Signal-averaged resting sympathetic transduction of blood pressure: is it time to account for prevailing muscle sympathetic burst frequency?

2021 ◽  
Author(s):  
Massimo Nardone ◽  
Anthony V. Incognito ◽  
Muhammad Mohtasham Kathia ◽  
Lucas Joseph Omazic ◽  
Jordan B. Lee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Linear Regression ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Signal Averaging ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Males And Females ◽  
Healthy Males

Calculating the blood pressure (BP) response to a burst of muscle sympathetic nerve activity (MSNA), termed sympathetic transduction, may be influenced by an individual's resting burst frequency. We examined the relationships between sympathetic transduction and MSNA in 107 healthy males and females and developed a normalized sympathetic transduction metric to incorporate resting MSNA. Burst-triggered signal-averaging was used to calculate the peak diastolic BP response following each MSNA burst (sympathetic transduction of BP) and following incorporation of MSNA burst cluster patterns and amplitudes (sympathetic transduction slope). MSNA burst frequency was negatively correlated with sympathetic transduction of BP (r=-0.42; P<0.01) and the sympathetic transduction slope (r=-0.66; P<0.01), independent of sex. MSNA burst amplitude was unrelated to sympathetic transduction of BP in males (r=0.04; P=0.78), but positively correlated in females (r=0.44; P<0.01) and with the sympathetic transduction slope in all participants (r=0.42; P<0.01). To control for MSNA, the linear regression slope of the log-log relationship between sympathetic transduction and MSNA burst frequency was used as a correction exponent. In sub-analysis of males (38±10 vs. 14±4bursts/min) and females (28±5 vs. 12±4bursts/min) with high vs. low MSNA, sympathetic transduction of BP and sympathetic transduction slope were lower in participants with high MSNA (all P<0.05). In contrast, normalized sympathetic transduction of BP and normalized sympathetic transduction slope were similar in males and females with high vs. low MSNA (all P>0.22). We propose that incorporating MSNA burst frequency into the calculation of sympathetic transduction will allow comparisons between participants with varying levels of resting MSNA.

scholarly journals Influence of Sex and Age on Muscle Sympathetic Nerve Activity of Healthy Normotensive Adults

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 997-1005 ◽  
Author(s):  
Daniel A. Keir ◽  
Mark B. Badrov ◽  
George Tomlinson ◽  
Catherine F. Notarius ◽  
Derek S. Kimmerly ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Body Mass ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Systematic Change ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Age Related

As with blood pressure, age-related changes in muscle sympathetic nerve activity (MSNA) may differ nonlinearly between sexes. Data acquired from 398 male (age: 39±17; range: 18–78 years [mean±SD]) and 260 female (age: 37±18; range: 18–81 years) normotensive healthy nonmedicated volunteers were analyzed using linear regression models with resting MSNA burst frequency as the outcome and the predictors sex, age, MSNA, blood pressure, and body mass index modelled with natural cubic splines. Age and body mass index contributed 41% and 11%, respectively, of MSNA variance in females and 23% and 1% in males. Overall, changes in MSNA with age were sigmoidal. At age 20, mean MSNA of males and females were similar, then diverged significantly, reaching in women a nadir at age 30. After 30, MSNA increased nonlinearly in both sexes. Both MSNA discharge and blood pressure were lower in females until age 50 (17±9 versus 25±10 bursts·min −1 ; P <1×10 −19 ; 106±11/66±8 versus 116±7/68±9 mm Hg; P <0.01) but converged thereafter (38±11 versus 35±12 bursts·min −1 ; P =0.17; 119±15/71±13 versus 120±13/72±9 mm Hg; P >0.56). Compared with age 30, MSNA burst frequency at age 70 was 57% higher in males but 3-fold greater in females; corresponding increases in systolic blood pressure were 1 (95% CI, −4 to 5) and 12 (95% CI, 6–16) mm Hg. Except for concordance in females beyond age 40, there was no systematic change with age in any resting MSNA-blood pressure relationship. In normotensive adults, MSNA increases after age 30, with ascendance steeper in women.

