Central chemoreflex sensitivity and sympathetic neural outflow in elite breath-hold divers

2008 ◽  
Vol 104 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Zeljko Dujic ◽  
Vladimir Ivancev ◽  
Karsten Heusser ◽  
Gordan Dzamonja ◽  
Ivan Palada ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Sympathetic Activity ◽  
Arterial Oxygen ◽  
System Response ◽  
Breath Holding ◽  
Breath Hold ◽  
Control Subjects ◽  
Obstructive Sleep ◽  
End Tidal

Repeated hypoxemia in obstructive sleep apnea patients increases sympathetic activity, thereby promoting arterial hypertension. Elite breath-holding divers are exposed to similar apneic episodes and hypoxemia. We hypothesized that trained divers would have increased resting sympathetic activity and blood pressure, as well as an excessive sympathetic nervous system response to hypercapnia. We recruited 11 experienced divers and 9 control subjects. During the diving season preceding the study, divers participated in 7.3 ± 1.2 diving fish-catching competitions and 76.4 ± 14.6 apnea training sessions with the last apnea 3–5 days before testing. We monitored beat-by-beat blood pressure, heart rate, femoral artery blood flow, respiration, end-tidal CO2, and muscle sympathetic nerve activity (MSNA). After a baseline period, subjects began to rebreathe a hyperoxic gas mixture to raise end-tidal CO2 to 60 Torr. Baseline MSNA frequency was 31 ± 11 bursts/min in divers and 33 ± 13 bursts/min in control subjects. Total MSNA activity was 1.8 ± 1.5 AU/min in divers and 1.8 ± 1.3 AU/min in control subjects. Arterial oxygen saturation did not change during rebreathing, whereas end-tidal CO2 increased continuously. The slope of the hypercapnic ventilatory and MSNA response was similar in both groups. We conclude that repeated bouts of hypoxemia in elite, healthy breath-holding divers do not lead to sustained sympathetic activation or arterial hypertension. Repeated episodes of hypoxemia may not be sufficient to drive an increase in resting sympathetic activity in the absence of additional comorbidities.

Short-term intermittent hypoxia enhances sympathetic responses to continuous hypoxia in humans

2007 ◽  
Vol 103 (3) ◽  
pp. 835-842 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Cynthia S. Hogeman ◽  
Sadeq Quraishi ◽  
Latoya Linton-Frazier ◽  
Kristen S. Gray
Keyword(s):  
Blood Pressure ◽  
Sleep Apnea ◽  
Sympathetic Activity ◽  
Intermittent Hypoxia ◽  
Muscle Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Short Term ◽  
Healthy Humans ◽  
Obstructive Sleep ◽  
Normal Humans

Short-term intermittent hypoxia leads to sustained sympathetic activation and a small increase in blood pressure in healthy humans. Because obstructive sleep apnea, a condition associated with intermittent hypoxia, is accompanied by elevated sympathetic activity and enhanced sympathetic chemoreflex responses to acute hypoxia, we sought to determine whether intermittent hypoxia also enhances chemoreflex activity in healthy humans. To this end, we measured the responses of muscle sympathetic nerve activity (MSNA, peroneal microneurography) to arterial chemoreflex stimulation and deactivation before and following exposure to a paradigm of repetitive hypoxic apnea (20 s/min for 30 min; O2 saturation nadir 81.4 ± 0.9%). Compared with baseline, repetitive hypoxic apnea increased MSNA from 113 ± 11 to 159 ± 21 units/min ( P = 0.001) and mean blood pressure from 92.1 ± 2.9 to 95.5 ± 2.9 mmHg ( P = 0.01; n = 19). Furthermore, compared with before, following intermittent hypoxia the MSNA (units/min) responses to acute hypoxia [fraction of inspired O2 (FiO2) 0.1, for 5 min] were enhanced (pre- vs. post-intermittent hypoxia: +16 ± 4 vs. +49 ± 10%; P = 0.02; n = 11), whereas the responses to hyperoxia (FiO2 0.5, for 5 min) were not changed significantly ( P = NS; n = 8). Thus 30 min of intermittent hypoxia is capable of increasing sympathetic activity and sensitizing the sympathetic reflex responses to hypoxia in normal humans. Enhanced sympathetic chemoreflex activity induced by intermittent hypoxia may contribute to altered neurocirculatory control and adverse cardiovascular consequences in sleep apnea.

