scholarly journals Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

2011 ◽  
Vol 300 (5) ◽  
pp. H1788-H1793 ◽  
Author(s):  
John J. Durocher ◽  
Jenna C. Klein ◽  
Jason R. Carter
Keyword(s):  
Arterial Pressure ◽  
Strong Correlation ◽  
Mental Stress ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Spontaneous Fluctuations

Mental stress consistently induces a pressor response that is often accompanied by a paradoxical increase of muscle sympathetic nerve activity (MSNA). The purpose of the present study was to evaluate sympathetic baroreflex sensitivity (BRS) by examining the relations between spontaneous fluctuations of diastolic arterial pressure (DAP) and MSNA. We hypothesized that sympathetic BRS would be attenuated during mental stress. DAP and MSNA were recorded during 5 min of supine baseline, 5 min of mental stress, and 5 min of recovery in 32 young healthy adults. Burst incidence and area were determined for each cardiac cycle and placed into 3-mmHg DAP bins; the slopes between DAP and MSNA provided an index of sympathetic BRS. Correlations between DAP and MSNA were strong (>0.5) during baseline in 31 of 32 subjects, but we evaluated the change in slope only for those subjects maintaining a strong correlation during mental stress (16 subjects). During baseline, the relation between DAP and MSNA was negative when expressed as either burst incidence [slope = −1.95 ± 0.18 bursts·(100 beats)−1·mmHg−1; r = −0.86 ± 0.03] or total MSNA [slope = −438 ± 91 units·(beat)−1 mmHg−1; r = −0.76 ± 0.06]. During mental stress, the slope between burst incidence and DAP was significantly reduced [slope = −1.14 ± 0.12 bursts·(100 beats)−1·mmHg−1; r = −0.72 ± 0.03; P < 0.01], indicating attenuation of sympathetic BRS. A more detailed analysis revealed an attenuation of sympathetic BRS during the first 2 min of mental stress ( P < 0.01) but no change during the final 3 min of mental stress ( P = 0.25). The present study demonstrates that acute mental stress attenuates sympathetic BRS, which may partially contribute to sympathoexcitation during the mental stress-pressor response. However, this attenuation appears to be isolated to the onset of mental stress. Moreover, variable MSNA responses to mental stress do not appear to be directly related to sympathetic BRS.

Does infusion of ANG II increase muscle sympathetic nerve activity in patients with primary aldosteronism?

2008 ◽  
Vol 294 (6) ◽  
pp. R1873-R1879 ◽  
Author(s):  
Toshiyoshi Matsukawa ◽  
Takenori Miyamoto
Keyword(s):  
Primary Aldosteronism ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Ang Ii ◽  
Nerve Activity ◽  
Unilateral Adrenalectomy

Patients with primary aldosteronism (PA) were shown to have suppressed muscle sympathetic nerve activity (MSNA) in our previous study. Although baroreflex inhibition probably accounts in part for this reduced MSNA in PA, we hypothesized that the lowered activity of the renin-angiotensin system in PA may also contribute to the suppressed SNA. We recorded MSNA in 9 PA and 16 age-matched normotensive controls (NC). In PA, the resting mean blood pressure (MBP) and serum sodium concentrations were increased, and MSNA was reduced. We examined the effects of infusion of a high physiological dose of ANG II (5.0 ng·kg−1·min−1) on MSNA in 6 of 9 PA and 9 of 16 NC. Infusion of ANG II caused a greater pressor response in PA than NC, but, in spite of the greater increase in pressure, MSNA increased in PA, whereas it decreased in NC. Simultaneous infusion of nitroprusside and ANG II, to maintain central venous pressure at the baseline level and reduce the elevation in MBP induced by ANG II, caused significantly greater increases in MSNA in PA than in NC. Baroreflex sensitivity of heart rate, estimated during phenylephrine infusions, was reduced in PA, but baroreflex sensitivity of MSNA was unchanged in PA compared with NC. All the abnormalities in PA were eliminated following unilateral adrenalectomy. In conclusion, the suppressed SNA in PA depends in part on the low level of ANG II in these patients.

