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Acute effects of Finnish sauna and cold-water immersion on haemodynamic variables and autonomic nervous system activity in patients with heart failure.
Radtke, T, Poerschke, D, Wilhelm, M, Trachsel, LD, Tschanz, H, Matter, F, Jauslin, D, Saner, H, Schmid, JP
European journal of preventive cardiology. 2016;(6):593-601
Abstract
BACKGROUND The haemodynamic response to Finnish sauna and subsequent cold-water immersion in heart failure patients is unknown. METHODS Haemodynamic response to two consecutive Finnish sauna (80℃) exposures, followed by a final head-out cold-water immersion (12℃) was measured in 37 male participants: chronic heart failure (n = 12, 61.8 ± 9.2 years), coronary artery disease (n = 13, 61.2 ± 10.6 years) and control subjects (n = 12, 60.9 ± 8.9 years). Cardiac output was measured non-invasively with an inert gas rebreathing method prior to and immediately after the first sauna exposure and after cold-water immersion, respectively. Blood pressure was measured before, twice during and after sauna. The autonomic nervous system was assessed by power spectral analysis of heart rate variability. Total power, low-frequency and high-frequency components were evaluated. The low frequency/high frequency ratio was used as a marker of sympathovagal balance. Sauna and cold-water immersion were well tolerated by all subjects. RESULTS Cardiac output and heart rate significantly increased in all groups after sauna and cold-water immersion (p < 0.05), except for coronary artery disease patients after sauna exposure. Systolic blood pressure during sauna decreased significantly in all groups with a nadir after 6 min (all p < 0.05). Cold-water immersion significantly increased systolic blood pressure in all groups (p < 0.05). No change in the low/high frequency ratio was found in chronic heart failure patients. In coronary artery disease patients and controls a prolonged increase in low frequency/high frequency ratio was observed after the first sauna exposure. CONCLUSIONS Acute exposure to Finnish sauna and cold-water immersion causes haemodynamic alterations in chronic heart failure patients similarly to control subjects and in particular did not provoke an excessive increase in adrenergic activity or complex arrhythmias.
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The development of selected cardiovascular parameters in patients with type 2 diabetes mellitus during a spa treatment.
Fialová, E, Kittnar, O
Physiological research. 2015;(Suppl 5):S661-7
Abstract
Diabetes mellitus is not just a simple metabolic disorder, however, it is considered to be a cardiovascular disease of a metabolic origin. This is apparent especially when speaking about type 2 diabetes (DM II). The objective of our study was to determine whether a comprehensive spa treatment (procedures and drinking cure) may affect the level of the sympathetic tone of patients suffering from DM II. As an indicator of the sympathetic tone, selected electrocardiographic parameters derived from the heart rate variability and microwave alternans were chosen. There were 96 patients enrolled in our study: 38 patients with poorly controlled DM II and two control groups: 9 patients with compensated DM II and 49 patients, average age without diabetes or other disorders of the glucose metabolism. All received an identical spa treatment and continued their medical therapy. The electrophysiological examination of patients was performed before and after a three-week spa treatment using the KARDiVAR system. Parameters derived from the analysis of heart rate variability (HRV), microvolt T-wave alternans, and microvolt R-wave alternans were analyzed in order to evaluate the tones of the autonomic nervous system (ANS). The control group showed a slight increase of parameter the index of activity of regulatory systems (IRSA) (4.4+/-1.3 vs. 3.8+/-1.4; p=0.006) after the spa treatment, while increased heart rate (80.9+/-11.0 vs. 74.6+/-9.6; p=0.028), reduced index of centralization (IC) (1.3+/-0.6 vs. 2.9+/-1.4; p=0.027) and reduced index of myocardium (IM) (9.9+/-7.4 vs. 18.0+/-6.3; p=0.041) were found in patients with a compensated DM II. Patients with a poorly compensated DM II showed a decreased IM (10.9+/-8.6 vs. 16.9+/-5.2; p=0.001) and also a reduced IRSA (4.1+/-3.5 vs. 6.3+/-1.9; p=0.001). The results proved favorable changes in ANS cardiovascular control of patients with DM II after a spa treatment, especially in terms of reducing the sympathoadrenal system activity (decreased IRSA), improving electrical stability of the myocardium and increasing centrally controlled heart rate variability without overloading the cardiovascular system (drop of IM).
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Effect of weight loss on sympatho-vagal balance in subjects with grade-3 obesity: restrictive surgery versus hypocaloric diet.
