Impaired insulin-mediated antilipolysis and lactate release in adipose tissue of upper-body obese women

Upper-body/visceral obesity is associated with abnormalities of free fatty acid (FFA) metabolism and greater risk of developing type 2 diabetes compared with lower-body obesity. In lean subjects lipolysis is readily suppressed by insulin; however, metabolic inflexibility with respect to antilipolysis is a frequent finding in obesity, partly determined by body composition. This study investigates effects of insulin on regional adipose tissue lipolysis and lactate levels in upper-body overweight/obese (UBO), lower-body overweight/obese (LBO), and lean women. The microdialysis technique was used to assess adipose tissue glycerol and lactate concentrations in abdominal and femoral fat during a 5-h basal period and a 2-h hyperinsulinemic euglycemic clamp. The main findings were that the antilipolytic effect of insulin was attenuated in abdominal fat of UBO (glycerol reduction, abd (%): UBO 40.4 (-14 to 66), LBO 46.0 (-8 to 66), lean 66.2 (2-78), ANOVA, P < 0.05), and in femoral fat in both obese groups (glycerol reduction, fem (%): UBO 44.4 (35-67), LBO 44.4 (0-63), lean 65.0 (43-79), ANOVA, P < 0.05). Further, abdominal fat insulin-mediated increase in lactate concentration was greater in lean women compared with UBO women (lactate increase, abd (%): UBO -6.1 (-37.1 to 57.4), LBO 16.5 (-32.2 to 112.5), lean 51.4 (-45.7 to 162.9), P < 0.05), whereas no differences were found between groups in femoral fat (lactate increase, fem (%), UBO -12.9 (-43 to 24), LBO 12.7 (-30.7 to 92), lean 27.6 (-9.5 to 123.8), not significant). Respiratory exchange ratio (RER) increased significantly and similarly in all groups. So, UBO women were metabolically inflexible with respect to insulins antilipolytic and lactate increasing effects in abdominal adipose tissue. These phenomena are probably both consequences of insulin resistance of adipose tissue.     

Body composition determines direct FFA storage pattern in overweight women

Direct FFA storage in adipose tissue is a recently appreciated pathway for postabsorptive lipid storage. We evaluated the effect of body fat distribution on direct FFA storage in women with different obesity phenotypes. Twenty-eight women [10 upper body overweight/obese (UBO; WHR >0.85, BMI >28 kg/m(2)), 11 lower body overweight/obese (LBO; WHR <0.80, BMI >28 kg/m(2)), and 7 lean (BMI <25 kg/m(2))] received an intravenous bolus dose of [9,10-(3)H]palmitate- and [1-(14)C]triolein-labeled VLDL tracer followed by upper body subcutaneous (UBSQ) and lower body subcutaneous (LBSQ) fat biopsies. Regional fat mass was assessed by combining DEXA and CT scanning. We report greater fractional storage of FFA in UBSQ fat in UBO women compared with lean women (P < 0.01). The LBO women had greater storage per 10(6) fat cells in LBSQ adipocytes compared with UBSQ adipocytes (P = 0.04), whereas the other groups had comparable storage in UBSQ and LBSQ adipocytes. Fractional FFA storage was significantly associated with fractional VLDL-TG storage in both UBSQ (P < 0.01) and LBSQ (P = 0.03) adipose tissue. In conclusion, UBO women store a greater proportion of FFA in the UBSQ depot compared with lean women. In addition, LBO women store FFA more efficiently in LBSQ fat cells compared with UBSQ fat cells, which may play a role in development of their LBO phenotype. Finally, direct FFA storage and VLDL-TG fatty acid storage are correlated, indicating they may share a common rate-limiting pathway for fatty acid storage in adipose tissue.     