Vestibulosympathetic reflex during mental stress

2002 ◽  
Vol 93 (4) ◽  
pp. 1260-1264 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray ◽  
William H. Cooke
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Neural Activity ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Neural Activation ◽  
Nerve Activity ◽  
Vestibulosympathetic Reflex ◽  
Mental Stimulation

Increases in sympathetic neural activity occur independently with either vestibular or mental stimulation, but it is unknown whether sympathetic activation is additive or inhibitive when both stressors are combined. The purpose of the present study was to investigate the combined effects of vestibular and mental stimulation on sympathetic neural activation and arterial pressure in humans. Muscle sympathetic nerve activity (MSNA), arterial pressure, and heart rate were recorded in 10 healthy volunteers in the prone position during 1) head-down rotation (HDR), 2) mental stress (MS; using arithmetic), and 3) combined HDR and MS. HDR significantly ( P< 0.05) increased MSNA (9 ± 2 to 13 ± 2 bursts/min). MS significantly increased MSNA (8 ± 2 to 13 ± 2 bursts/min) and mean arterial pressure (87 ± 2 to 101 ± 2 mmHg). Combined HDR and MS significantly increased MSNA (9 ± 1 to 16 ± 2 bursts/min) and mean arterial pressure (89 ± 2 to 100 ± 3 mmHg). Increases in MSNA (7 ± 1 bursts/min) during the combination trial were not different from the algebraic sum of each trial performed alone (8 ± 2 bursts/min). We conclude that the interaction for MSNA and arterial pressure is additive during combined vestibular and mental stimulation. Therefore, vestibular- and stress-mediated increases of MSNA appear to occur independently in humans.

Human sympathetic and vagal baroreflex responses to sequential nitroprusside and phenylephrine

1999 ◽  
Vol 276 (5) ◽  
pp. H1691-H1698 ◽  
Author(s):  
László Rudas ◽  
Alexandra A. Crossman ◽  
Carlos A. Morillo ◽  
John R. Halliwill ◽  
Kari U. O. Tahvanainen ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Finger Arterial Pressure ◽  
Baseline Levels ◽  
Regression Slopes ◽  
Nerve Muscle ◽  
Spontaneous Fluctuations

We evaluated a method of baroreflex testing involving sequential intravenous bolus injections of nitroprusside followed by phenylephrine and phenylephrine followed by nitroprusside in 18 healthy men and women, and we drew inferences regarding human sympathetic and vagal baroreflex mechanisms. We recorded the electrocardiogram, photoplethysmographic finger arterial pressure, and peroneal nerve muscle sympathetic activity. We then contrasted least squares linear regression slopes derived from the depressor (nitroprusside) and pressor (phenylephrine) phases with 1) slopes derived from spontaneous fluctuations of systolic arterial pressures and R-R intervals, and 2) baroreflex gain derived from cross-spectral analyses of systolic pressures and R-R intervals. We calculated sympathetic baroreflex gain from integrated muscle sympathetic nerve activity and diastolic pressures. We found that vagal baroreflex slopes are less when arterial pressures are falling than when they are rising and that this hysteresis exists over pressure ranges both below and above baseline levels. Although pharmacological and spontaneous vagal baroreflex responses correlate closely, pharmacological baroreflex slopes tend to be lower than those derived from spontaneous fluctuations. Sympathetic baroreflex slopes are similar when arterial pressure is falling and rising; however, small pressure elevations above baseline silence sympathetic motoneurons. Vagal, but not sympathetic baroreflex gains vary inversely with subjects’ ages and their baseline arterial pressures. There is no correlation between sympathetic and vagal baroreflex gains. We recommend repeated sequential nitroprusside followed by phenylephrine doses as a simple, efficientmeans to provoke and characterize human vagal and sympathetic baroreflex responses.

scholarly journals Neurovascular responses to mental stress in prehypertensive humans

2011 ◽  
Vol 110 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Christopher E. Schwartz ◽  
John J. Durocher ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Mental Arithmetic ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Vascular Responses ◽  
Forearm Vascular Conductance

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120–139 and/or diastolic 80–89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

Neural mechanism of the pressor response to obstructive and nonobstructive apnea

1997 ◽  
Vol 83 (6) ◽  
pp. 2048-2054 ◽  
Author(s):  
Srinivas Katragadda ◽  
Ailiang Xie ◽  
Dominic Puleo ◽  
James B. Skatrud ◽  
Barbara J. Morgan
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Neural Mechanism ◽  
Nerve Activity ◽  
Saturation Pulse ◽  
Ganglionic Blockade ◽  
Pressor Responses

