women had higher galanin responses (4.9-fold increase) than men (3.5-fold, P = 0.017) to PCS exposure. Overall, PCS increased pGal to 186 ± 5 pg/ml ( P = 0.0003), without significant differences between presyncope vs. orthostatic intolerance, pre- vs. postcentrifuge, or active vs. passive gravitational training. Increases in pGal were poorly related to synchronous elevations in plasma vasopressin. We conclude that galanin is regularly increased in healthy humans under conditions of presyncopal orthostatic stress, the response being independent of gravity training but larger in women than in men.
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32

Lipatova, Aksinia, Azamat Kade, Artem Trofimenko, Viktor Ovsiannikov, Oleg Tcymbalov, and Aleksandr Sidorenko. "Assessment of the tDCS Influence on Stress-Induced Disorders in Rats with Low Stress Sustainability and Endurance." Serbian Journal of Experimental and Clinical Research 20, no. 3 (September 1, 2019): 207–14. http://dx.doi.org/10.2478/sjecr-2018-0057.

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Abstract The aim of study is to analyze the tDCS influence on stress-induced disorders in rats with low stress sustainability and endurance. The animals with a low stress sustainability and endurance were divided into 3 groups: the comparison 1, the comparison 2 and the main. The control group consisted of intact rats. The rats of the comparison group 1 were subjected to orthostatic stress 24 hours after the 1st forced swimming test. The rats of the comparison group 2 and the main one were conducted the 2nd forced swimming test on the 7th day of the experiment, and 24 hours later they were subjected to the orthostatic stress. Rats of the main group got tDCS sessions after the 1st forced swimming test. The development of the orthostatic stress is accompanied by an increase in plasma content the following components: adrenaline by 88.9%, ACTH in 10.5 times, corticosterone by 70.1%, IL-1β by 178.2%, IL-6 in 6.7 times, IL-10 by 37.1% in comparison with intact animals. The usage of tDCS in rats with low stress sustainability and endurance increased the swimming duration by 47.7%. During the OS it was also accompanied by a decrease in plasma content: adrenaline in 1.4 times, ACTH in 8.2 times, corticosterone in 1.4 times, IL-1β in 1.5 times, IL-6 in 2.2 times, IL-10 in 1.2 times, relative to the comparison group 2. The obtained data showed the essential effect of tDCS on stress-related changes in the content of cytokines and hormones of blood.
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33

Savard, Gabrielle K., and Mark A. Stonehouse. "Cardiovascular Response to Orthostatic Stress: Effects of Exercise Training Modality." Canadian Journal of Applied Physiology 20, no. 2 (June 1, 1995): 240–54. http://dx.doi.org/10.1139/h95-018.

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The effects of exercise training posture on cardiovascular and baroreflex responses to orthostatic challenge were assessed in highly trained cyclists (CT, n = 8) and swimmers (ST, n = 8), and in untrained men (UT, n = 8). CT demonstrated the lowest orthostatic tolerance to lower body negative pressure (LBNP, 0 to −50 mmHg), with only 3 subjects completing the full LBNP procedure; 5 UT and all ST completed the testing. During LBNP, stroke volume (SV) decreases were similar in CT and ST, but greater than in UT. Mean pulse pressure and systemic vascular resistance (SVR) were reduced in CT relative to ST and UT at the highest levels of LBNP; the slope of the ΔSVR/ΔZ0 and ΔSVR/ΔSV relationships in CT, used to assess peripheral vascular baroreflex function, were attenuated relative to the other groups. There were no between-group differences in the heart rate response to LBNP. The greater incidence of orthostatic intolerance observed in upright-versus supine-trained athletes during passive LBNP was linked to attenuated baroreflex control of peripheral vascular resistance. Key words: arterial baroreflex, arterial pressure, cardiopulmonary baroreceptor, endurance training, vascular resistance
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34

Tonkin, A. L., L. M. H. Wing, M. J. Morris, and V. Kapoor. "Afferent baroreflex dysfunction and age-related orthostatic hypotension." Clinical Science 81, s25 (October 1, 1991): 531–38. http://dx.doi.org/10.1042/cs0810531.

