Contrasting effects of hypoxia and hypercapnia on ventilation and sympathetic activity in humans

1989 ◽  
Vol 67 (5) ◽  
pp. 2101-2106 ◽  
Author(s):  
V. K. Somers ◽  
A. L. Mark ◽  
D. C. Zavala ◽  
F. M. Abboud
Keyword(s):  
Sympathetic Activity ◽  
Peroneal Nerve ◽  
Sympathetic Nerve Activity ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inhibitory Influence ◽  
Nerve Activity ◽  
Peripheral Chemoreceptor ◽  
Absolute Increase ◽  
Hypercapnic Hypoxia

We compared the effects of isocapnic hypoxia (IHO) and hyperoxic hypercapnia (HC) on sympathetic nerve activity (SNA) recorded from a peroneal nerve in 13 normal subjects. HC caused greater increases in blood pressure (BP), minute ventilation (VE), and SNA [53 +/- 14% (SE) during HC vs. 21 +/- 7% during IHO; P less than 0.05]. Even at equivalent levels of VE, HC still elicited greater SNA than IHO. However, apnea during HC caused a lesser (P less than 0.05) increase in SNA (91 +/- 26% compared with apnea on room air) than apnea during IHO (173 +/- 50%). Hypercapnic hypoxia resulted in a greater absolute increase in VE (23.6 +/- 2.8 l/min) than the additive increases due to HC alone plus IHO alone (18.0 +/- 1.8 l/min, P less than 0.05). SNA also increased synergistically by 108 +/- 23% with the combined stimulus compared with the additive effect of HC alone plus IHO alone (68 +/- 19%; P less than 0.05). We conclude that 1) HC causes greater increases in VE and SNA than does hypoxia; 2) for the same increase in VE, hypercapnia still causes a greater increase in SNA than hypoxia; however, during apnea, hypoxia causes a much greater increase in SNA than hypercapnia; 3) the inhibitory influence of ventilation on SNA is greater during hypoxia (i.e., predominantly peripheral chemoreceptor stimulation) than hypercapnia (i.e., predominantly central chemoreceptor stimulation); and 4) combined hypoxia and hypercapnia have a synergistic effect on SNA as well as on VE.

Influence of ventilation and hypocapnia on sympathetic nerve responses to hypoxia in normal humans

1989 ◽  
Vol 67 (5) ◽  
pp. 2095-2100 ◽  
Author(s):  
V. K. Somers ◽  
A. L. Mark ◽  
D. C. Zavala ◽  
F. M. Abboud
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inhibitory Influence ◽  
Sympathetic Response ◽  
Normal Humans ◽  
Breathing Room ◽  
Baroreceptor Activation ◽  
Voluntary Apnea

The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.

Carotid baroreceptor-muscle sympathetic relation in humans

1987 ◽  
Vol 253 (6) ◽  
pp. R929-R934 ◽  
Author(s):  
R. F. Rea ◽  
D. L. Eckberg
Keyword(s):  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Normal Subjects ◽  
Threshold Level ◽  
Sigmoid Function ◽  
Nerve Activity ◽  
Carotid Baroreceptor ◽  
Neck Pressure

The purpose of this study was to define the relation between carotid distending pressure and muscle sympathetic activity in humans. Carotid baroreceptors of nine healthy subjects were compressed or stretched for 5 s with graded neck pressure or suction (+40 to -65 mmHg), and muscle sympathetic nerve activity was recorded. The results delineate several features of human baroreflex function. First, the carotid-muscle sympathetic relation is well described by an inverse sigmoid function. Second, a linear relation exists between carotid distending pressure and sympathetic outflow over a range of approximately 25 mmHg. Third, sympathetic responses to changes of carotid pressures are asymmetric; increases of sympathetic activity during carotid compression are much greater than reductions of sympathetic activity during carotid stretch. Fourth, at rest, normal subjects operate near the threshold level for sympathetic excitation. Thus the carotid-muscle sympathetic baroreflex is poised to oppose reductions more effectively than elevations of arterial pressure, and the range of pressures over which the reflex is active is wider than thought hitherto.