Katragadda, Srinivas, Ailiang Xie, Dominic Puleo, James B. Skatrud, and Barbara J. Morgan. Neural mechanism of the pressor response to obstructive and nonobstructive apnea. J. Appl. Physiol. 83(6): 2048–2054, 1997.—Obstructive and nonobstructive apneas elicit substantial increases in muscle sympathetic nerve activity and arterial pressure. The time course of change in these variables suggests a causal relationship; however, mechanical influences, such as release of negative intrathoracic pressure and reinflation of the lungs, are potential contributors to the arterial pressure rise. To test the hypothesis that apnea-induced pressor responses are neurally mediated, we measured arterial pressure (photoelectric plethysmography), muscle sympathetic nerve activity (peroneal microneurography), arterial O2 saturation (pulse oximeter), and end-tidal CO2 tension (gas analyzer) during sustained Mueller maneuvers, intermittent Mueller maneuvers, and simple breath holds in six healthy humans before, during, and after ganglionic blockade with trimethaphan (3–4 mg/min, titrated to produce complete disappearance of sympathetic bursts from the neurogram). Ganglionic blockade abolished the pressor responses to sustained and intermittent Mueller maneuvers (−4 ± 1 vs. +15 ± 3 and 0 ± 2 vs. +15 ± 5 mmHg) and breath holds (0 ± 3 vs. +11 ± 3, all P < 0.05). We conclude that the acute pressor response to obstructive and nonobstructive voluntary apnea is sympathetically mediated.

scholarly journals Muscle sympathetic nerve activity and hemodynamic responses to venous distension: does sex play a role?

2019 ◽  
Vol 316 (3) ◽  
pp. H734-H742 ◽  
Author(s):  
Daniel E. Mansur ◽  
Monique O. Campos ◽  
João D. Mattos ◽  
Adrielle C. S. Paiva ◽  
Marcos P. Rocha ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Young Women ◽  
Femoral Artery ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Compliance ◽  
Nerve Activity

Peripheral venous distension mechanically stimulates type III/IV sensory fibers in veins and evokes pressor and sympathoexcitatory reflex responses in humans. As young women have reduced venous compliance and impaired sympathetic transduction, we tested the hypothesis that pressor and sympathoexcitatory responses to venous distension may be attenuated in women compared with men. Mean arterial pressure (photoplethysmography), heart rate (HR), stroke volume (SV; Modelflow), cardiac output (CO = HR × SV), muscle sympathetic nerve activity (MSNA), femoral artery blood flow, and femoral artery conductance (Doppler ultrasound) were quantified in eight men (27 ± 4 yr) and nine women (28 ± 4 yr) before [control (CON)], during (INF), and immediately after (post-INF) a local infusion of saline [5% of the total forearm volume (30 ml/min); the infusion time was 2 ± 1 and 1 ± 1 min ( P = 0.0001) for men and women, respectively] through a retrograde catheter inserted into an antecubital vein, to which venous drainage and arterial supply had been occluded. Mean arterial pressure increased during and after infusion in both groups (vs. the CON group, P < 0.05), but women showed a smaller pressor response in the post-INF period (Δ+7.2 ± 2.0 vs. Δ+18.3 ± 3.9 mmHg in men, P = 0.019). MSNA increased and femoral artery conductance decreased similarly in both groups (vs. the CON group, P < 0.05) at post-INF. Although HR changes were similar, increases in SV (Δ+20.4 ± 8.6 vs. Δ+2.6 ± 2.7 ml, P = 0.05) and CO (Δ+0.84 ± 0.17 vs. Δ+0.34 ± 0.10 l/min, P = 0.024) were greater in men compared with women. Therefore, venous distension evokes a smaller pressor response in young women due to attenuated cardiac adjustments rather than reduced venous compliance or sympathetic transduction. NEW & NOTEWORTHY We found that the pressor response to venous distension was attenuated in young women compared with age-matched men. This was due to attenuated cardiac adjustments rather than reduced venous compliance, sympathetic activation, or impaired transduction and vascular control. Collectively, these findings suggest that an attenuated venous distension reflex could be involved in orthostatic intolerance in young women.

