scholarly journals Superentrainment of muscle sympathetic nerve activity during sinusoidal galvanic vestibular stimulation

2016 ◽  
Vol 116 (6) ◽  
pp. 2689-2694 ◽  
Author(s):  
Vaughan G. Macefield ◽  
Cheree James

Sinusoidal galvanic vestibular stimulation (sGVS), delivered at frequencies ranging from 0.08 to 2.0 Hz, induces vestibular illusions of side-to-side motion and robust modulation of muscle sympathetic nerve activity (MSNA) to the lower legs. We have previously documented, in seated subjects, de novo synthesis of bursts of MSNA that are temporally locked to the sinusoidal stimulus rather than to the cardiac-related rhythm. Here we tested the hypothesis that this vestibular entrainment of MSNA is higher in the upright than in the supine position. MSNA was recorded from the common peroneal nerve in 10 subjects lying on a tilt table. Bipolar binaural sGVS (±2 mA, 200 cycles) was applied to the mastoid processes at 0.2, 0.8, and 1.4 Hz in the supine and upright (75°) positions. In four subjects, “superentrainment” of MSNA occurred during sGVS, with strong bursts locked to one phase of the sinusoidal stimulus. This occurred more prominently in the upright position. On average, cross-correlation analysis revealed comparable vestibular modulation of MSNA in both positions at 0.2 Hz (84.9 ± 3.6% and 78.7 ± 5.7%), 0.8 Hz (77.4 ± 3.9% and 74.4 ± 8.9%), and 1.4 Hz (69.8 ± 4.6% and 80.2 ± 7.4%). However, in the supine position there was a significant linear fall in the magnitude of vestibular modulation with increasing frequency, whereas this was not present in the upright position. We conclude that vestibular contributions to the control of blood pressure are higher in the upright position.

2019 ◽  
Vol 121 (5) ◽  
pp. 1644-1649 ◽  
Author(s):  
Natasha Singh ◽  
Elie Hammam ◽  
Vaughan G. Macefield

We have previously shown that sinusoidal galvanic vestibular stimulation (sGVS), delivered at 0.2–2.0 Hz, evokes a partial entrainment of muscle sympathetic nerve activity (MSNA). Moreover, at lower frequencies of stimulation (0.08–0.18 Hz) sGVS produces two peaks of modulation: one (primary) peak associated with the positive peak of the sinusoidal stimulus and a smaller (secondary) peak associated with the trough. Here we assessed whether sGVS delivered at 0.05 Hz causes a more marked modulation of MSNA than at higher frequencies and tested the hypothesis that the primary and secondary peaks are of identical amplitude because of the longer cycle length. MSNA was recorded via tungsten microelectrodes inserted into the left peroneal nerve in 11 seated subjects. Bipolar binaural sGVS (±2 mA, 100 cycles) was applied to the mastoid processes at 0.05, 0.5, and 5.0 Hz (500 cycles). Cross-correlation analysis revealed two bursts of modulation of MSNA for each cycle at 0.05 and 0.5 Hz but only one at 5 Hz. There was a significant inverse linear relationship between vestibular modulation (primary peak) and frequency ( P < 0.0001), with the amplitudes of the peaks being highest at 0.05 Hz. Moreover, the secondary peak at this frequency was not significantly different from the primary peak. These results indicate that vestibular modulation of MSNA operates over a large range of frequencies but is greater at lower frequencies of sGVS. We conclude that the vestibular apparatus, through its influence on muscle sympathetic outflow, preferentially contributes to the control of blood pressure at low frequencies. NEW & NOTEWORTHY Vestibulosympathetic reflexes have been documented in experimental animals and humans. Here we show that sinusoidal galvanic vestibular stimulation, a means of selectively exciting vestibular afferents in humans, induces greater modulation of muscle sympathetic nerve activity when delivered at a very low frequency (0.05 Hz) than at 0.5 or 5.0 Hz.


2015 ◽  
Vol 309 (7) ◽  
pp. H1218-H1224 ◽  
Author(s):  
Fatima El-Hamad ◽  
Elisabeth Lambert ◽  
Derek Abbott ◽  
Mathias Baumert

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.


1993 ◽  
Vol 74 (4) ◽  
pp. 1719-1722 ◽  
Author(s):  
C. A. Ray

We previously demonstrated that brief dynamic one-legged knee extensions (DKE) performed in the upright position decreased muscle sympathetic nerve activity (MSNA). The present study was undertaken to investigate MSNA responses to prolonged DKE. DKE was performed for 40 min in the upright (sitting) position, and MSNA was recorded in the peroneal nerve of the contralateral leg by microneurography. DKE elicited a significant increase in mean arterial pressure (MAP) from 83 +/- 3 to 101 +/- 6 (SE) mmHg during the 5th min of exercise. The increase in MAP persisted for the remainder of exercise. In contrast, heart rate (HR) showed a gradual increase throughout the 40 min of exercise (80 +/- 3 to 110 +/- 5 beats/min at 40 min of exercise; P < 0.05). MSNA decreased from 34 +/- 3 to 28 +/- 3 bursts/min (P < 0.05) from control to the 5th min of DKE and then returned to control levels by 20 min (35 +/- 3 bursts/min) and remained unchanged for the remainder of exercise. During recovery, MSNA was significantly increased above control for 10 min postexercise (40 bursts/min) when HR and MAP had returned to control levels. These results confirm our previous finding that MSNA is decreased during the early stage of upright DKE. The two new findings are as follows: 1) prolonged DKE failed to increase MSNA above control levels, and 2) during recovery when HR and MAP are at control levels, MSNA is significantly elevated.


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