Relation between QT interval variability and muscle sympathetic nerve activity in normal subjects

2015 ◽  
Vol 309 (7) ◽  
pp. H1218-H1224 ◽  
Author(s):  
Fatima El-Hamad ◽  
Elisabeth Lambert ◽  
Derek Abbott ◽  
Mathias Baumert
Keyword(s):  
Supine Position ◽  
Sympathetic Nerve ◽  
Qt Interval ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Normal Subjects ◽  
Nerve Activity ◽  
Head Up Tilt ◽  
Low Frequency Power

Beat-to-beat variability of the QT interval (QTV) is sought to provide an indirect noninvasive measure of sympathetic nerve activity, but a formal quantification of this relationship has not been provided. In this study we used power contribution analysis to study the relationship between QTV and muscle sympathetic nerve activity (MSNA). ECG and MSNA were recorded in 10 healthy subjects in the supine position and after 40° head-up tilt. Power spectrum analysis was performed using a linear autoregressive model with two external inputs: heart period (RR interval) variability (RRV) and MSNA. Total and low-frequency power of QTV was decomposed into contributions by RRV, MSNA, and sources independent of RRV and MSNA. Results show that the percentage of MSNA power contribution to QT is very small and does not change with tilt. RRV power contribution to QT power is notable and decreases with tilt, while the greatest percentage of QTV is independent of RRV and MSNA in the supine position and after 40° head-up tilt. In conclusion, beat-to-beat QTV in normal subjects does not appear to be significantly affected by the rhythmic modulations in MSNA following low to moderate orthostatic stimulation. Therefore, MSNA oscillations may not represent a useful surrogate for cardiac sympathetic nerve activity at moderate levels of activation, or, alternatively, sympathetic influences on QTV are complex and not quantifiable with linear shift-invariant autoregressive models.

Importance of ventilation in modulating interaction between sympathetic drive and cardiovascular variability

2001 ◽  
Vol 280 (2) ◽  
pp. H722-H729 ◽  
Author(s):  
Philippe Van De Borne ◽  
Nicola Montano ◽  
Krzysztof Narkiewicz ◽  
Jean P. Degaute ◽  
Alberto Malliani ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Minute Ventilation ◽  
Low Frequency ◽  
Nerve Activity ◽  
Cardiovascular Variability ◽  
Controlled Breathing ◽  
End Tidal ◽  
Cardiovascular Rhythms

Chemoreflex stimulation elicits both hyperventilation and sympathetic activation, each of which may have different influences on oscillatory characteristics of cardiovascular variability. We examined the influence of hyperventilation on the interactions between changes in R-R interval (RR) and muscle sympathetic nerve activity (MSNA) and changes in neurocirculatory variability, in 14 healthy subjects. We performed spectral analysis of RR and MSNA variability during each of the following interventions: 1) controlled breathing, 2) maximal end-expiratory apnea, 3) isocapnic voluntary hyperventilation, and 4) hypercapnia-induced hyperventilation. MSNA increased from 100% during controlled breathing to 170 ± 25% during apnea ( P = 0.02). RR was unchanged, but normalized low-frequency (LF) variability of both RR and MSNA increased markedly ( P < 0.001). During isocapnic hyperventilation, minute ventilation increased to 20.2 ± 1.4 l/min ( P < 0.0001). During hypercapnic hyperventilation, minute ventilation also increased (to 19.7 ± 1.7 l/min) as did end-tidal CO2 (both P < 0.0001). MSNA remained unchanged during isocapnic hyperventilation (104 ± 7%) but increased to 241 ± 49% during hypercapnic hyperventilation ( P < 0.01). RR decreased during both isocapnic and hypercapnic hyperventilation ( P < 0.05). However, normalized LF variability of RR and of MSNA decreased ( P < 0.05) during both isocapnic and hypercapnic hyperventilation, despite the tachycardia and heightened sympathetic nerve traffic. In conclusion, marked respiratory oscillations in autonomic drive induced by hyperventilation may induce dissociation between RR, MSNA, and neurocirculatory variability, perhaps by suppressing central genesis and/or inhibiting transmission of LF cardiovascular rhythms.

scholarly journals Acute effects of device-guided slow breathing on sympathetic nerve activity and baroreflex sensitivity in posttraumatic stress disorder

2018 ◽  
Vol 315 (1) ◽  
pp. H141-H149 ◽  
Author(s):  
Ida T. Fonkoue ◽  
Paul J. Marvar ◽  
Seth D. Norrholm ◽  
Melanie L. Kankam ◽  
Yunxiao Li ◽  
...  
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Sympathetic Activity ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Sham Group ◽  
Stress Disorder ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Slow Breathing