Abstract P161: Inspiratory Muscle Training and Aerobic Training in the Treatment of Hypertension: Baroreflex Sensitivity, Sympathetic Activity and Endothelial Function Responses

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Janaina B Ferreira ◽  
Valéria Hong ◽  
Otávio Coelho ◽  
Silvia Cavasin ◽  
Fernando Santos ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Function ◽  
Arterial Hypertension ◽  
Vascular Function ◽  
Sympathetic Activity ◽  
Baroreflex Sensitivity ◽  
Aerobic Training ◽  
Inspiratory Muscle ◽  
Inspiratory Muscle Training ◽  
Muscle Training

Arterial hypertension is associated to sympathetic hyperactivity and endothelial dysfunction. Aerobic training (AT) is highly recommended to improve vascular function minimizing complications and Inspiratory muscle training (IMT) has demonstrated beneficial effects in this population, especially improving cardiovascular autonomic control. We sought to observe the effects of both training modalities on baroreflex sensitivity, sympathetic activity and endothelial function, in patients with controlled arterial hypertension. 10 patients (55±4 years old, both genders) were included and allocated into two groups: IMT (n=5, 7days/week, 30min/day, load=30%PImax) and AT (n=5, 2days/week, 1hour/day, load=70%HRmax). Both training protocols were performed during 12 weeks. Blood pressure (BP) and heart rate (HR) signals were recorded before and after protocols, as well as the other evaluations, by pulse telemetry (Finometer®PRO) and ECG (PowerLab®). Arterial baroreflex sensitivity was analysed by sequence method. Sympathetic activity was evaluated by microneurography (PowerLab®) and the endothelial function was evaluated by flow mediated dilation (EnVisor CHD, Philips, Bothell, WA, USA). After 12 weeks treatment IMT improved baroreflex sensitvity to both tachycardic and bradycardic responses respectively (BRR Down Gain (mean): IMT=26.51(±1.7)vs15.57(±6.7), AT=13.94(±5.5)vs17.92(±1.6); BRR Up Gain (mean): IMT=17.16(±1.2)vs16.28(±1.1), AT=12.39(±5)vs12.69(±3.3)). Additionally, we observed reduction of sympathetic activity in both groups (IMT:33.23±11.79vs25.07±13.28; AT:29.88±7.07vs24.09±6.37) and improvement of endothelial function independent of the treatment (IMT:6.4±2.18vs7.22±2.08; AT:5.49±7.43vs7.06±3.12). Regarding the responses to inspiratory muscle training and aerobic training on autonomic cardiovascular control and endothelial function in Hypertension, we demonstrated for the first time that IMT and AT present quite similar effects in patients with controlled blood pressure.

Obstructive Sleep Apnea in Children With Down Syndrome

PEDIATRICS ◽  
1991 ◽  
Vol 88 (1) ◽  
pp. 132-139
Author(s):  
Carole L. Marcus ◽  
Thomas G. Keens ◽  
Daisy B. Bautista ◽  
Walter S. von Pechmann ◽  
Sally L. Davidson Ward
Keyword(s):  
Obstructive Sleep Apnea ◽  
Down Syndrome ◽  
Sleep Apnea ◽  
Arterial Oxygen Saturation ◽  
Sleep Apnea Syndrome ◽  
Arterial Oxygen ◽  
Children With Down Syndrome ◽  
Obstructive Sleep ◽  
Apnea Syndrome ◽  
End Tidal

Children with Down syndrome have many predisposing factors for the obstructive sleep apnea syndrome (OSAS), yet the type and severity of OSAS in this population has not been characterized. Fifty-three subjects with Down syndrome (mean age 7.4 ± 1.2 [SE] years; range 2 weeks to 51 years) were studied. Chest wall movement, heart rate, electrooculogram, end-tidal Po2 and Pco2, transcutaneous Po2 and Pco2, and arterial oxygen saturation were measured during a daytime nap polysomnogram. Sixteen of these children also underwent overnight polysomnography. Nap polysomnograms were abnormal in 77% of children; 45% had obstructive sleep apnea (OSA), 4% had central apnea, and 6% had mixed apneas; 66% had hypoventilation (end-tidal Pco2, >45 mm Hg) and 32% desaturation (arterial oxygen saturation <90%). Overnight studies were abnormal in 100% of children, with OSA in 63%, hypoventilation in 81%, and desaturation in 56%. Nap studies significantly underestimated the presence of abnormalities when compared to overnight polysomnograms. Seventeen (32%) of the children were referred for testing because OSAS was clinically suspected, but there was no clinical suspicion of OSAS in 36 (68%) children. Neither age, obesity, nor the presence of congenital heart disease affected the incidence of OSA, desaturation, or hypoventilation. Polysomnograms improved in all 8 children who underwent tonsilletomy and adenoidectomy, but they normalized in only 3. It is concluded that children with Down syndrome frequently have OSAS, with OSA, hypoxemia, and hypoventilation. Obstructive sleep apnea syndrome is seen frequently in those children in whom it is not clinically suspected. It is speculated that OSAS may contribute to the unexplained pulmonary hypertension seen in children with Down syndrome.