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1. To test the hypothesis that in apparently healthy elderly subjects with orthostatic hypotension there is afferent baroreflex dysfunction, cardiovascular and neurohumoral responses were measured after separate stimuli which activated baroreceptor (head-up tilt) and non-baroreceptor (cold stress, isometric exercise) afferent pathways. 2. In 15 healthy elderly control subjects blood pressure did not change with 60° head-up tilting and there was a moderate increase in heart rate, whereas in 13 subjects with age-related orthostatic hypotension head-up tilting was associated with a marked fall in blood pressure but a similar heart rate response to that in the elderly control group. In contrast, both groups of subjects had similar blood pressure and heart rate responses to cold stress and sustained isometric exercise. 3. Nine subjects with autonomic neuropathy also showed a marked hypotensive response to head-up tilt, but produced no pressor response to cold stress or isometric exercise. 4. The plasma concentrations of noradrenaline, adrenaline and neuropeptide-Y-like immunoreactivity rose and that of atrial natriuretic peptide fell after head-up tilt in the study population as a whole. There were no significant differences between groups despite the much greater blood pressure drops in the subjects with autonomic neuropathy and in those with age-associated orthostatic hypotension. 5. The aorto-iliac pulse wave velocity index was significantly higher in subjects with age-associated orthostatic hypotension compared with that in control subjects. 6. The pattern of responses to the separate stresses observed in the group with age-associated orthostatic hypotension is characteristic and different from that in the elderly control subjects and the subjects with autonomic neuropathy. It suggests that age-associated orthostatic hypotension is related predominantly to dysfunction in the afferent limb of the baroreflex arc, possibly partially caused by a splinting of arterial baroreceptors by non-compliant arterial walls.
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35

Cooper, Victoria L., and Roger Hainsworth. "Carotid Baroreceptor Reflexes in Humans During Orthostatic Stress." Experimental Physiology 86, no. 5 (September 2001): 677–81. http://dx.doi.org/10.1113/eph8602213.

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36

Joyner, Michael J. "Orthostatic stress, haemorrhage and a bankrupt cardiovascular system." Journal of Physiology 587, no. 21 (October 30, 2009): 5015–16. http://dx.doi.org/10.1113/jphysiol.2009.181495.

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37

Fluet, N., C. Richter, and Cahalin P. Lawrence. "CARDIOVASCULAR RESPONSE TO ORTHOSTATIC STRESS: A SYSTEMATIC REVIEW." Cardiopulmonary Physical Therapy Journal 15, no. 4 (December 2004): 37. http://dx.doi.org/10.1097/01823246-200415040-00038.

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38

Wilson, Luke C., James D. Cotter, Jui-lin Fan, Rebekah A. I. Lucas, Kate N. Thomas, and Philip N. Ainslie. "Mechanisms Of Orthostatic Intolerance During Passive Heat Stress." Medicine & Science in Sports & Exercise 41 (May 2009): 342. http://dx.doi.org/10.1249/01.mss.0000355592.71566.a5.

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39

Lipsitz, Lewis A., Carolyn M. Connelly, Margaret Kelley-Gagnon, Dan K. Kiely, Darrell Abernethy, and Carol Waksmonski. "Cardiovascular adaptation to orthostatic stress during vasodilator therapy*." Clinical Pharmacology & Therapeutics 60, no. 4 (October 1996): 461–71. http://dx.doi.org/10.1016/s0009-9236(96)90203-9.

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40

Wilson, Timothy D., Jorge M. Serrador, and J. Kevin Shoemaker. "Head position modifies cerebrovascular response to orthostatic stress." Brain Research 961, no. 2 (January 2003): 261–68. http://dx.doi.org/10.1016/s0006-8993(02)03965-3.

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41

Larsson, Gunilla, Peter O. O. Julu, Ingegerd Witt Engerström, Marlene Sandlund, and Britta Lindström. "Normal reactions to orthostatic stress in Rett syndrome." Research in Developmental Disabilities 34, no. 6 (June 2013): 1897–905. http://dx.doi.org/10.1016/j.ridd.2013.02.027.

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42

Appenzeller, Peter, Marlowe Eldridge, Otto Appenzeller, and Stephen Wood. "Standing orthostatic stress at low and high altitude." Journal of the Autonomic Nervous System 31, no. 2 (November 1990): 171–72. http://dx.doi.org/10.1016/0165-1838(90)90074-s.