Sympathetic Responses to Valsalva's Manoeuvre Following Bed Rest

2003 ◽  
Vol 28 (3) ◽  
pp. 342-355 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Cynthia S. Hogeman ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Bed Rest ◽  
Pressure Control ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Head Up Tilt ◽  
Valsalva's Manoeuvre

The purpose of this study was to examine whether 14 days of head-down tilt bed rest (HDBR) alters autonomic regulation during Valsalva's manoeuvre (VM) and if this would predict blood pressure control during a 60° head-up tilt (HUT) test. To examine autonomic control of blood pressure, we measured the changes in systolic (ΔSBP) and diastolic (ΔDBP) blood pressure between baseline and the early straining (Phase IIE) period of VM (20 sec straining to 40 mmHg; N = 7) in conjunction with changes in muscle sympathetic nerve activity (MSNA; microneurography) burst frequency (B/min) and total activity (%Δ) from baseline over the 20-sec straining period. MSNA data were successfully recorded from 6 of the 7 individuals. The averaged responses from three repeated VMs performed in the supine position were compared between the pre- and post-HDBR tests. Compared with the pre-HDBR test, a greater reduction in SBP, DBP, and MAP was observed during Phase IIE following HDBR, p < 0.05. The increase in MSNA burst frequency during straining was augmented in the post- compared with the pre-HDBR test, p < 0.0001, as was the Phase IV blood pressure overshoot, p < 0.05. Although all subjects completed the 20-min pre-HDBR tilt test without evidence of hypotension or orthostatic intolerance, the post-HDBR test was stopped early in 5 of the 7 subjects due to systolic hypotension. The responses during the VM suggest that acute autonomic adjustments to rapid blood pressure changes are preserved after bed rest. Furthermore, MSNA and blood pressure responses during VM did not predict blood pressure control during orthostasis following HDBR. Key words: muscle sympathetic nerve activity, blood pressure, orthostatic tolerance, head-up tilt

scholarly journals Effects of dynamic arm and leg exercise on muscle sympathetic nerve activity and vascular conductance in the inactive leg

2019 ◽  
Vol 127 (2) ◽  
pp. 464-472
Author(s):  
Connor J. Doherty ◽  
Trevor J. King ◽  
Anthony V. Incognito ◽  
Jordan B. Lee ◽  
Andrew D. Shepherd ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Burst Frequency ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Leg Cycling ◽  
Concurrent Exercise

The influence of muscle sympathetic nerve activity (MSNA) responses on local vascular conductance during exercise are not well established. Variations in exercise mode and active muscle mass can produce divergent MSNA responses. Therefore, we sought to examine the effects of small- versus large-muscle mass dynamic exercise on vascular conductance and MSNA responses in the inactive limb. Thirty-five participants completed two study visits in a randomized order. During visit 1, superficial femoral artery (SFA) blood flow (Doppler ultrasound) was assessed at rest and during steady-state rhythmic handgrip (RHG; 1:1 duty cycle, 40% maximal voluntary contraction), one-leg cycling (17 ± 3% peak power output), and concurrent exercise at the same intensities. During visit 2, MSNA (contralateral fibular nerve microneurography) was acquired successfully in 12/35 participants during the same exercise modes. SFA blood flow increased during RHG ( P < 0.0001) and concurrent exercise ( P = 0.03) but not cycling ( P = 0.91). SFA vascular conductance was unchanged during RHG ( P = 0.88) but reduced similarly during concurrent and cycling exercise (both P < 0.003). RHG increased MSNA burst frequency ( P = 0.04) without altering burst amplitude ( P = 0.69) or total MSNA ( P = 0.26). In contrast, cycling and concurrent exercise had no effects on MSNA burst frequency (both P ≥ 0.10) but increased burst amplitude (both P ≤ 0.001) and total MSNA (both P ≤ 0.007). Across all exercise modes, the changes in MSNA burst amplitude and SFA vascular conductance were correlated negatively ( r = −0.43, P = 0.02). In summary, the functional vascular consequences of alterations in sympathetic outflow to skeletal muscle are most closely associated with changes in MSNA burst amplitude, but not frequency, during low-intensity dynamic exercise. NEW & NOTEWORTHY Low-intensity small- versus large-muscle mass exercise can elicit divergent effects on muscle sympathetic nerve activity (MSNA). We examined the relationships between changes in MSNA (burst frequency and amplitude) and superficial femoral artery (SFA) vascular conductance during rhythmic handgrip, one-leg cycling, and concurrent exercise in the inactive leg. Only changes in MSNA burst amplitude were inversely associated with SFA vascular conductance responses. This result highlights the functional importance of measuring MSNA burst amplitude during exercise.