Patients with posttraumatic stress disorder (PTSD) have elevated sympathetic nervous system reactivity and impaired sympathetic and cardiovagal baroreflex sensitivity (BRS). Device-guided slow breathing (DGB) has been shown to lower blood pressure (BP) and sympathetic activity in other patient populations. We hypothesized that DGB acutely lowers BP, heart rate (HR), and improves BRS in PTSD. In 23 prehypertensive veterans with PTSD, we measured continuous BP, ECG, and muscle sympathetic nerve activity (MSNA) at rest and during 15 min of DGB at 5 breaths/min ( n = 13) or identical sham device breathing at normal rates of 14 breaths/min (sham; n = 10). Sympathetic and cardiovagal BRS was quantified using pharmacological manipulation of BP via the modified Oxford technique at baseline and during the last 5 min of DGB or sham. There was a significant reduction in systolic BP (by −9 ± 2 mmHg, P < 0.001), diastolic BP (by −3 ± 1 mmHg, P = 0.019), mean arterial pressure (by −4 ± 1 mmHg, P = 0.002), and MSNA burst frequency (by −7.8 ± 2.1 bursts/min, P = 0.004) with DGB but no significant change in HR ( P > 0.05). Within the sham group, there was no significant change in diastolic BP, mean arterial pressure, HR, or MSNA burst frequency, but there was a small but significant decrease in systolic BP ( P = 0.034) and MSNA burst incidence ( P = 0.033). Sympathetic BRS increased significantly in the DGB group (−1.08 ± 0.25 to −2.29 ± 0.24 bursts·100 heart beats−1·mmHg−1, P = 0.014) but decreased in the sham group (−1.58 ± 0.34 to –0.82 ± 0.28 bursts·100 heart beats−1·mmHg−1, P = 0.025) (time × device, P = 0.001). There was no significant difference in the change in cardiovagal BRS between the groups (time × device, P = 0.496). DGB acutely lowers BP and MSNA and improves sympathetic but not cardiovagal BRS in prehypertensive veterans with PTSD. NEW & NOTEWORTHY Posttraumatic stress disorder is characterized by augmented sympathetic reactivity, impaired baroreflex sensitivity, and an increased risk for developing hypertension and cardiovascular disease. This is the first study to examine the potential beneficial effects of device-guided slow breathing on hemodynamics, sympathetic activity, and arterial baroreflex sensitivity in prehypertensive veterans with posttraumatic stress disorder.

Alterations in sympathetic neurovascular transduction during acute hypoxia in humans

2013 ◽  
Vol 304 (11) ◽  
pp. R959-R965 ◽  
Author(s):  
Can Ozan Tan ◽  
Yu-Chieh Tzeng ◽  
Jason W. Hamner ◽  
Renaud Tamisier ◽  
J. Andrew Taylor
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Sympathetic Outflow ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Hypoxic Exercise

Resting vascular sympathetic outflow is significantly increased during and beyond exposure to acute hypoxia without a parallel increase in either resistance or pressure. This uncoupling may indicate a reduction in the ability of sympathetic outflow to effect vascular responses (sympathetic transduction). However, the effect of hypoxia on sympathetic transduction has not been explored. We hypothesized that transduction would either remain unchanged or be reduced by isocapnic hypoxia. In 11 young healthy individuals, we measured beat-by-beat pressure, multiunit sympathetic nerve activity, and popliteal blood flow velocity at rest and during isometric handgrip exercise to fatigue, before and during isocapnic hypoxia (∼80% SpO2), and derived sympathetic transduction for each subject via a transfer function that reflects Poiseuille's law of flow. During hypoxia, heart rate and sympathetic nerve activity increased, whereas pressure and flow remained unchanged. Both normoxic and hypoxic exercise elicited significant increases in heart rate, pressure, and sympathetic activity, although sympathetic responses to hypoxic exercise were blunted. Hypoxia slightly increased the gain relation between pressure and flow (0.062 ± 0.006 vs. 0.074 ± 0.004 cm·s−1·mmHg−1; P = 0.04), but markedly increased sympathetic transduction (−0.024 ± 0.005 vs. −0.042 ± 0.007 cm·s−1·spike−1; P < 0.01). The pressor response to isometric handgrip was similar during normoxic and hypoxic exercise due to the balance of interactions among the tachycardia, sympathoexcitation, and transduction. This indicates that the ability of sympathetic activity to affect vasoconstriction is enhanced during brief exposure to isocapnic hypoxia, and this appears to offset the potent vasodilatory stimulus of hypoxia.