Autonomic nervous nonlinear interactions lead to frequency modulation between low- and high-frequency bands of the heart rate variability spectrum

Cardiac sympathetic and parasympathetic neural activities have been found to interact with each other to efficiently regulate the heart rate and maintain homeostasis. Quantitative and noninvasive methods used to detect the presence of interactions have been lacking, however. This may be because interactions among autonomic nervous systems are nonlinear and nonstationary. The goal of this work was to identify nonlinear interactions between the sympathetic and parasympathetic nervous systems in the form of frequency and amplitude modulations in human heart rate data. To this end, wavelet analysis was performed, followed by frequency analysis of the resultant wavelet decomposed signals in several frequency brackets defined as very low frequency (f < 0.04 Hz), low frequency (LF; 0.04-0.15 Hz), and high frequency (HF; 0.15-0.4 Hz). Our analysis suggests that the HF band is significantly modulated by the LF band in the heart rate data obtained in both supine and upright body positions. The strength of modulations is stronger in the upright than supine position, which is consistent with elevated sympathetic nervous activities in the upright position. Furthermore, significantly stronger frequency modulation than in the control condition was also observed with the cold pressor test. The results with the cold pressor test, as well as the body position experiments, further demonstrate that the frequency modulation between LF and HF is most likely due to sympathetic and parasympathetic nervous interactions during sympathetic activations. The modulation phenomenon suggests that the parasympathetic nervous system is frequency modulated by the sympathetic nervous system. In this study, there was no evidence of amplitude modulation among these frequencies.     

Impact of body composition on very-low-density lipoprotein-triglycerides kinetics

Upper body obese (UBO) subjects have greater cardiovascular disease risk than lower body obese (LBO) or lean subjects. Obesity is also associated with hypertriglyceridemia that may involve greater production and impaired removal of very-low-density lipoprotein (VLDL)-triglycerides (TG). In these studies, we assessed the impact of body composition on basal VLDL-TG production, VLDL-TG oxidation, and VLDL-TG storage. VLDL-TG kinetics were assessed in 10 UBO, 10 LBO, and 10 lean women using a bolus injection of [1-(14)C]VLDL-TG. VLDL-TG oxidation was measured by (14)CO(2) production (hyamine trapping) and VLDL-TG adipose tissue storage by fat biopsies. Insulin sensititvity was assessed by the hyperinsulinemic-euglycemic clamp technique and body composition by dual X-ray absorptiometry in combination with computed tomography. Hepatic VLDL-TG production was significantly greater in UBO than in lean women [(mumol/min) UBO: 64.8 (SD 40.0) vs. LBO: 42.5 (SD 25.6) vs. lean: 31.8 (SD 13.3), P = 0.04], whereas VLDL-TG oxidation was similar in the three groups and averaged 20% of resting energy expenditure [(mumol/min) UBO: 38.3 (SD 26.5) vs. LBO: 23.5 (SD 13.5) vs. lean: 21.1 (SD 9.7), P = 0.09]. In UBO women, more VLDL-TG was deposited in upper body subcutaneous fat [VLDL-TG redeposition in abdominal adipose tissue (mumol/min): UBO: 5.0 (SD 2.9) vs. LBO: 4.0 (SD 3.2) vs. lean: 1.3 (SD 1.0), ANOVA P = 0.01]; in LBO women, more VLDL-TG was deposited in femoral fat [VLDL-TG redeposition in femoral adipose tissue (mumol/min): UBO: 5.1 (SD 3.1) vs. LBO: 5.8 (SD 4.3) vs. lean: 2.3 (SD 1.5), ANOVA P = 0.04]. Only a small proportion of VLDL-TG (8-16%) was partitioned into redeposition in either group. We found that elevated VLDL-TG production without concomitant increased clearance via oxidation and adipose tissue redeposition contributes to hypertriglyceridemia in UBO women.     

Evidence of dominant parasympathetic nervous activity of great cormorants (<Emphasis Type="Italic">Phalacrocorax carbo</Emphasis>)

The characteristics of autonomic nervous activity were examined on captive great cormorants Phalacrocorax carbo hanedae, using a power spectral analysis of heart rate variability. Heart rates were calculated from recordings of the electrocardiograms of the birds via embarked data loggers. We investigated the effects of blockades of the sympathetic or parasympathetic nervous systems using the indices of autonomic nervous activity such as high frequency (0.061–1.5 Hz) component, low frequency (0.02–0.060 Hz) component and the low frequency power component to high frequency power component ratio. Resting heart rate (85.5 ± 6.1 bpm) was lower than the intrinsic heart rate (259.2 ± 15.3 bpm). The heart rate drastically increased after the injection of the parasympathetic nervous blocker, on the other hand it slightly decreased after the injection of the sympathetic nervous blocker. The sympathetic, parasympathetic and net autonomic nervous tones calculated from heart rate with and without blockades were 40.9 ± 27.6, −44.5 ± 7.4 and −29.5 ± 9.0%, respectively. The effect of the parasympathetic nervous blockade on low frequency and high frequency power was greater than that of the sympathetic nervous blockade. Those data suggested that the parasympathetic nervous activity was dominant for great cormorants.     