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43

Mader, Greg, Mette Olufsen, and Adam Mahdi. "Modeling Cerebral Blood Flow Velocity During Orthostatic Stress." Annals of Biomedical Engineering 43, no. 8 (December 31, 2014): 1748–58. http://dx.doi.org/10.1007/s10439-014-1220-4.

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44

Fogelman, Amy, Charity Sauder, Matthew Kearney, Damian Dyckman, Nathan Kuipers, and Chester Ray. "Endurance Training Reduces Renal Vasoconstriction to Orthostatic Stress." Medicine & Science in Sports & Exercise 38, Supplement (May 2006): S44—S45. http://dx.doi.org/10.1249/00005768-200605001-01077.

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45

Charleston-Villalobos, Sonia, Sina Reulecke, Andreas Voss, Mahmood R. Azimi-Sadjadi, Ramón González-Camarena, Mercedes J. Gaitán-González, Jesús A. González-Hermosillo, Guadalupe Hernández-Pacheco, Steffen Schulz, and Tomás Aljama-Corrales. "Time-Frequency Analysis of Cardiovascular and Cardiorespiratory Interactions During Orthostatic Stress by Extended Partial Directed Coherence." Entropy 21, no. 5 (May 5, 2019): 468. http://dx.doi.org/10.3390/e21050468.

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In this study, the linear method of extended partial directed coherence (ePDC) was applied to establish the temporal dynamic behavior of cardiovascular and cardiorespiratory interactions during orthostatic stress at a 70° head-up tilt (HUT) test on young age-matched healthy subjects and patients with orthostatic intolerance (OI), both male and female. Twenty 5-min windows were used to analyze the minute-wise progression of interactions from 5 min in a supine position (baseline, BL) until 18 min of the orthostatic phase (OP) without including pre-syncopal phases. Gender differences in controls were present in cardiorespiratory interactions during OP without compromised autonomic regulation. However in patients, analysis by ePDC revealed considerable dynamic alterations within cardiovascular and cardiorespiratory interactions over the temporal course during the HUT test. Considering the young female patients with OI, the information flow from heart rate to systolic blood pressure (mechanical modulation) was already increased before the tilt-up, the information flow from systolic blood pressure to heart rate (neural baroreflex) increased during OP, while the information flow from respiration to heart rate (respiratory sinus arrhythmia) decreased during the complete HUT test. Findings revealed impaired cardiovascular interactions in patients with orthostatic intolerance and confirmed the usefulness of ePDC for causality analysis.
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46

Monahan, Kevin D., and Chester A. Ray. "Vestibulosympathetic reflex during orthostatic challenge in aging humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 5 (November 1, 2002): R1027—R1032. http://dx.doi.org/10.1152/ajpregu.00298.2002.

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Aging attenuates the increase in muscle sympathetic nerve activity (MSNA) and elicits hypotension during otolith organ engagement in humans. The purpose of the present study was to determine the neural and cardiovascular responses to otolithic engagement during orthostatic stress in older adults. We hypothesized that age-related impairments in the vestibulosympathetic reflex would persist during orthostatic challenge in older subjects and might compromise arterial blood pressure regulation. MSNA, arterial blood pressure, and heart rate responses to head-down rotation (HDR) performed with and without lower body negative pressure (LBNP) in prone subjects were measured. Ten young (27 ± 1 yr) and 11 older subjects (64 ± 1 yr) were studied prospectively. HDR performed alone elicited an attenuated increase in MSNA in older subjects (Δ106 ± 28 vs. Δ20 ± 7% for young and older subjects). HDR performed during simultaneous orthostatic stress increased total MSNA further in young (Δ53 ± 15%; P < 0.05) but not older subjects (Δ−5 ± 4%). Older subjects demonstrated consistent significant hypotension during HDR performed both alone (Δ−6 ± 2 mmHg) and during LBNP (Δ−7 ± 2 mmHg). These data provide experimental support for the concept that age-related impairments in the vestibulosympathetic reflex persist during orthostatic challenge in older adults. Furthermore, these findings are consistent with the concept that age-related alterations in vestibular function might contribute to altered orthostatic blood pressure regulation with age in humans.
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47

Butler, G. C., Y. Yamamoto, and R. L. Hughson. "Fractal nature of short-term systolic BP and HR variability during lower body negative pressure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R26—R33. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r26.