Abstract 2470: Augmented Tonic Activation Of Chemoreceptors May Contribute To Sympathetic Overactivity In Patients With Essential Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Maciej Sinski ◽  
Jacek Lewandowski ◽  
Joanna Bidiuk ◽  
Piotr Abramczyk ◽  
Anna Dobosiewicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Hemoglobin Saturation ◽  
Ambient Oxygen ◽  
Young Subjects ◽  
End Tidal ◽  
Carotid Body Chemoreceptors

Rationale : Peripheral chemoreflex contributes to regulation of arterial blood pressure and chemoreceptors respond not only to hypoxia but they are also continuously activated by normal ambient oxygen concentration. Stimulation of chemoreceptors activates sympathetic traffic and this response may be altered in subjects with essential hypertension.. Objective: The aim of our study was to investigate the effect of deactivation of carotid body chemoreceptors on sympathetic activity directly measured as MSNA (muscle sympathetic nerve activity) in young subjects with mild to moderate untreated hypertension. Methods: Twelve patients with essential hypertension (36±9 years, all men, BMI 29±4 kg/m 2 ,) and 8 controls (37±7, men BMI 27±5kg/m 2 ) participated in the study. None of the patients or controls received any medications. MSNA (burst/minute and mean burst amplitude - au), systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate (HR), ECG, hemoglobin saturation with oxygen (Sat%), end tidal CO 2 and respiratory movements were monitored and measured after 10 minute of respiration by non-rebreathing mask with 100% 0 2 or 21% O 2 applied in blinded fashion. Results: Hypertensives had higher resting MSNA (38.6 ±8.6 burst/min vs. 30.3±.7 burst/min, p<0.05), SBP (149.1± 9.9 vs. 124.1 ±11.6, p < 0.05) and DBP (92.1 ±8.6 vs. 78.1 ± 8.9, p< 0.05) than controls. Breathing with 100% oxygen caused significant decrease in MSNA in hypertensives (from 38.6 ± 8.6 burst/min to 26.3 burst/min ± 6.8 and from 100 ± 0 au to 86 ± 18 au, p< 0.05) and no change in MSNA in controls (30.3 ± 5.7 burst/min initially and 27.3 burst/min ± 6.2 after 100% 0 2 , 100 ± 0 au vs. 98 ± 11 au). Blood pressure, end tidal CO 2 , respiration frequency did not change significantly after hyperoxia while HR decreased (from 69.6 ± 9 to 64.1 ± 7 in hypertensives p<0.05 and from 67± 8 to 62.5 ± 7 in controls, p< 0.05). Sat% increased significantly in both groups to 99%. Conclusions: Increased sympathetic activity in young, untreated hypertensives may be caused by the elevated tonic chemoreflex activation.

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.

Blood pressure increase detected by ambulatory monitoring correlates with hypoxemia reflecting sleep apnea severity

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 222-232 ◽  
Author(s):  
Soňa Grešová ◽  
Zoltán Tomori ◽  
Martin Kurpas ◽  
Alexander Marossy ◽  
Adela Vrbenská ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sleep Apnea ◽  
Continuous Positive Airway Pressure ◽  
Arterial Hypertension ◽  
Oxygen Saturation ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Arterial Oxygen Saturation ◽  
Secondary Component ◽  
Arterial Oxygen

AbstractAmbulatory blood pressure monitoring and parallel polysomnographic study were performed in 116 adult males divided into 6 groups. Thirty blood-pressure (BP) and polysomnographic variables were measured to test their usefulness for screening for both arterial hypertension and sleep apnea-hypopnea syndrome (SAHS). The development of severe breathing disorders and hypoxemia during sleep was attributed to SAHS, when compared with measurements in healthy controls and in patients with arterial hypertension. Such disorders manifested as an increased apnea-hypopnea index, apnea index, duration of arterial oxygen saturation of less than 85%, and decrease of average arterial oxygen saturation that correlated with nocturnal average diastolic BP (p=0.0049, p=0.0027, p=0.049 and p=0.0457, respectively). These respiratory disorders resulted in various nocturnal, rather than diurnal, and diastolic and systolic BP variables. The acute antihypertensive effect of continuous positive airway pressure therapy for SAHS significantly reduced the episodes of apnea and hypopnea and the secondary component of hypertension caused by excessive sympathetic stimulation. For the SAHS-induced, dose-dependent component of hypertension that responded to continuous positive airway pressure, the following variables, in decreasing significance, were useful: nocturnal average systolic and diastolic BP and 24-hour average systolic and diastolic BP, as well as percent time elevation and mean blood pressure load. The monitoring of these variables could contribute to early diagnostic and prognostic stratification of complications and adequate therapy of the secondary component of hypertension caused by SAHS.