Supine and standing sympathovagal balance in athletes and controls

Differences in autonomic nerve activity between athletes and controls during supine rest and standing were investigated by recording the cardiac rhythm in 18 professional cyclists and 11 controls. We computed four indexes of autonomic control: the standard deviation (SD) of the interbeat intervals, the coefficient of variance (CV) of the interbeat intervals, the percentage of successive intervals differing by more than 50 ms (pNN50), and the fraction low-frequency (0.07–0.14 Hz) spectral power (LF), and we also measured the mean interbeat interval (MI). Significant differences (Student's t-test, P < 0.005) between the athletes and the controls in the supine position were found for pNN50 [mean 52.6 (SEM 2.5) vs 37.1 (SEM 3.4)%], LF [mean 32.2 (SEM 1.6) vs 40.7 (SEM 2.1) normalized units], and MI [mean 1241 (SEM 20) vs 1021 (SEM 25) ms]. A significant difference between the athletes and the controls in the standing position was found for MI [mean 888 (SEM 13) vs 801 (SEM 23) ms]. These results would suggest that there is a parasympathetic predominance in athletes in the supine, but not in the standing position. The finding that pNN50 and LF, but not SD and CV, differed between the athletes and the controls, would seem to demonstrate that the differences in autonomic control between the athletes and the controls are reflected in the quality (balance between slow and fast heart rate fluctuations) rather than in the quantity of heart rate variability.     

Effects of glucagon-like peptide-1, yohimbine, and nitrergic modulation on sympathetic and parasympathetic activity in humans

Glucagon-like peptide-1 (GLP-1), an incretin, which is used to treat diabetes mellitus in humans, inhibited vagal activity and activated nitrergic pathways. In rats, GLP-1 also increased sympathetic activity, heart rate, and blood pressure (BP). However, the effects of GLP-1 on sympathetic activity in humans are unknown. Our aims were to assess the effects of a GLP-1 agonist with or without alpha(2)-adrenergic or -nitrergic blockade on autonomic nervous functions in humans. In this double-blind study, 48 healthy volunteers were randomized to GLP-1-(7-36) amide, the nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-l-arginine acetate (l-NMMA), the alpha(2)-adrenergic antagonist yohimbine, or placebo (i.e., saline), alone or in combination. Hemodynamic parameters, plasma catecholamines, and cardiac sympathetic and parasympathetic modulation were measured by spectral analysis of heart rate. Thereafter, the effects of GLP-1-(7-36) amide on muscle sympathetic nerve activity (MSNA) were assessed by microneurography in seven subjects. GLP-1 increased (P = 0.02) MSNA but did not affect cardiac sympathetic or parasympathetic indices, as assessed by spectral analysis. Yohimbine increased plasma catecholamines and the low-frequency (LF) component of heart rate power spectrum, suggesting increased cardiac sympathetic activity. l-NMMA increased the BP and reduced the heart rate but did not affect the balance between sympathetic and parasympathetic activity. GLP-1 increases skeletal muscle sympathetic nerve activity but does not appear to affect cardiac sympathetic or parasympathetic activity in humans.     

Cardiac Autonomic Activity During Human Sleep: Analysis of Sleep Stages and Sleep Cycles

In this study characteristics of cardiac functioning were investigated in nine subjects during their nocturnal sleep. The pre-ejection period and the high frequency component of heart rate variability were used as indices of cardiac sympathetic and parasympathetic activity of the autonomic nervous system respectively. Heart rate and the autonomic indices were assessed across physiological determined sleep stages and consecutive temporal sleep cycles. Repeated measures ANOVA analyses indicated a significant pattern of heart rate as a function of sleep stages, which was mirrored by parasympathetic activity. Further, a significant decrease of heart rate as a function of sleep cycles was mirrored by an increase of sympathetic activity. Moreover, non-REM/REM differences revealed a dominant role of parasympathetic activity during sleep stages as well as sleep cycles. These findings demonstrate that sympathetic activity is influenced by time asleep, whereas parasympathetic activity is influenced by the depth of sleep.     