The impact of 6 months of exercise-based cardiac rehabilitation on sympathetic neural recruitment during apneic stress

2021 ◽  
Author(s):  
Andrew D'Souza ◽  
Mark B. Badrov ◽  
Katelyn N. Wood ◽  
Sophie Lalande ◽  
Neville Gordon Suskin ◽  
...  
Keyword(s):  
Cardiac Rehabilitation ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Firing Frequency ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
Discharge Patterns ◽  
The Impact

The current study evaluated the hypothesis that six months of exercise-based cardiac rehabilitation (CR) would improve sympathetic neural recruitment in patients with ischemic heart disease (IHD). Microneurography was used to evaluate action potential (AP) discharge patterns within bursts of muscle sympathetic nerve activity (MSNA), in eleven patients with IHD (1 female; 61±9 years) pre- (Pre-CR) and post- six months of aerobic and resistance training-based CR (Post-CR). Measures were made at baseline and during maximal voluntary end-inspiratory (EI-APN) and end-expiratory apneas (EE-APN). Data were analyzed during 1-minute of baseline and the second half of apneas. At baseline, overall sympathetic activity was less Post-CR (all P<0.01). During EI-APN, AP recruitment was not observed Pre-CR (all P>0.05) but increases in both within-burst AP firing frequency (∆Pre-CR: 2±3 AP spikes/burst vs. ∆Post-CR: 4±3 AP spikes/burst; P=0.02) and AP cluster recruitment (∆Pre-CR: -1±2 vs. ∆Post-CR: 2±2; P<0.01) were observed in Post-CR tests. In contrast, during EE-APN, AP firing frequency was not different Post-CR compared to Pre-CR tests (∆Pre-CR: 269±202 spikes/min vs. ∆Post-CR: 232±225 spikes/min; P=0.54), and CR did not modify the recruitment of new AP clusters (∆Pre-CR: -1±3 vs. ∆Post-CR: 0±1; P=0.39), or within-burst firing frequency (∆Pre-CR: 3±3 AP spikes/burst vs. ∆Post-CR: 2±2 AP spikes/burst; P=0.21). These data indicate that CR improves some of the sympathetic nervous system dysregulation associated with cardiovascular disease, primarily via a reduction in resting sympathetic activation. However, the benefits of CR on sympathetic neural recruitment may depend upon the magnitude of initial impairment.

Changes in efferent pulmonary sympathetic nerve activity during systemic hypoxia in anesthetized cats

1995 ◽  
Vol 269 (6) ◽  
pp. R1404-R1409 ◽  
Author(s):  
M. Shirai ◽  
K. Matsukawa ◽  
N. Nishiura ◽  
A. T. Kawaguchi ◽  
I. Ninomiya
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Peripheral Chemoreceptor ◽  
Renal Sympathetic Nerve Activity ◽  
O2 Partial Pressure ◽  
Systemic Hypoxia ◽  
Before And After ◽  
The Central Nervous System ◽  
Pulmonary Arterial

Changes in efferent sympathetic nerve activity to the pulmonary vessels during systemic hypoxia have yet to be elucidated. The purpose of this study was to determine the pulmonary sympathetic nerve activity (PSNA) changes in response to acute systemic hypoxia before and after sinoaortic denervation plus vagotomy in anesthetized cats. The denervation was performed to estimate the central nervous system-mediated peripheral chemoreceptor- and baroreceptor-independent PSNA change. PSNA was recorded from the central end of the cut nerve bundle, which was isolated from the lobar artery supplying the diaphragmatic lobe. Renal sympathetic nerve activity (RSNA) and systemic and pulmonary arterial pressures were also measured simultaneously. The animals were submitted to approximately 3-min periods of graded hypoxia (16, 12, 8, 5, and 3% O2 inhalations). PSNA did not change from normoxia down to an arterial O2 partial pressure (PaO2) of approximately 45 Torr (with 12-21% O2 inhalations). Below this level, PSNA began to increase, and markedly so (approximately 2.5-fold) at a PaO2 of approximately 15 Torr (with 3% O2). The hypoxic PSNA increase was significantly larger than that for RSNA, with a PaO2 of less than approximately 30 Torr (with 3-8% O2). Particularly at a PaO2 of approximately 15 Torr, the magnitude of the PSNA increase was two times greater than that for RSNA. After denervation, the hypoxic PSNA increase was significantly attenuated at a PaO2 of approximately 25 to approximately 45 Torr (with 5-12% O2), but the attenuation was very small; therefore most of the PSNA increase persisted. The hypoxic RSNA increase, in contrast, was mostly abolished after denervation. The data indicate that the neural reflex effect of systemic hypoxia on PSNA is significantly greater than that on RSNA and suggest that the hypoxic PSNA increase is mostly mediated by central mechanisms, whereas that for RSNA is chiefly caused by peripheral chemoreceptors.

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.

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