The human spleen as an erythrocyte reservoir in diving-related interventions

2002 ◽  
Vol 92 (5) ◽  
pp. 2071-2079 ◽  
Author(s):  
Kurt Espersen ◽  
Hans Frandsen ◽  
Torben Lorentzen ◽  
Inge-Lis Kanstrup ◽  
Niels J. Christensen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Indirect Method ◽  
Hemoglobin Concentration ◽  
Breath Holding ◽  
Breath Hold ◽  
Peripheral Blood Flow ◽  
Diving Response ◽  
Human Spleen ◽  
The Face

Twelve subjects without and ten subjects with diving experience performed short diving-related interventions. After labeling of erythrocytes, scintigraphic measurements were continuously performed during these interventions. All interventions elicited a graduated and reproducible splenic contraction, depending on the type, severity, and duration of the interventions. The splenic contraction varied between ∼10% for “apnea” (breath holding for 30 s) and “cold clothes” (cold and wet clothes applied on the face with no breath holding for 30 s) and ∼30–40% for “simulated diving” (simulated breath-hold diving for 30 s), “maximal apnea” (breath holding for maximal duration), and “maximal simulated diving” (simulated breath-hold diving for maximal duration). The strongest interventions (simulated diving, maximal apnea, and maximal simulated diving) elicited modest but significant increases in hemoglobin concentration (0.1–0.3 mmol/l) and hematocrit (0.3–1%). By an indirect method, the splenic venous hematocrit was calculated to 79%. No major differences were observed between the two groups. The splenic contraction should, therefore, be included in the diving response on equal terms with bradycardia, decreased peripheral blood flow, and increased blood pressure.

scholarly journals The effect of antihypertensive therapy and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea syndrome in association with arterial hypertension

2017 ◽  
Vol 14 (1) ◽  
pp. 37-40
Author(s):  
E M Elfimova ◽  
A V Rvacheva ◽  
M I Tripoten ◽  
O V Pogorelova ◽  
T V Balakhonova ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Antihypertensive Therapy ◽  
Adhesion Molecule ◽  
Severe Obstructive Sleep Apnea ◽  
Cpap Therapy ◽  
Obstructive Sleep

Objective. To evaluate the effect of antihypertensive therapy (AHT) and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea (OSA) syndrome in association with arterial hypertension (AH). Materials and methods. The study included 43 male patients with severe OSA syndrome (Apnea-Hypopnea Index 52.4 [46.1; 58.6]) and AH (systolic blood pressure 144.0 [142.0; 156.0] mm Hg, diastolic blood pressure 90.9 [88.3; 93.5] mm Hg). Treatment with angiotensin-converting enzyme inhibitors, calcium antagonists, and thiazide-like diuretics was performed till target BP level measured with Korotkoff method was achieved. The patients who had reached target BP level (BP≤140/90 mm Hg) were randomized into two groups: group 1 included 23 patients who continued taking the AHT, group 2 included 22 patients who continued taking the AHT to which CPAP therapy was added. Peripheral blood lymphocyte immunophenotyping, cytokine panel test (IL-1β, IL-6, tumor necrosis factor a, IL-2Ra, sCD40L), adhesion molecule analysis (ICAM-1, VCAM-1), thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1a), and endothelin-1 levels in blood serum were evaluated at admission, after target BP level achievement (2nd visit) and after 3 months of AHT or AHT+CPAP therapy (3rd visit). Flow-mediated dilation of brachial artery was assessed using reactive hyperemia test by D.Celermajer. Results. Against the background of combined AHT the target BP level was achieved by 95% of patients. After target BP level achievement a significant decrease of IL-1β -0.16 [-0.5; 0], p=0.000 level and number of CD50+ cells (lymphocytes with inter-cellular adhesion molecule ICAM-3) from 2158.5 [1884.7; 2432.3] to 1949.6 [1740.9; 2158.3], p=0.050 were observed in patients with severe OSA associated with AH. There were no significant changes in vascular endothelial function observed in patients taking only AHT. Significant decrease of fibrinogen (-0.3 [-0.4; -0.1], p=0.002) and homocystein (-2.03 [-3.8; -0.2], p=0.03) levels was observed in patients taking both AHT and CPAP therapy. Conclusion. The combination of AHT and CPAP therapy in patients with severe OSA and AH not only allows reaching the target BP level but also leads to inflammatory and endothelial dysfunction markers levels decrease.

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