Cardiac Autonomic Activity During Human Sleep: Analysis of Sleep Stages and Sleep Cycles

In this study characteristics of cardiac functioning were investigated in nine subjects during their nocturnal sleep. The pre-ejection period and the high frequency component of heart rate variability were used as indices of cardiac sympathetic and parasympathetic activity of the autonomic nervous system respectively. Heart rate and the autonomic indices were assessed across physiological determined sleep stages and consecutive temporal sleep cycles. Repeated measures ANOVA analyses indicated a significant pattern of heart rate as a function of sleep stages, which was mirrored by parasympathetic activity. Further, a significant decrease of heart rate as a function of sleep cycles was mirrored by an increase of sympathetic activity. Moreover, non-REM/REM differences revealed a dominant role of parasympathetic activity during sleep stages as well as sleep cycles. These findings demonstrate that sympathetic activity is influenced by time asleep, whereas parasympathetic activity is influenced by the depth of sleep.     

Effects of sleep pressure on endogenous cardiac autonomic activity and body temperature.

This study investigated the effects of variations in sleep pressure on cardiac autonomic activity and body temperature. In a counterbalanced design, 12 healthy, young subjects (6 men and 6 women) remained recumbent during 30 h of wakefulness (high sleep pressure) and 6 h of wakefulness (low sleep pressure). Both periods of wakefulness were immediately followed by a sleep opportunity, and the first 2 h of sleep were analyzed. During extended hours of wakefulness, a reduction in heart rate was mediated by a decline in cardiac sympathetic activity (measured via preejection period) and the maintenance of cardiac parasympathetic activity (measured via respiratory sinus arrhythmia). In subsequent high-pressure sleep, parasympathetic activity was amplified and sympathetic activity was negatively associated with electroencephalographic slow-wave activity. Sleep deprivation had no impact on foot temperature, but it did alter the pattern of change in core body temperature. A downregulation of cardiac autonomic activity during both extended hours of wakefulness and subsequent sleep may respectively provide "protection" and "recovery" from the temporal extension of cardiac demand.     

A trial of the use of aekol in preventing psychoautonomic disorders

Autonomic dysfunction in chronic emotional stress is well documented. The aim of this study was to analyze the effects of natural antioxidant vitamin E (aekol). Twenty persons (16 women and 4 men, mean age 38 +/- 4 years) who reported recent occurrence of emotional stress were examined before and after a 4-week treatment with aekol (5 ml twice a day). Heart rate variability (taking into account very low-frequency (VLF, 0.003-0.04 Hz), low-frequency (LF, 0.04-0.15 Hz), and high-frequency (HF, 0.15-0.40 Hz) components) was computed from the power spectra (5-min epochs) of the EKG recorded in the patients in supine position. After the treatment, the HF power of the heart rate variability (an index of cardiac parasympathetic activity) increased (p < 0.05), whereas the VLF power (an index of the cerebral sympathetic activity) decreased (p < 0.01). The decrease in the VLF was accompanied by a reduction of anxiety level (p < 0.01). According to our hypothesis, the absolute and relative power of the VLF can be used as an index of anxiety or cerebral sympathetic activity, which significantly decreases after the aekol treatment.     

Autonomic Nervous System Regulation of Epicardial Adipose Tissue: Potential Roles for Regulator of G Protein Signaling-4

The epicardial adipose tissue (EAT) or epicardial fat is a visceral fat depot in the heart that contains intrinsic adrenergic and cholinergic nerves, through which it interacts with the cardiac sympathetic (adrenergic) and parasympathetic (cholinergic) nervous systems. These EAT nerves represent a significant source of several adipokines and other bioactive molecules, including norepinephrine, epinephrine, and free fatty acids. The production of these molecules is biologically relevant for the heart, since abnormalities in EAT secretion are implicated in the development of pathological conditions, including coronary atherosclerosis, atrial fibrillation, and heart failure. Sympathetic hyperactivity and parasympathetic (cholinergic) derangement are associated with EAT dysfunction, leading to a variety of adverse cardiac conditions, such as heart failure, diastolic dysfunction, atrial fibrillation, etc.; therefore, several studies have focused on exploring the autonomic regulation of EAT as it pertains to heart disease pathogenesis and progression. In addition, Regulator of G protein Signaling (RGS)-4 is a protein with significant regulatory roles in both adrenergic and muscarinic receptor signaling in the heart. In this review, we provide an overview of the autonomic regulation of EAT, with a specific focus on cardiac RGS4 and the potential roles this protein plays in this regulation.     

