165 EVIDENCE FOR INCREASED SYMPATHETIC NERVOUS ACTIVITY IN EXERCISE BY HEART RATE SPECTRAL ANALYSIS

1990 ◽  
Vol 22 (2) ◽  
pp. S28
Author(s):  
Y. Yamamoto ◽  
R. L. Hughson ◽  
J. C. Peterson
2018 ◽  
Vol 80 (1-2) ◽  
pp. 50-54 ◽  
Author(s):  
Masafumi Nozoe ◽  
Miho Yamamoto ◽  
Miki Kobayashi ◽  
Masashi Kanai ◽  
Hiroki Kubo ◽  
...  

Autonomic dysfunction is one of the predictors of poor outcome in patients with acute ischemic stroke. We compared the heart rate variability (HRV) during early mobilization in patients with or without neurological deterioration (ND). We enrolled 7 acute ischemic patients with ND and 14 without ND and measured their HRV in the rest and mobilization by electrocardiography. There was a significant difference in sympathetic nervous activity during mobilization between the 2 groups. However, no significant differences in blood pressure, heart rate, and parasympathetic nerve activity were observed. In patients with acute ischemic stroke, it is likely that the increase in sympathetic nervous activity during mobilization is associated with ND.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ivani C Trombetta ◽  
Cristiane M Nunes ◽  
Luciano F Drager ◽  
Raffael F Fraga ◽  
Maria Janieire N Alves ◽  
...  

Obstructive sleep apnoea (OSA) and metabolic syndrome (MetS) independently increases muscular sympathetic nervous activity (MSNA). Unknown is whether OSA has an additive effect on MSNA in patients with MetS. We tested the hypothesis that: OSA would have an additive effect on MSNA in patients with MetS. In addition, we studied whether the increase in MSNA in patients with MetS is associated with alteration in arterial baroreflex sensitivity (BRS). Twenty four patients with MetS diagnosed according ATP-III were divided in two groups: MetS+OSA (n=14) and MetS (n=10). They were matched for age, body mass index, waist circumference, and metabolic profile: OSA was defined by an apnoea/hypopnoea index (AHI)>15 events/hour by polysonography. MSNA was recorded directly from the peroneal nerve using the technique of microneurography. Blood pressure (BP) was monitored on a beat-by-beat basis (Finapress) and heart rate by ECG. BRS was analyzed by spontaneous BP and heart rate fluctuations. AHI was higher (42±9 vs. 7±1 events/h, P =0.0001) and minimum oxygen saturation lower (77±2 vs. 87±1 %, P =0.001) in MetS+OSA patients. Patients MetS+OSA had higher MSNA (55±3 vs. 43±2 bursts/100 beats, P =0.01) and systolic BP (158±4 vs.144±3 mmHg, P =0.01) when compared with patients with MetS without OSA. Further analysis showed that AHI and minimum oxygen saturation have significant correlation with MSNA (r=0.65; P =0.001 and r=−0.48; P =0.017, respectively). Patients with MetS+OSA had lower BRS for increases (7.8±0.9 vs. 13.4 ± 1.4 msec/mmHg, P =0.01) and decreases (7.2±0.9 vs. 13.2 ± 2.0 msec/mmHg, P =0.03) in blood pressure than patients with MetS without OSA. MSNA significantly correlated with BRS during spontaneous increases in blood pressure (r=−0.56, P =0.01). OSA exacerbates MSNA in patients with MetS. In addition, the augmented MSNA in patients with MetS+OSA is associated with reduced BRS. These findings suggest that OSA increases the risk for cardiovascular disease in patients with MetS.


1995 ◽  
Vol 89 (4) ◽  
pp. 349-357 ◽  
Author(s):  
Mario Vaz ◽  
Andrea Turner ◽  
Bronwyn Kingwell ◽  
Jaye Chin ◽  
Elizabeth Koff ◽  
...  

1. Sympatho-adrenal activity was measured after the consumption of a 3.15 MJ mixed meal. Whole-body noradrenaline spillover rates, forearm plasma noradrenaline spillover and adrenaline secretion rates were derived using isotope dilution methodology. Heart rate and blood pressure spectral analysis measurements were also made. The relation of sympatho-adrenal activity to thermogenic and cardiovascular events was studied. Sympathetic nervous and thermogenic responses were measured for 120 min after the single 3.15 MJ meal and compared with those after three 1.05 MJ meals, given 30 min apart. 2. Whole-body and forearm plasma noradrenaline spillover, and the 0.1 Hz component of systolic pressure power all increased significantly postprandially, while the 0.1 Hz component of heart rate variability, an indirect index of cardiac sympathetic nervous activity, remained unaltered. Adrenaline secretion was unaltered postprandially. Whole-body plasma noradrenaline spillover and thermogenesis during the 120 min postprandial period were 37% and 36% higher after the single meal as compared with the multiple meals, although this was not statistically significant. 3. The sympathetic neural responses were delayed in relation to peak plasma insulin levels and sustained in the face of declining insulin levels. Energy expenditure increased significantly postprandially, but there was no direct quantitative relationship to plasma noradrenaline spillover. Forearm oxygen consumption did not increase postprandially despite significant increases in regional noradrenaline spillover. Thus, no close relation was demonstrated between postprandial sympathetic nervous activation and either insulin secretion or thermogenesis.


