scholarly journals Muscle sympathetic nerve activity response to heat stress is attenuated in chronic heart failure patients

2017 ◽  
Vol 312 (6) ◽  
pp. R873-R882 ◽  
Author(s):  
Jian Cui ◽  
John Boehmer ◽  
Cheryl Blaha ◽  
Lawrence I. Sinoway
Keyword(s):  
Heart Failure ◽  
Heat Stress ◽  
Chronic Heart Failure ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Hot Environment

Heat stress evokes significant increases in muscle sympathetic nerve activity (MSNA) in healthy individuals. The MSNA response to heat stress in chronic heart failure (CHF) is unknown. We hypothesized that the MSNA response to heat stress is attenuated in CHF. Passive whole body heating was applied with water-perfused suits in 13 patients (61 ± 2 yr) with stable class II-III CHF, 12 age-matched (62 ± 2 yr) healthy subjects, and 14 young (24 ± 1 yr) healthy subjects. Mild heating (i.e., increases in skin temperature ΔTsk ~2–4°C, internal temperature ΔTcore <0.3°C) significantly decreased MSNA in CHF patients; however, it did not significantly alter the MSNA in the age-matched and young healthy subjects. Heat stress (i.e., ΔTsk ~4°C and ΔTcore ~0.6°C) raised MSNA in the age-matched (32.9 ± 3.2 to 45.6 ± 4.2 bursts/min; P < 0.001) and young (14.3 ± 1.7 to 26.3 ± 2.4 bursts/min; P < 0.001) controls, but not in CHF (46.2 ± 5.3 to 50.5 ± 5.3 bursts/min; P = 0.06). The MSNA increase by the heat stress in CHF (Δ4.2 ± 2.0 bursts/min) was significantly less than those seen in the age-matched (Δ12.8 ± 1.7 bursts/min, P < 0.05) and young (Δ12.0 ± 2.7 bursts/min, P < 0.05) control groups. These data suggest that the MSNA response to heat stress is attenuated in CHF patients. We speculate that the attenuated MSNA response to heat stress may contribute to impaired cardiovascular adjustments in CHF in a hot environment.

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

1999 ◽  
Vol 277 (6) ◽  
pp. H2348-H2352 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
D. B. Farr
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Whole Body ◽  
Nerve Activity ◽  
Arterial Blood

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

scholarly journals Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia

2009 ◽  
Vol 106 (4) ◽  
pp. 1125-1131 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David A. Low ◽  
David M. Keller ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Whole Body Heat Stress ◽  
Body Heat

Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature ∼ 0.7°C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (−4.34 ± 0.40 to −3.57 ± 0.31 units·beat−1·mmHg−1, respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating ( P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation.

Frequency domain characteristics of muscle sympathetic nerve activity in heart failure and healthy humans

1997 ◽  
Vol 273 (1) ◽  
pp. R205-R212 ◽  
Author(s):  
S. Ando ◽  
H. R. Dajani ◽  
J. S. Floras
Keyword(s):  
Heart Failure ◽  
Frequency Domain ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Power ◽  
Breathing Frequency ◽  
Nerve Activity ◽  
Significant Difference

The purpose of this study was to characterize oscillations in muscle sympathetic nerve activity (MSNA) in the frequency domain in healthy subjects and patients with congestive heart failure (CHF) and to relate these to blood pressure (BP), heart rate (HR), and breathing frequency. MSNA burst frequency was significantly greater in CHF [52 +/- 21 (n = 12) vs. 35 +/- 11 (n = 19) bursts/min, P < 0.05], whereas breathing frequency and HR were similar. There was no significant difference between CHF and healthy subjects in total power, harmonic power, and nonharmonic power in the MSNA spectrum from 0 to 0.5 Hz, but low frequency power (LF, 0.05-0.15 Hz, P < 0.05) was reduced in heart failure patients. There was less coherence between BP and MSNA in the LF range, but similar spectral power in both groups in the very LF (VLF, 0-0.05 Hz) and high frequency (0.15-0.5 Hz) ranges. The transfer of MSNA oscillations into BP in the VLF (P < 0.05) and LF (P < 0.02) ranges was significantly lower in CHF, but gains in the transfer function and in the coherence between BP and MSNA and in the coherence between respiration and MSNA were similar in the two groups. These observations indicate that modulation of MSNA by the arterial baroreflex and respiration is preserved in CHF. The loss of LF power in the MSNA signal may be due to impaired neuroeffector transduction. The higher sympathetic nerve firing rate in CHF would therefore appear to be caused by factors other than the loss of regulation by these two inhibitory influences.

