Changes In Muscle Sympathetic Activity Research Articles

The differential modulation of the baroreflex control mechanism in fight, flight or freeze behaviour.

The differential modulation of the baroreflex control mechanism in fight, flight or freeze behaviour.

Heart rate turbulence parameters correlate with post–premature ventricular contraction changes in muscle sympathetic activity

Heart rate turbulence (HRT) has been shown to be vagally mediated with a strong correlation to baroreflex indices. However, the relationship between HRT and peripheral sympathetic nerve activity (SNA) after a premature ventricular contraction (PVC) remains unclear. We sought to evaluate the relationship between HRT and the changes in peripheral SNA after PVCs. We recorded postganglionic muscle SNA during electrocardiogram monitoring in eight patients with spontaneous PVCs. Fifty-two PVCs were observed and analyzed for turbulence onset (TO) and slope (TS). SNA was quantified during (1) the dominant burst after the PVC (dominant burst area) and (2) the 10 seconds after the dominant burst (postburst SNA). The mean TO was 0.1% +/- 4.6%, and the mean TS was 6.1 +/- 6.6. The dominant burst area negatively correlated with TO (r = -0.50, P = .0002). The postburst SNA showed a significant positive correlation with TO (r = 0.44, P = .001) and a negative correlation with TS (r = -0.42, P = .002). These correlations remained significant after controlling for either the PVC coupling interval or the left ventricular ejection fraction. Our findings highlight the relationship between perturbations in HRT and pathology in the sympathetic limb of the autonomic nervous system. Future studies are needed to evaluate the prognostic role of baroreflex control of sympathetic activity in patients with structural heart disease.

Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 85

The aim of this study is to report changes in muscle sympathetic activity (MSA) and other cardiovascular variables during central apnea occurring during a relaxed wakefulness. We describe a 47‐year‐old man with a five‐year history of apnea. Polysomnographic recording showed repeated central apnea, without an obstructive peripheral component, during sleep or relaxed wakefulness. Neuromuscular disease was excluded by EMG investigation. During relaxed wake, MSA was evaluated by a microneurographic recording from the left peroneal nerve in association with blood pressure (BP), heart rate (HR), thoracoabdominal respiration and sympathetic skin response (SSR). Microneurographic polygraphic recording was performed during normal respiration (5 minutes) and during repeated apnea episodes (4 consecutive episodes with mean duration of 26.2 s; range 18–45). During normal respiration, MSA was 39.5 burst/min and 64.7 bursts/100 heartbeats, the heart rate was 61.1 beat/min. During the apnea episodes, both MSA (29% and 27%: 50.9 burst/min e 82.1 bursts/100 heartbeats respectively; mean values) and HR (1%: 61.9 beat/min; mean values) increased. The maximum MSA and HR increase was reached at the end of apnea and was followed by a BP increase. Spontaneous SSR were absent during apnea episodes whereas sporadic responses were recorded after the apnea episodes when the breathing acts were wide and prolonged. In conclusion, central apnea caused an increase in MSA and minor increase in HR leading to a BP increase following the apnea episode.

Relation of plasma norepinephrine and sympathetic traffic during hypotension in humans

We compared changes in antecubital venous plasma levels of norepinephrine (NE) and peroneal nerve muscle sympathetic activity (MSA) during and after nitroprusside (NP)-induced hypotension in nine healthy volunteers. During NP, MSA increased at 98.7%/min, peaked at 4 min at 399 +/- 77% (SE) of base line, and then decreased, so that at the end of the infusion MSA was 298 +/- 39% of base line. NE increased at 9.2%/min and peaked at 14.5 min at 231 +/- 31% of base line just before the end of the infusion. Percent increases of MSA and NE near the end of NP were not significantly different. The time-to-peak NE lagged the time-to-peak MSA by nearly 10 min. These results suggest that during increases of sympathetic outflow diffusion and washout of NE from neuroeffector junctions result in delayed increases in NE in the venous drainage; percent changes in MSA and NE during prolonged stable mild hypotension are similar. The findings provide conditional support for the use of changes in NE to indicate changes in sympathetic traffic.