Effect of autonomic blockers on heart period variability in calves: evaluation of the sympathovagal balance

This study was designed to validate the measures of heart period variability for assessing of autonomic nervous system control in calves. Eight calves received an injection of either 0.5 mg/kg atenolol (sympathetic tone blockade), 0.2 mg/kg atropine sulfate (parasympathetic tone blockade), 0.5 mg/kg atenolol + 0.2 mg/kg atropine sulfate (double autonomic blockade) or saline. In the time-domain, we calculated the mean instantaneous heart rate (HR), mean of RR intervals (MeanRR), standard deviation of RR intervals (SDRR) and that of the difference between adjacent intervals (RMSSD). In the frequency-domain, the power of the spectral band 0-1 Hz (TPW), the power of the 0-0.15 Hz band (LF), that of the 0.15-1 Hz band (HF), and the LF/HF ratio were considered. The net vago-sympathetic effect (VSE) was calculated as the ratio of MeanRR in a defined situation to MeanRR during the double blockade. Atenolol injection had no effect on cardiac activity, whereas atropine induced large modifications which were moderated when atenolol was administered at the same time. VSE, HR, MeanRR and RMSSD were found to be valid indicators of the parasympathetic tone of calves because of large variations due to the drug and low individual variations. No measure reflected the sympathetic tone.     

Quantifying cardiac sympathetic and parasympathetic nervous activities using principal dynamic modes analysis of heart rate variability

The ratio between low-frequency (LF) and high-frequency (HF) spectral power of heart rate has been used as an approximate index for determining the autonomic nervous system (ANS) balance. An accurate assessment of the ANS balance can only be achieved if clear separation of the dynamics of the sympathetic and parasympathetic nervous activities can be obtained, which is a daunting task because they are nonlinear and have overlapping dynamics. In this study, a promising nonlinear method, termed the principal dynamic mode (PDM) method, is used to separate dynamic components of the sympathetic and parasympathetic nervous activities on the basis of ECG signal, and the results are compared with the power spectral approach to assessing the ANS balance. The PDM analysis based on the 28 subjects consistently resulted in a clear separation of the two nervous systems, which have similar frequency characteristics for parasympathetic and sympathetic activities as those reported in the literature. With the application of atropine, in 13 of 15 supine subjects there was an increase in the sympathetic-to-parasympathetic ratio (SPR) due to a greater decrease of parasympathetic than sympathetic activity (P=0.003), and all 13 subjects in the upright position had a decrease in SPR due to a greater decrease of sympathetic than parasympathetic activity (P<0.001) with the application of propranolol. The LF-to-HF ratio calculated by the power spectral density is less accurate than the PDM because it is not able to separate the dynamics of the parasympathetic and sympathetic nervous systems. The culprit is equivalent decreases in both the sympathetic and parasympathetic activities irrespective of the pharmacological blockades. These findings suggest that the PDM shows promise as a noninvasive and quantitative marker of ANS imbalance, which has been shown to be a factor in many cardiac and stress-related diseases.     

Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation.

Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.     

Early autonomic malfunction in normotensive individuals with a genetic predisposition to essential hypertension

One of the primary pathologies associated with hypertension is a complex autonomic dysfunction with evidence of sympathetic hyperactivity and/or vagal withdrawal. We investigated the possibility for early detection of essential hypertension on the basis of the analysis of heart rate (HR) and blood pressure fluctuations, which reflect autonomic control. Young adult normotensive offspring of one hypertensive parent (KHT; n = 12) and normotensive offspring of two normotensive parents (YN; n = 14) participated in this study. ECG, continuous blood pressure, and respiration were recorded during steady-state conditions and under various autonomic challenges. Time-frequency decomposition of these signals was performed with the use of a continuous wavelet transform. The use of the wavelet transform enables the extension of typical HR variability analysis to non-steady-state conditions. This time-dependent spectral analysis of HR allows time-dependent quantification of different spectral components reflecting the sympathetic and parasympathetic activity during rapid transitions, such as an active change in posture (CP). During an active CP from the supine to standing position, KHT demonstrated a significantly greater increase in the low-frequency fluctuations in HR than YN, indicating enhanced sympathetic involvement in the HR response to CP, and a reduced alpha-index, indicating decreased baroreceptor sensitivity. On recovery from handgrip, vagal reactivation was more sluggish in KHT. These results indicate the early existence of malfunctions in both branches of autonomic control in individuals at increased risk of hypertension.     

