A new method of quantifying human muscle sympathetic nerve activity for frequency domain analysis

1996 ◽  
Vol 101 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Yoshiki Sugiyama ◽  
Toshiyoshi Matsukawa ◽  
Hatsue Suzuki ◽  
Satoshi Iwase ◽  
A.S.M. Shamsuzzaman ◽  
...  
Keyword(s):  
Frequency Domain ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Domain Analysis ◽  
Frequency Domain Analysis ◽  
Human Muscle ◽  
New Method ◽  
Nerve Activity

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.

A signal-averaging technique for the analysis of human muscle sympathetic nerve activity

1992 ◽  
Vol 73 (1) ◽  
pp. 376-381 ◽  
Author(s):  
C. L. Birkett ◽  
C. A. Ray ◽  
E. A. Anderson ◽  
R. F. Rea
Keyword(s):  
Data Collection ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Human Muscle ◽  
Hard Copy ◽  
Signal Acquisition ◽  
Signal Averaging ◽  
Nerve Activity ◽  
Averaging Technique

We present a signal-averaging technique for analysis of human muscle sympathetic nerve activity (SNA). Nerve traffic was averaged by coupling signal acquisition to electrocardiographic R waves. The amplitude of the averaged waveform was multiplied by the number of R waves sampled to provide a measure of SNA in arbitrary units. This was compared with SNA measured by manual digitization of hard-copy records. In nine volunteers, SNA was increased or decreased with stepwise infusions of nitroprusside or phenylephrine: there were 10 5-min periods of data in each subject. Across all subjects, the correlation between manual and signal-averaged measures of SNA was excellent during both nitroprusside (r = 0.98) and phenylephrine infusions (r = 0.91) and the slopes of the regression lines were near unity. In three periods of data collection, electrical artifacts were added randomly at frequencies of 0.5 and 0.07 Hz during playback of the signal into the computer. Signal-averaged estimates of SNA were unaffected by artifacts. This technique provides reliable observer-independent measures of SNA.

Relationship between size and latency of action potentials in human muscle sympathetic nerve activity

2011 ◽  
Vol 105 (6) ◽  
pp. 2830-2842 ◽  
Author(s):  
Aryan Salmanpour ◽  
Lyndon J. Brown ◽  
Craig D. Steinback ◽  
Charlotte W. Usselman ◽  
Ruma Goswami ◽  
...  
Keyword(s):  
Action Potential ◽  
Sympathetic Nerve ◽  
Action Potentials ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Burst Size ◽  
Muscle Sympathetic Nerve Activity ◽  
Peak Height ◽  
Human Muscle ◽  
Nerve Activity

We employed a novel action potential detection and classification technique to study the relationship between the recruitment of sympathetic action potentials (i.e., neurons) and the size of integrated sympathetic bursts in human muscle sympathetic nerve activity (MSNA). Multifiber postganglionic sympathetic nerve activity from the common fibular nerve was collected using microneurography in 10 healthy subjects at rest and during activation of sympathetic outflow using lower body negative pressure (LBNP). Burst occurrence increased with LBNP. Integrated burst strength (size) varied from 0.22 ± 0.07 V at rest to 0.28 ± 0.09 V during LBNP. Sympathetic burst size (i.e., peak height) was directly related to the number of action potentials within a sympathetic burst both at baseline ( r = 0.75 ± 0.13; P < 0.001) and LBNP ( r = 0.75 ± 0.12; P < 0.001). Also, the amplitude of detected action potentials within sympathetic bursts was directly related to the increased burst size at both baseline ( r = 0.59 ± 0.16; P < 0.001) and LBNP ( r = 0.61 ± 0.12; P < 0.001). In addition, the number of detected action potentials and the number of distinct action potential clusters within a given sympathetic burst were correlated at baseline ( r = 0.7 ± 0.1; P < 0.001) and during LBNP ( r = 0.74 ± 0.03; P < 0.001). Furthermore, action potential latency (i.e., an inverse index of neural conduction velocity) was decreased as a function of action potential size at baseline and LBNP. LBNP did not change the number of action potentials and unique clusters per sympathetic burst. It was concluded that there exists a hierarchical pattern of recruitment of additional faster conducting neurons of larger amplitude as the sympathetic bursts become stronger (i.e., larger amplitude bursts). This fundamental pattern was evident at rest and was not altered by the level of baroreceptor unloading applied in this study.

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