scholarly journals Plasma Leptin Concentrations and Cardiac Autonomic Nervous System in Healthy Subjects with Different Body Weights

2000 ◽  
Vol 85 (5) ◽  
pp. 1810-1814 ◽  
Author(s):  
Giuseppe Paolisso ◽  
Daniela Manzella ◽  
Nicola Montano ◽  
Antonio Gambardella ◽  
Michele Varricchio

Abstract Previous studies have shown that leptin stimulates sympathetic nervous system; heart rate variability (HRV) is a widely used technique for assessing the sympathovagal balance at the cardiac level. The aim of our study was to investigate a possible relationship between plasma leptin levels and the autonomic regulation using spectral analysis of HRV. In 120 healthy nonobese subjects the plasma leptin concentration was determined, and HRV was recorded at baseline and during tilt. All subjects were categorized in quartiles of plasma leptin concentration. Analysis of data showed a significant increase in body mass index, body fat, fasting plasma insulin, triglyceride concentration, and homeostatic model assessment values throughout the different quartiles of plasma leptin concentration. Concerning cardiovascular parameters, heart rate, arterial blood pressures, and RR intervals were not significantly different among the quartiles. Total power and high frequency (HF) in normalized units were significantly decreased, whereas low frequency (LF) normalized units was progressively increased from the first to the fourth quartile. Thus, the LF/HF ratio rose gradually and significantly from the lowest to the highest quartile. Such results were independent of the body fat estimate (P < 0.03 for the trend). The change in the LF/HF ratio was significantly enhanced during tilt (P < 0.001 vs. rest values for all quartiles); the effect was stronger in subjects in the fourth quartile of plasma leptin concentration (P < 0.005 for the trend). The latter parameter was also independent of body fat content and distribution (P < 0.01). Our study shows that increasing fasting plasma leptin concentrations are associated with a shift of the sympathovagal balance toward a progressive increase in sympathetic activation and an increased response to orthostatic stimulus in nonobese subjects with different body fat contents.

2020 ◽  
Author(s):  
Bharti Bhandari ◽  
Manisha Mavai ◽  
Yogendra Raj Singh ◽  
Bharati Mehta ◽  
Omlata Bhagat

A single episode of breath-holding (BH) is known to elevate the blood pressure, and regular breathing exercise lowers the blood pressure. This prompted us to investigate how a series of BH epochs would affect the cardiovascular system. To observe arterial blood pressure (ABP) and heart rate (HR) changes associated with a series of “BH epochs” following maximum inspiration and maximum expiration and find the underlying mechanisms for the change by autonomic activity. Thirty-five healthy young adults were instructed to hold their breath repetitively, for 5 minutes, in two patterns, one following maximum inspiration and other following maximum expiration. ABP and ECG (for Heart Rate Variability) were continuously recorded at rest and during both the maneuvers. Capillary blood gases (BG) were zanalyzed at baseline and at the breakpoint of the last epoch of BH. ABP rose significantly at the breakpoint during both the maneuvers. No change in HR was observed. There was significant fall in PO2 from 94.7 (4.1) mmHg at baseline to 79.1 (9.0) mmHg during inspiratory and 76.90 (12.1) mmHg during expiratory BH. Similarly, SPO2 decreased from 96.3 (1.9) % at baseline to 95.4 (1.5) % and 94.5 (2.7) % during inspiratory and expiratory BH, respectively. Rise in PCO2 from 39.5(3.1) mmHg at baseline to 42.9 (2.7) mmHg and 42.1 (2.8) mmHg during inspiratory and expiratory BH respectively was observed. There was no significant correlation between blood gases and arterial blood pressure. Among HRV parameters, a significant decrease in SDNN, RMSSD, HFnu, total power and SD1/SD2 and the significant increase in LFnu, LF/HF and SD2 were observed during both BH patterns. Rhythmic BH patterns affect the cardiovascular system in similar way as a single episode of BH. Sympathetic overactivity could be the postulated mechanism for the same. © 2019 Tehran University of Medical Sciences. All rights reserved. Acta Med Iran 2019;57(8):492-498.


2018 ◽  
Vol 7 (9) ◽  
pp. 270 ◽  
Author(s):  
Hasthi Dissanayake ◽  
Rowena McMullan ◽  
Yang Kong ◽  
Ian Caterson ◽  
David Celermajer ◽  
...  

Birth weight is associated with cardiovascular disease, with those at both ends of the spectrum at increased risk. However, birth weight is a crude surrogate of fetal growth. Measures of body composition may more accurately identify high risk infants. We aimed to determine whether aortic wall thickening, cardiac autonomic control, and cardiac structure/function differ in newborns with high or low body fatness compared to those with average body fatness. 189 healthy singleton term born neonates were recruited and stratified by body fat percentiles (sex and gestation-specific). Infants with low body fat had higher aortic intima-media thickness (43 µm (95% confidence interval (CI) 7, 78), p = 0.02), lower heart rate variability (log total power, −0.5 (95% CI −0.8, −0.1), p = 0.008), and thicker ventricular walls (posterior wall thickness, 3.1 mm (95% CI 1.6, 4.6), p < 0.001) compared to infants with average body fatness. Infants with high body fat showed no differences in aortic intima-media thickness (−2 µm (95% CI −37, 33), p = 0.91) or cardiac structure compared to average body fatness, although stroke volume (−0.3 mL/kg (95% CI −0.6, −0.0), p = 0.003) and heart rate variability were lower (log total power, −0.8 (95% CI −1.1, −0.5), p < 0.001). The non-linear association of body fatness with heart rate variability was independent of birth weight. Infants born with low or high body fat have altered markers of cardiovascular health. Assessment of body fatness alongside birth weight may assist in identifying high risk individuals.