Pontiroli, AE, Merlotti, C, Veronelli, A, Lombardi, F
Acta diabetologica. 2013;(6):843-50
Abstract
Few and mostly uncontrolled studies indicate that weight loss improves heart rate variability (HRV) in grade-3 obesity. The aim of this study was to compare in grade-3 obesity surgery and hypocaloric diet on clinical and metabolic variables and on autonomic indices of HRV. Twenty-four subjects (body mass index, BMI 45.5 ± 9.13 kg/m(2)) underwent surgery (n = 12, gastric banding, LAGB) or received hypocaloric diet (n = 12, 1,000-1,200 kg/day). Clinical [BMI, systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate] and metabolic variables [glucose, cholesterol, HDL- and LDL-cholesterol, triglycerides, AST and ALT transaminases] and 24-h Holter electrocardiographic-derived HRV parameters [R-R interval, standard deviation of R-R intervals (SDNN); low/high-frequency (LF/HF) ratio, and QT interval] were measured at baseline and after 6 months. The two groups were identical at baseline. BMI (-7.5 ± 3.57 kg/m(2), mean ± SD), glucose (-24.1 ± 26.77 mg/dL), SBP (-16.7 ± 22.19 mmHg) and DBP (-6.2 ± 8.56 mmHg) decreased in LAGB subjects (p < 0.05) and remained unchanged in controls. At 6 months, SDNN increased in LAGB subjects (+25.0 ± 37.19 ms, p < 0.05) and LF/HF ratio diminished (2.9 ± 1.84 vs. 4.9 ± 2.78; p = 0.01), with no change in controls; LF (daytime) and HF (24 h and daytime) increased in LAGB subjects, with no change in controls. Decrease in BMI correlated with SBP and DBP decrease (p < 0.05), and DBP decrease correlated with HR decrease (p < 0.05) and QT shortening (p < 0.05). Weight loss is associated with improvement of glucose metabolism, of blood pressure, and with changes in time and frequency domain parameters of HRV; all these changes indicate recovery of a more physiological autonomic control, with increase in parasympathetic and reduction in sympathetic indices of HRV.
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Vascular adrenergic responsiveness is inversely related to tonic activity of sympathetic vasoconstrictor nerves in humans.
Charkoudian, N, Joyner, MJ, Sokolnicki, LA, Johnson, CP, Eisenach, JH, Dietz, NM, Curry, TB, Wallin, BG
The Journal of physiology. 2006;(Pt 3):821-7
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Abstract
In humans, sympathetic nerve activity (SNA) at rest can vary several-fold among normotensive individuals with similar blood pressures. We recently showed that a balance exists between SNA and cardiac output, which may contribute to the maintenance of normal blood pressures over the range of resting SNA levels. In the present studies, we assessed whether variability in vascular adrenergic responsiveness has a role in this balance. We tested the hypothesis that forearm vascular responses to noradrenaline (NA) and tyramine (TYR) are related to SNA such that individuals with lower resting SNA have greater adrenergic responsiveness, and vice-versa. We measured multifibre muscle SNA (MSNA; microneurography), arterial pressure (brachial catheter) and forearm blood flow (plethysmography) in 19 healthy subjects at baseline and during intrabrachial infusions of NA and TYR. Resting MSNA ranged from 6 to 34 bursts min(-1), and was inversely related to vasoconstrictor responsiveness to both NA (r = 0.61, P = 0.01) and TYR (r = 0.52, P = 0.02), such that subjects with lower resting MSNA were more responsive to NA and TYR. We conclude that interindividual variability in vascular adrenergic responsiveness contributes to the balance of factors that maintain normal blood pressure in individuals with differing levels of sympathetic neural activity. Further understanding of this balance may have important implications for our understanding of the pathophysiology of hypertension.
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Sympathetic neural regulation in endurance-trained humans: fitness vs. fatness.
Alvarez, GE, Halliwill, JR, Ballard, TP, Beske, SD, Davy, KP
Journal of applied physiology (Bethesda, Md. : 1985). 2005;(2):498-502
Abstract
We tested the hypothesis that muscle sympathetic nerve activity (MSNA) would be higher in endurance-trained (ET) compared with sedentary (Sed) men with similar levels of total body and abdominal adiposity. We further hypothesized that sympathetic baroreflex gain would be augmented in ET compared with Sed men independent of the level of adiposity. To address this, we measured MSNA (via microneurography), sympathetic and vagal baroreflex responses (the modified Oxford technique), body composition (dual-energy X-ray absorptiometry), and waist circumference (Gulick tape) in Sed (n = 22) and ET men (n = 8). The ET men were also compared with a subgroup of Sed men (n = 6) with similar levels of total body and abdominal adiposity. Basal MSNA was greater in the ET compared with Sed men with similar levels of total body and abdominal adiposity (28 +/- 2.0 vs. 21 +/- 2.0 bursts/min; P < 0.05) but similar to the larger group of Sed men (n = 22) with higher total body and abdominal adiposity (vs. 26 +/- 3 bursts/min; P > 0.05). In contrast to our hypothesis, sympathetic baroreflex gain was lower in the ET compared with Sed men (-6.4 +/- 0.8 vs. -8.4 +/- 0.4 arbitrary integrative units x beat(-1) x mmHg(-1); P < 0.05) regardless of the level of adiposity. Taken together, the results of the present study suggest that MSNA is higher in ET compared with Sed men with similar levels of total body and abdominal adiposity. In addition, sympathetic baroreflex gain is lower in ET compared with Sed men. That sympathetic baroreflex gain was lower in ET compared with Sed men regardless of the level of adiposity suggests an influence of the ET state per se.