Spontaneous fluctuations in the peripheral photoplethysmographic waveform: roles of arterial pressure and muscle sympathetic nerve activity

2012 ◽  
Vol 302 (3) ◽  
pp. H826-H836 ◽  
Author(s):  
Gregory S. H. Chan ◽  
Azharuddin Fazalbhoy ◽  
Ingvars Birznieks ◽  
Vaughan G. Macefield ◽  
Paul M. Middleton ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Arterial Pressure Waveform ◽  
Clinical Value ◽  
Nerve Activity ◽  
Sympathetic Influence ◽  
Spontaneous Fluctuations

Assessment of spontaneous slow waves in the peripheral blood volume using the photoplethysmogram (PPG) has shown potential clinical value, but the physiological correlates of these fluctuations have not been fully elucidated. This study addressed the contribution of arterial pressure and muscle sympathetic nerve activity (MSNA) in beat-to-beat PPG variability in resting humans under spontaneous breathing conditions. Peripheral PPG waveforms were measured from the fingertip, earlobe, and toe in young and healthy individuals ( n = 13), together with the arterial pressure waveform, electrocardiogram, respiration, and direct measurement of MSNA by microneurography. Cross-spectral coherence analysis revealed that among the PPG waveforms, low-frequency fluctuations (0.04–0.15 Hz) in the ear PPG had the highest coherence with arterial pressure (0.71 ± 0.15) and MSNA (0.44 ± 0.18, with a peak of 0.71 ± 0.16 at 0.10 ± 0.03 Hz). The normalized midfrequency powers (0.08–0.15 Hz), with an emphasis on the 0.1-Hz region, were positively correlated between MSNA and the ear PPG ( r = 0.77, P = 0.002). Finger and toe PPGs had lower coherence with arterial pressure (0.35 ± 0.10 and 0.30 ± 0.11, respectively) and MSNA (0.33 ± 0.10 and 0.26 ± 0.10, respectively) in the LF band but displayed higher coherence between themselves (0.54 ± 0.09) compared with the ear ( P < 0.001), which may suggest the dominance of regional vasomotor activities and a common sympathetic influence in the glabrous skin. These findings highlight the differential mechanisms governing PPG waveform fluctuations across different body sites. Spontaneous PPG variability in the ear includes a major contribution from arterial pressure and MSNA, which may provide a rationale for its clinical utility.

Acute effects of electronic cigarettes on arterial pressure and peripheral sympathetic activity in young non-smokers

2020 ◽  
Author(s):  
Joshua Eric Gonzalez ◽  
William Harold Cooke
Keyword(s):  
Arterial Pressure ◽  
Health Risks ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Electronic Cigarettes ◽  
Muscle Sympathetic Nerve Activity ◽  
Crossover Design ◽  
Acute Effects ◽  
Nerve Activity ◽  
Peripheral Sympathetic Activity

E-cigarettes like the JUUL are marketed as an alternative to smoking for those who want to decrease the health risks of tobacco. Tobacco cigarettes increase heart rate (HR) and arterial pressure (AP), while reducing muscle sympathetic nerve activity (MSNA) through sympathetic baroreflex inhibition. The acute effects of e-cigarettes on AP and MSNA have not been reported: our purpose was to clarify this issue. Using a randomized crossover design, participants inhaled on a JUUL containing nicotine (59 mg/ml) and a similar placebo e-cigarette (0 mg/ml). Experiments were separated by ~1 month. We recorded baseline ECG, AP (n=15), and MSNA (n=10). Subjects rested for 10 min, (BASE) and then inhaled once every 30 s on an e-cigarette that contained nicotine or placebo (VAPE) for 10 min followed by a 10-min recovery (REC). Data were expressed as Δmeans±SE from BASE. HR increased in the nicotine condition during VAPE and returned to BASE values in REC (5.0±1.3 nicotine vs 0.1±0.8 b/min placebo, during VAPE P<.01). AP increased in the nicotine condition during VAPE and remained elevated during REC. (6.5±1.6 nicotine vs 2.6±1 mmHg placebo, during VAPE and 4.6.0±1.7 nicotine vs 1.4±1.4 mmHg placebo during REC; p<.05). MSNA decreased from BASE to VAPE and did not restore during REC (-7.1±1.6 nicotine vs 2.6±2 bursts/min placebo during VAPE and -5.8±1.7 nicotine vs 0.5±1.4 placebo during REC; p<.05). Our results show that acute e-cigarette usage increases mean arterial pressure leading to a baroreflex mediated inhibition of MSNA.