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We have shown previously that the heart rate variability (HRV) signal is fractal in nature with a high degree of complexity, as given by the calculated fractal dimension (DF). We have also reported that loss of complexity, as indicated by a reduction in DF of HRV, is associated with orthostatic hypotension and impending syncope. To extend this investigation of cardiovascular responses, we have investigated the signal characteristics of short-term systolic blood pressure variability (BPV) coincident with measurements of HRV during orthostatic stress. Eight healthy men completed a test protocol of 20 min supine rest followed sequentially by 10 min at each of -5, -15, -25, -40, and -50 mmHg lower body negative pressure (LBNP) and 10 min supine recovery. We found that resting BPV and HRV were fractal with approximately 70% of both variables in the fractal component of the variability signal. The slope of the 1/f beta relationship was 1.16 +/- 0.12 for HRV and 2.31 +/- 0.17 for BPV. With increasing levels of orthostatic stress, the 1/f beta slope of HRV increased significantly to 1.68 +/- 0.08 at -50 mmHg LBNP, whereas the 1/f beta slope was unchanged for BPV. Indicators of parasympathetic and sympathetic nervous system activity derived from heart rate variability suggested reduced and increased values, respectively, as the LBNP increased. These data indicate important differences in heart rate and blood pressure control under orthostatic stress.
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48

Miller, Judith A., John S. Floras, Bernard Zinman, Karl L. Skorecki, and Alexander G. Logan. "Effect of Hyperglycaemia on Arterial Pressure, Plasma Renin Activity and Renal Function in Early Diabetes." Clinical Science 90, no. 3 (March 1, 1996): 189–95. http://dx.doi.org/10.1042/cs0900189.

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1. In insulin-dependent diabetes mellitus, hyperglycaemia has a profound effect on renal and systemic haemodynamic function. The mechanism for this is unknown. 2. We conducted a study in 11 males with insulin-dependent diabetes mellitus, within 6 years of diagnosis. We examined the neurohumoral, haemodynamic and renal variables during euglycaemia (4.0–6.0 mmol/l) and after a 12 h period of hyperglycaemia (8.5–10.5 mmol/l). Subjects were examined in a sodium-replete state during supine rest and during simulated orthostatic stress induced by lower body negative pressure at –15 mmHg. 3. Variations in glycaemia markedly influenced plasma renin activity, which was increased at baseline during hyperglycaemia (3.82 ± 0.66 pmol of angiotensin I h−1 ml−1 compared with 2.13 ± 033 pmol of angiotensin I h−1 ml−1 during euglycaemia, P = 0.009), and rose further during simulated orthostatic stress. Mean arterial pressure was also elevated during hyperglycaemia (89 ± 2 mmHg compared with 81 ± 3 mmHg during euglycaemia, P = 0.03), both at rest and during orthostatic stress. 4. The renal haemodynamic effects of hyperglycaemia included maintenance of glomerular filtration rate in the face of significant declines in renal blood flow, and a probable increase in filtration fraction (0.21 ± 0.01 compared with 0.18 ± 0.01 during euglycaemia, P = 0.06). The responses of mean arterial pressure and renal blood flow to simulated orthostatic stress were not affected by hyperglycaemia, but the forearm vascular response was significantly augmented. 5. These data suggest that sustained hyperglycaemia activates the renin—angiotensin system, thereby increasing systemic and renal vasomotor tone. Over time such changes may have deleterious microvascular consequences.
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49

Ichinose, Masashi, Mitsuru Saito, Takeshi Ogawa, Keiji Hayashi, Narihiko Kondo, and Takeshi Nishiyasu. "Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 5 (November 2004): H2147—H2153. http://dx.doi.org/10.1152/ajpheart.00215.2004.

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We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: −15 and −35 mmHg). At −15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at −35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at −15 mmHg LBNP (vs. CON) and further shifted upward at −35 mmHg LBNP. At −15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at −35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.
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50

Carter, Jason R., Sarah F. Stream, John J. Durocher, and Robert A. Larson. "Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans." American Journal of Physiology-Endocrinology and Metabolism 300, no. 5 (May 2011): E771—E778. http://dx.doi.org/10.1152/ajpendo.00674.2010.

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Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (−5, −10, −15, −20, −30, and −40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo ( n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.
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