1993 ◽  
Vol 84 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Alastair J. McCance ◽  
J. Colin Forfar

1. To investigate the effects of acute β1-adrenoceptor blockade on sympathetic nervous activity, cardiac and whole-body noradrenaline kinetics were determined during intravenous infusions of saline placebo and of metoprolol (10-15 mg plus 150 μg min−1 kg−1) in 10 patients undergoing diagnostic cardiac catheterization, in whom β-adrenoceptor antagonists had been discontinued for 7 days. 2. Coronary haemodynamics were measured in these 10 patients plus two others. Compared with saline placebo, metoprolol administration was associated with decreases in heart rate (68 ± 2 to 59 ± 3 beats/min, P < 0.001) and coronary sinus blood flow (86 ± 8 to 68 ± 6 ml/min, P < 0.001) and an increase in calculated coronary vascular resistance (1.42 ± 0.19 to 1.75 ± 0.22 mmHg min ml−1, P < 0.001). Arterial and femoral venous noradrenaline concentrations, whole-body noradrenaline clearance and whole-body noradrenaline spillover to arterial plasma did not change. In contrast, cardiac noradrenaline spillover (33.7 ± 5.1 to 20.2 ± 4.3 pmol/min, P < 0.05) and cardiac noradrenaline clearance (31 ± 3 to 23 ± 3 ml/min, P < 0.001) were significantly decreased during metoprolol administration. 3. These results may be explained by inhibition of pre-junctional facilitatory β-adrenoceptors, which we hypothesize may be predominantly of the β1-subtype in the heart and of the β2-subtype in the periphery.


1981 ◽  
Vol 51 (4) ◽  
pp. 812-815 ◽  
Author(s):  
F. Peronnet ◽  
J. Cleroux ◽  
H. Perrault ◽  
D. Cousineau ◽  
J. de Champlain ◽  
...  

Plasma norepinephrine (NE) concentration was measured by means of a sensitive radioenzymatic assay in blood collected from an antecubital vein in 10 healthy male subjects (37 +/- 2 yr, mean +/- SE). The subjects were evaluated at rest and during exercise before and after a 20-wk training program on bicycle ergometer (three 30-min sessions per week at 80% of maximal heart rate). Following the training program, maximal oxygen uptake increased significantly from 33 +/- 2 to 42 +/- 1 ml . kg-1 . min-1. Resting plasma NE remained unchanged after training (167 +/- 38 before and 185 +/- 29 pg . ml-1 after training). For a given absolute work load (735 +/- 51 kg . m. min-1) the sympathetic nervous response was lower after training as reflected by the decrease in NE concentration (1,371 +/- 286 vs. 687 +/- 64 pg . ml-1). At the same relative work load (heart rate: 158 +/- 5 before and 157 +/- 5 beats . min-1 after training) plasma NE concentration was unchanged after training (1,371 +/- 286 vs. 1,729 +/0 371 pg . ml-1). Results from the present study show that the sympathetic nervous activity is closely linked to the exercise demands and confirm earlier suggestions that it remains constant in relation to the relative work load.


1984 ◽  
Vol 57 (5) ◽  
pp. 1507-1511 ◽  
Author(s):  
P. Escourrou ◽  
D. G. Johnson ◽  
L. B. Rowell

To determine whether plasma catecholamine concentrations (a measure of sympathetic nervous activity [SNA]) rise above normoxic levels during exercise with hypoxemia, we exercised seven men for 15 min at three loads that required from 40 to 88% of maximal O2 uptake (VO2max). Subjects breathed room air on one day and 11–12% O2 on another with relative work loads corrected for the 24% fall in VO2max during hypoxemia. Hypoxemia caused large increments in norepinephrine (NE) concentration (radioenzyme technique) to 1.21 +/- 0.20 ng/ml (mean +/- SE), 2.79 +/- 0.38, and up to 5.90 +/- 0.75 (hypoxemia) compared with 0.89 +/- 0.06, 1.66 +/- 0.16, and 3.95 +/- 0.39 in normoxia at the three loads, respectively (P less than 0.001). Epinephrine (E) concentration approximately doubled (P less than 0.001) in hypoxemia at each load when compared with normoxic levels (i.e., 0.10 +/- 0.01 ng/ml, 0.23 +/- 0.03, and 0.46 +/- 0.06 in normoxia). However, hypoxemia did not significantly alter linear relationships between log plasma NE concentration and either heart rate (HR) or percent VO2max utilized, or between HR and percent VO2max. Thus NE concentration, like HR, appeared to reflect relative severity of exercise and overall SNA in both hypoxemia and normoxia. Above 40% VO2max during hypoxemia, circulating NE and E far exceeded levels known to have direct vasoconstrictor and metabolic effects in normoxic humans, but hypoxemia may blunt vasoconstriction in some regions.


2007 ◽  
Vol 71 (3) ◽  
pp. 671-676 ◽  
Author(s):  
Sachiko HACHIYA ◽  
Fuminori KAWABATA ◽  
Koichiro OHNUKI ◽  
Naohiko INOUE ◽  
Hirotsugu YONEDA ◽  
...  

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