scholarly journals Altered firing pattern of single-unit muscle sympathetic nerve activity during handgrip exercise in chronic heart failure

2009 ◽  
Vol 587 (11) ◽  
pp. 2613-2622 ◽  
Author(s):  
Hisayoshi Murai ◽  
Masayuki Takamura ◽  
Michirou Maruyama ◽  
Manabu Nakano ◽  
Tatsunori Ikeda ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Sympathetic Nerve ◽  
Single Unit ◽  
Firing Pattern ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Handgrip Exercise ◽  
Nerve Activity

scholarly journals Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

Circulation ◽  
2001 ◽  
Vol 104 (4) ◽  
pp. 418-423 ◽  
Author(s):  
Yukiko Goso ◽  
Hidetsugu Asanoi ◽  
Hisanari Ishise ◽  
Tomoki Kameyama ◽  
Tadakazu Hirai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Respiratory Modulation

Abstract 17981: Decreased Oscillatory Pattern of Sympathetic Nerve Activity is Associated With Arterial Baroreflex Dysfunction in Chronic Heart Failure Patients

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Edgar Toschi-Dias ◽  
Raphaela V Groehs ◽  
Ligia M Antunes-Correa ◽  
Patrícia F Trevizan ◽  
Denise M Lobo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Inverse Association ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Oscillatory Pattern

Background: Sympathetic activation and arterial baroreflex (ABR) dysfunction typify chronic heart failure (CHF). In addition, decreased oscillatory pattern of muscle sympathetic nerve activity (MSNA, LF MSNA /HF MSNA ) seems to contribute to sympathetic exacerbation in patients with CHF. Unknown is whether the LF MSNA /HF MSNA is associated with ABR dysfunction in CHF patients. To answer this question, we investigated the association between gain, latency and coupling of ABR function and LF MSNA /HF MSNA in CHF patients. Methods and Results: Forty-three CHF patients, Functional Class II to III, NYHA, ejection fraction ≤40% were allocated into two groups according to the level of LF MSNA /HF MSNA index: 1) Higher LF MSNA /HF MSNA (n=21, 52±2 years) and 2) Lower LF MSNA /HF MSNA (n=22, 54±1 years). Blood pressure (BP, oscillometric beat-to-beat basis) and MSNA (microneurography technique) were recorded during 10 min at rest. Spectral and cross-spectral analyses of BP and MSNA variabilities were conducted to assess the LF MSNA /HF MSNA and the gain, latency and coupling between BP and MSNA of ABR function. Etiology, ejection fraction, gain and latency of ABR function were similar between groups. However, the patients with lower LF MSNA /HF MSNA had increased MSNA bursts frequency (53±2vs. 39±3 bursts/min, P<0.01) and total activity (180±15 vs. 126±17 a.u, P=0.03) compared to the patients with higher LF MSNA /HF MSNA . In contrast, the patients with lower LF MSNA /HF MSNA had reduced coupling of ABR function (69±3 vs. 80±2 %, P<0.01). Further analysis showed a significant association between the coupling of ABR function and LF MSNA /HF MSNA (R=0.36, P=0.02). Conclusions: There is an inverse association between the LF MSNA /HF MSNA index and sympathetic nerve activity. In addition, there is a direct association between the LF MSNA /HF MSNA index and the coupling of ABR, which suggests that the ABR dysfunction explains, at least in part, the augmented sympathetic nerve activity in CHF patients.

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