Blood pressure oscillations impact signal-averaged sympathetic transduction of blood pressure: implications for the association with resting sympathetic outflow

2021 ◽  
Vol 321 (4) ◽  
pp. H798-H806
Author(s):  
Massimo Nardone ◽  
Carlin Katerberg ◽  
Anthony V. Incognito ◽  
André L. Teixeira ◽  
Lauro C. Vianna ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Operating Pressure ◽  
Sympathetic Outflow ◽  
Current Signal ◽  
Signal Averaging ◽  
Nerve Activity ◽  
Pressure Oscillations

The current signal-averaging technique for calculating sympathetic transduction of blood pressure does not consider the arterial pressure at which each muscle sympathetic burst occurs. A burst firing when mean arterial pressure is above the operating pressure was associated with a decrease in blood pressure. Thus, individuals with higher muscle sympathetic nerve activity demonstrate a reduced sympathetic transduction owing to the weighted contribution of more sympathetic bursts at higher levels of arterial pressure.

Endotoxemia causes central downregulation of sympathetic vasomotor tone in healthy humans

2008 ◽  
Vol 295 (3) ◽  
pp. R891-R898 ◽  
Author(s):  
Friedhelm Sayk ◽  
Alexander Vietheer ◽  
Bernhard Schaaf ◽  
Peter Wellhoener ◽  
Gunther Weitz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Blood Levels ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Healthy Humans ◽  
Vascular Bed

Experimental endotoxemia as a model of the initial septic response affects the autonomic nervous system with profound cardiovascular sequelae. Whether the postsynaptic sympathoneural activity to the muscle vascular bed is altered in the early septic phase remains to be determined. The present study aimed to elucidate the early effects of LPS on muscle sympathetic nerve activity (MSNA) and cardiovascular regulation in healthy humans. Young, healthy volunteers randomly received either an LPS bolus (4 ng/kg body wt, n = 11) or placebo (saline; n = 7). Experimental baroreflex assessment (baseline measurements followed by infusion of vasoactive drugs nitroprusside/phenylephrine) was done prior to and 90 min following LPS or placebo challenge. MSNA, heart rate, blood pressure, and blood levels of catecholamines, TNF-α and IL-6 were measured sequentially. Endotoxin but not placebo-induced flu-like symptoms and elevated cytokine levels. In contrast to placebo, LPS significantly suppressed MSNA burst frequency 90 min after injection [mean ± SE: 12.1 ± 2.9 vs. 27.5 ± 3.3 burst/min (post- vs. pre-LPS); P < 0.005] but increased heart rate [78.4 ± 3.1 vs. 60.6 ± 2.0 beats/min (post- vs. pre-LPS); P < 0.001]. Baseline blood pressure was not altered, but baroreflex testing demonstrated a blunted MSNA response and uncoupling of heart rate modulation to blood pressure changes in the endotoxin group. We conclude that endotoxin challenge in healthy humans has rapid suppressive effects on postsynaptic sympathetic nerve activity to the muscle vascular bed and alters baroreflex function which may contribute to the untoward cardiovascular effects of sepsis.