Effects of bright light and melatonin on sleep propensity, temperature, and cardiac activity at night.

Melatonin increases sleepiness, decreases core temperature, and increases peripheral temperature in humans. Melatonin may produce these effects by activating peripheral receptors or altering autonomic activity. The latter hypothesis was investigated in 16 supine subjects. Three conditions were created by using bright light and exogenous melatonin: normal endogenous, suppressed, and pharmacological melatonin levels. Data during wakefulness from 1.5 h before to 2.5 h after each subject's estimated melatonin onset (wake time + 14 h) were analyzed. Respiratory sinus arrhythmia (cardiac parasympathetic activity) and preejection period (cardiac sympathetic activity) did not vary among conditions. Pharmacological melatonin levels significantly decreased systolic blood pressure [5.75 +/- 1.65 (SE) mmHg] but did not significantly change heart rate. Suppressed melatonin significantly increased rectal temperature (0.27 +/- 0.06 degrees C), decreased foot temperature (1.98 +/- 0.70 degrees C), and increased sleep onset latency (5.53 +/- 1.87 min). Thus melatonin does not significantly alter cardiac autonomic activity and instead may bind to peripheral receptors in the vasculature and heart. Furthermore, increases in cardiac parasympathetic activity before normal nighttime sleep cannot be attributed to the concomitant increase in endogenous melatonin.     

Altered autonomic cardiac regulation in individuals with Down syndrome

We tested the hypothesis that individuals with Down syndrome, but without congenital heart disease, exhibit altered autonomic cardiac regulation. Ten subjects with Down syndrome (DS) and ten gender-and age-matched healthy control subjects were studied at rest and during active orthostatism, which induces reciprocal changes in sympathetic and parasympathetic traffic to the heart. Autoregressive power spectral analysis was used to investigate R-R interval variability. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. No significant differences between DS and control subjects were observed in arterial blood pressure at rest or in response to standing. Also, R-R interval did not differ at rest. R-R interval decreased significantly less during standing in DS vs. control subjects. Low-frequency (LFNU) and high-frequency (HFNU) (both expressed in normalized units) components of R-R interval variability did not differ between DS and control subjects at rest. During standing, significant increase in LFNU and decrease in HFNU were observed in control subjects but not in DS subjects. Baroreflex sensitivity (BRS) did not differ between DS and control subjects at rest and underwent significant decrease on going from supine to upright in both groups. However, BRS was greater in DS vs. control subjects during standing. These data indicate that subjects with DS exhibit reduced HR response to orthostatic stress associated with blunted sympathetic activation and vagal withdrawal and with a lesser reduction in BRS in response to active orthostatism. These findings suggest overall impairment in autonomic cardiac regulation in DS and may help to explain the chronotropic incompetence typically reported during exercise in subjects with DS without congenital heart disease.     

体位改变对Beagle犬心脏自主神经控制的影响

目的观察体位改变对Beagle犬心脏自主神经控制的影响。方法利用大动物无创生理遥测技术,监测清醒活动状态下雌性Beagle犬在静态姿势（lying、standing、sitting、hanging）和运动（walking）姿势下的心电图（ECG）,并用HRV功率谱分析其自主神经功能。结果在静态姿势下,Beagle犬RR间期（RRI）、RR间期的标准差SDNN（SDNN）、相邻RR间期差值平方和的均方根RMSSD（RMSSD）、相邻R-R间期差值〉50 ms的窦性个数占心搏总数的百分比pNNabs（50）（pNNabs（50））、TP总功率（TP）、VLF极低频功率（VLF）、标准化高频功率（HFnorm）均明显高于运动状态（P〈0.05,P〈0.01）,而心率（HR）、标准化低频功率（LFnorm）和低频功率/高频功率（LF/HF）平衡指数则明显低于运动状态（P〈0.05,P〈0.01）。结论不同体位姿势在静息状态下以迷走神经活动兴奋为主,相反,在运动状态下以交感神经活动兴奋为主;体位姿势改变能引起心率的变化,必然影响心脏自主神经控制能力,其主要取决于迷走神经活动强弱有关,且导致LF/HF均衡性的破坏。