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Sympathetic nerve activity in end-stage renal disease.
Hausberg, M, Kosch, M, Harmelink, P, Barenbrock, M, Hohage, H, Kisters, K, Dietl, KH, Rahn, KH
Circulation. 2002;(15):1974-9
Abstract
BACKGROUND Uremia is proposed to increase sympathetic nerve activity (SNA) in hemodialysis patients. The aims of the present study were to determine whether reversal of uremia by successful kidney transplantation (RTX) eliminates the increased SNA and whether signals arising in the diseased kidneys contribute to the increased SNA in renal failure. METHODS AND RESULTS We compared muscle sympathetic nerve activity (MSNA) in 13 hemodialysis patients wait-listed for RTX and in renal transplantation patients with excellent graft function treated with cyclosporine (RTX-CSA, n=13), tacrolimus (RTX-FK, n=13), or without calcineurin inhibitors (RTX-Phi, n=6), as well as in healthy volunteers (CON, n=15). In addition to the above patients with present diseased native kidneys, we studied 16 RTX patients who had undergone bilateral nephrectomy (RTX-NE). Data are mean+/-SEM. MSNA was significantly elevated in hemodialysis patients (43+/-4 bursts/min), RTX-CSA (44+/-5 bursts/min), RTX-FK (34+/-3 bursts/min), and RTX-Phi (44+/-5 bursts/min) as compared with CON (21+/-3 bursts/min), despite excellent graft function after RTX. RTX-NE had significantly reduced MSNA (20+/-3 bursts/min) when compared with RTX patients. MSNA did not change significantly with RTX in 4 hemodialysis patients studied before and after RTX (44+/-6 versus 43+/-5 bursts/min, P=NS). In contrast, nephrectomy resulted in reduced MSNA in all 6 RTX patients studied before and after removal of the second native kidney. CONCLUSIONS Despite correction of uremia, increased SNA is observed in renal transplant recipients with diseased native kidneys at a level not significantly different from chronic hemodialysis patients. The increased SNA seems to be mediated by signals arising in the native kidneys that are independent of circulating uremia related toxins.
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Limited effect of systemic beta-blockade on sympathetic outflow.
Tank, J, Diedrich, A, Schroeder, C, Stoffels, M, Franke, G, Sharma, AM, Luft, FC, Jordan, J
Hypertension (Dallas, Tex. : 1979). 2001;(6):1377-81
Abstract
Central beta-adrenoreceptors may augment sympathetic outflow. We tested the hypothesis that beta-blockade attenuates central sympathetic outflow by inhibiting central adrenoreceptors. We studied 18 healthy controls (4 female, 14 male; age, 26+/-6 years, body mass index, 23+/-3 kg/m(2)). ECG, brachial, and finger arterial blood pressure, muscle sympathetic nerve activity, and respiration were measured continuously before and during complete beta-blockade. Subjects received a total intravenous dose of 0.21 mg/kg of propranolol in 15 minutes. Spontaneous baroreflex slopes were calculated using the sequence technique (BRSup, BRSdown). The sympathetic baroreflex slope was determined at baseline using phenylephrine and sodium nitroprusside infusions. The subjects underwent cold pressor testing before and during beta-blockade. The R-R interval increased from 861+/-119 ms at baseline to 952+/-141 ms during beta-blockade (P<0.01). Blood pressure was 117+/-9/65+/-8 mm Hg at baseline and 117+/-10/67+/-8 mm Hg during beta-Blockade (P=NS). beta-Blockade did not affect baroreflex sensitivity (BRSup: 21+/-10 versus 28+/-11 ms/mmHg, P<0.1; BRSdown: 17+/-8 versus 20+/-8 ms/mmHg, P=NS). Muscle sympathetic nerve activity increased significantly during beta-blockade (number of bursts/100 beats: 32+/-9 versus 40+/-14, P<0.05), compared with baseline. However, the operating points of the parasympathetic and sympathetic baroreflex during beta-blockade were on the baroreflex curves obtained at baseline. beta-Blockade blunted the heart rate response to cold pressor testing; blood pressure and muscle sympathetic nerve activity responses were similar. Our study demonstrates that propranolol does not cause an acute decrease in sympathetic activity in normotensive young subjects. This, observation is not consistent with an important tonic stimulatory effect of beta-adrenoreceptors in the brain.