Hormone phase dependency of neural responses to chemoreflex-driven sympathoexcitation in young women using hormonal contraceptives

2013 ◽  
Vol 115 (10) ◽  
pp. 1415-1422 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Torri A. Luchyshyn ◽  
Tamara I. Gimon ◽  
Chantelle A. Nielson ◽  
Stan H. M. Van Uum ◽  
...  
Keyword(s):  
Young Women ◽  
Sympathetic Nerve Activity ◽  
Contraceptive Use ◽  
Muscle Sympathetic Nerve Activity ◽  
Hormonal Contraceptives ◽  
Neural Responses ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Burst Amplitude ◽  
Progressive Hypoxia

Hormone fluctuations in women may influence muscle sympathetic nerve activity (MSNA) in a manner dependent on the severity of the sympathoexcitatory stimulus. This study examined MSNA patterns at rest and during chemoreflex stimulation in low- (LH) vs. high-hormone (HH) phases of contraceptive use in healthy young women ( n = 7). We tested the hypothesis that MSNA would be greater in the HH phase at baseline and in response to chemoreflex stimulation. MSNA recordings were obtained through microneurography in LH and HH at baseline, during rebreathing causing progressive hypoxia and hypercapnia, and during a hypercapnic-hypoxic end-inspiratory apnea. Baseline MSNA burst incidence ( P = 0.03) and burst frequency ( P = 0.02) were greater in the HH phase, while MSNA burst amplitude distributions and hemodynamic measures were similar between phases. Rebreathing elicited increases in all MSNA characteristics from baseline ( P < 0.05), but was not associated with hormone phase-dependent changes to MSNA patterns. Apnea data were considered in two halves, both of which caused large increases in all MSNA variables from baseline in each hormone phase ( P < 0.01). Increases in burst incidence and frequency were greater in LH during the first half of the apnea ( P = 0.03 and P = 0.02, respectively), while increases in burst amplitude and total MSNA were greater in LH during the second half of the apnea ( P < 0.05). These results indicate that change in hormone phase brought on through use of hormonal contraceptives influences MSNA patterns such that baseline MSNA is greater in the HH phase, but responses to severe chemoreflex stimulation are greater in the LH phase.

scholarly journals Chronic intermittent hypoxia in humans during 28 nights results in blood pressure elevation and increased muscle sympathetic nerve activity

2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Chronic Intermittent Hypoxia ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Healthy Humans

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

scholarly journals Sympathetic and cardiovascular responses to venous distension in an occluded limb

2011 ◽  
Vol 301 (6) ◽  
pp. R1831-R1837 ◽  
Author(s):  
Jian Cui ◽  
Urs A. Leuenberger ◽  
Zhaohui Gao ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Present Report ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Nerve Activity ◽  
Sympathetic Response ◽  
Venous Circulation ◽  
Blood Pressure Responses

We recently showed that a fixed volume (i.e., 40 ml) of saline infused into the venous circulation of an arterially occluded vascular bed increases muscle sympathetic nerve activity (MSNA) and blood pressure. In the present report, we hypothesized that the volume and rate of infusion would influence the magnitude of the sympathetic response. Blood pressure, heart rate, and MSNA were assessed in 13 young healthy subjects during forearm saline infusions (arrested circulation). The effects of different volumes of saline (i.e., 2%, 3%, 4%, or 5% forearm volume at 30 ml/min) and different rates of infusion (i.e., 5% forearm volume at 10, 20, or 30 ml/min) were evaluated. MSNA and blood pressure responses were linked with the infusion volume. Infusion of 5% of forearm volume evoked greater MSNA responses than did infusion of 2% of forearm volume (Δ11.6 ± 1.9 vs. Δ3.1 ± 1.8 bursts/min and Δ332 ± 105 vs. Δ38 ± 32 units/min, all P < 0.05). Moreover, greater MSNA responses were evoked by saline infusion at 30 ml/min than 10 ml/min ( P < 0.05). Sonographic measurements confirmed that the saline infusions induced forearm venous distension. The results suggest that volume and rate of saline infusion are important factors in evoking sympathetic activation. We postulate that venous distension contributes to cardiovascular autonomic adjustment in humans.

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