Baroreflex attenuation after hypotension induced by vena caval occlusion in anesthetized dogs

1995 ◽  
Vol 268 (4) ◽  
pp. R859-R864
Author(s):  
F. Sawano ◽  
T. Shibamoto ◽  
T. Hayashi ◽  
Y. Saeki
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Systemic Hypotension ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors ◽  
Pressure Fall

We determined effects of vena caval occlusion-induced systemic hypotension of 50 mmHg lasting 10 min (VCO) on efferent sympathetic nerve activity (SNA) and sympathetic baroreflex responsiveness. We recorded simultaneously SNA to the kidney (RNA), heart (CNA), spleen (SpNA), and liver (HNA) in anesthetized dogs. Baroreflex sensitivity was assessed using the ratio of a reflex SNA increase to a mean arterial pressure fall, which was also induced by caval occlusion. During VCO, SNA initially and equivocally increased, followed by recovery toward baseline. Cervical vagotomy attenuated the VCO-induced initial sympathoexcitation and subsequently maintained SNA at higher levels than those of intact animals, a finding basically similar to hemorrhagic hypotension [S. Koyama, F. Sawano, Y. Matsuda, Y. Saeki, T. Shibamoto, T. Hayashi, Jr., Y. Matsubayashi, and M. Kawamoto. Am. J. Physiol. 262 (Regulatory Integrative Comp. Physiol. 31): R579-R585, 1992]. At 5 min after releasing VCO, the baroreflex responsiveness was significantly attenuated: RNA, 79 +/- 11%; CNA, 78 +/- 8%; HNA, 60 +/- 16%; SpNA, 81 +/- 13% of the corresponding baseline. Fifteen minutes after VCO, this attenuation disappeared. Either vagotomy or pretreatment with intravenous vasopressin V1 receptor antagonist abolished this baroreflex attenuation. In conclusion, systemic hypotension to 50 mmHg for 10 min causes transient attenuation of sympathetic baroreflex sensitivity due to circulating vasopressin released by unloading of cardiopulmonary receptors during hypotension.

Arterial pressure and muscle sympathetic nerve activity are increased after two hours of sustained but not cyclic hypoxia in healthy humans

2005 ◽  
Vol 98 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Renaud Tamisier ◽  
Amit Anand ◽  
Luz M. Nieto ◽  
David Cunnington ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sustained Hypoxia

Sustained and episodic hypoxic exposures lead, by two different mechanisms, to an increase in ventilation after the exposure is terminated. Our aim was to investigate whether the pattern of hypoxia, cyclic or sustained, influences sympathetic activity and hemodynamics in the postexposure period. We measured sympathetic activity (peroneal microneurography), hemodynamics [plethysmographic forearm blood flow (FBF), arterial pressure, heart rate], and peripheral chemosensitivity in normal volunteers on two occasions during and after 2 h of either exposure. By design, mean arterial oxygen saturation was lower during sustained relative to cyclic hypoxia. Baseline to recovery muscle sympathetic nerve activity and blood pressure went from 15.7 ± 1.2 to 22.6 ± 1.9 bursts/min ( P < 0.01) and from 85.6 ± 3.2 to 96.1 ± 3.3 mmHg ( P < 0.05) after sustained hypoxia, respectively, but did not exhibit significant change from 13.6 ± 1.5 to 17.3 ± 2.5 bursts/min and 84.9 ± 2.8 to 89.8 ± 2.5 mmHg after cyclic hypoxia. A significant increase in FBF occurred after sustained, but not cyclic, hypoxia, from 2.3 ± 0.2 to 3.29 ± 0.4 and from 2.2 ± 0.1 to 3.1 ± 0.5 ml·min−1·100 g of tissue−1, respectively. Neither exposure altered the ventilatory response to progressive isocapnic hypoxia. Two hours of sustained hypoxia increased not only muscle sympathetic nerve activity but also arterial blood pressure. In contrast, cyclic hypoxia produced slight but not significant changes in hemodynamics and sympathetic activity. These findings suggest the cardiovascular response to acute hypoxia may depend on the intensity, rather than the pattern, of the hypoxic exposure.

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