2018 ◽  
Vol 105 (4) ◽  
pp. 386-396 ◽  
Author(s):  
ZZ Taralov ◽  
KV Terziyski ◽  
PK Dimov ◽  
BI Marinov ◽  
SS Kostianev

Purpose The purpose of this study is to establish the alterations in the activity of the autonomic nervous system (ANS) via heart rate variability (HRV) in subjects exposed to 1 h of exogenous hypoxia for 10 consecutive days. Methods Twelve healthy non-smoker males at mean age of 29.8 ± 7.4 (mean ± SD) breathed hypoxic air delivered through hypoxicator (FiО2 = 12.3% ± 1.5%) for 1 h in 10 consecutive days. Pulse oximetry and electrocardiography were monitored during the visit and HRV was calculated for the entire 1-h hypoxic period. Results Comparing the last hypoxic visit to the first, subjects had higher standard deviation of normal-to-normal interbeat intervals (SDNNs) (65.7 ± 32.5 vs. 81.1 ± 32.0 ms, p = 0.013) and root mean square of successive R–R interval difference (RMSSD) (58.1 ± 30.9 vs. 76.5 ± 34.6 ms, p = 0.029) as well as higher lnTotal power (8.1 ± 1.1 vs. 8.5 ± 0.9 ms2, p = 0.015) and high frequency (lnHF) (6.8 ± 1.3 vs. 7.5 ± 1.2 ms2, p = 0.05) and lower LF/HF (2.4 ± 1.4 vs. 1.5 ± 1.0, p = 0.026). Changes in saturation (87.0 ± 7.1 vs. 90.8 ± 5.0%, p = 0.039) and heart rate (67.1 ± 8.9 vs. 62.5 ± 6.0 beats/min, p = 0.040) were also observed. Conclusions Intermittent hypoxic training consisting of 1-h hypoxic exposure for 10 consecutive days could diminish the effects of acute exogenous hypoxia on the ANS characterized by an increased autonomic control (SDNN and total power) with augmentation of the parasympathetic nervous system activity (increased RMSSD and HF and decreased LF/HF). Therefore, it could be applied as a pre-acclimatization technique aiming at an increase in the autonomic control and oxygen saturation in subjects with upcoming sojourn to high altitude.


1989 ◽  
Vol 256 (1) ◽  
pp. R112-R119 ◽  
Author(s):  
D. N. Darlington ◽  
M. Miyamoto ◽  
L. C. Keil ◽  
M. F. Dallman

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.


1989 ◽  
Vol 256 (6) ◽  
pp. H1573-H1579 ◽  
Author(s):  
J. B. Madwed ◽  
P. Albrecht ◽  
R. G. Mark ◽  
R. J. Cohen

We have previously reported that low-frequency oscillations in arterial blood pressure (ABP) and heart rate (HR) occur when conscious dogs experience severe blood loss. These low-frequency oscillations are generated by enhancement of the sympathetic nervous system and inhibition of the parasympathetic nervous system. We have developed a simple computer model to elucidate those properties critical to the generation of these oscillations. Our model incorporates several important features: 1) arterial baroreceptor feedback loops, which relate ABP to targeted HR and total peripheral resistance (TPR) values; 2) two effector outputs, HR and TPR, which are controlled by the outputs of vagal, beta-adrenergic, and alpha-adrenergic effector mechanisms; 3) a fixed beat-to-beat stroke volume; and 4) a wind-kessel model, which represents the peripheral circulation. Each effector mechanism is modeled as a low-pass filter in series with a delay. The vagal effector mechanism slows the HR after a 100-ms delay and reaches maximal HR at that time. The beta-adrenergic effector mechanism speeds HR after a 2.5-s delay and then increases to maximal HR 7.5 s later. The alpha-adrenergic effector mechanism begins vasoconstriction after a 5-s delay and then reaches maximal contraction 15 s later. Computer simulations of inhibition of the vagal effector mechanism and activation of the adrenergic effector mechanisms elicit low-frequency oscillations in ABP and HR. These oscillations are similar to those observed experimentally in the dog during hemorrhage. We conclude that the slow temporal response of the alpha-adrenergic effector mechanism controlling TPR is the critical element in predicting the observed low-frequency oscillations in ABP and HR.


2007 ◽  
Vol 16 (4) ◽  
pp. 336-342
Author(s):  
Nicolas Olivier ◽  
Renaud Legrand ◽  
Jacques Rogez ◽  
FX Gamelin ◽  
Serge Berthoin ◽  
...  

Objective:To analyze the consequences on heart rate variability (HRV) of a hospitalization period due to surgery of the knee in sportsmen.Patients:Ten soccer players who had undergone knee surgery took part in this study.Design:HRV was measured before and after hospitalization within a 7-day interval.Results:After the hospitalization phase, heart rate at rest increased significantly (3 beats/minute). A significant decrease of 7% in the cardiac inter beat interval (R-R interval), P < 0.05 and a 66% decrease in total power spectral density: −66%, P < 0.05 were observed. The disturbance of the autonomic nervous system could be due to a variation in cardiac vagal activity resulting in a 64% decrease in the high frequencies (P < 0.05). This variation was not associated with a modification in normalized markers (LFn.u., HFn.u.) and LF/HF ratio (P > 0.05).Conclusion:In sportsmen, a hospitalization period led to an increase in resting heart rate and was associated with a disturbance of the autonomic nervous system.


2021 ◽  
Vol 99 (12) ◽  
pp. 1370-1375
Author(s):  
Svetlana V. Ivanova ◽  
Svetlana A. Skovronskaya ◽  
Mihail E. Goshin ◽  
Olga V. Budarina ◽  
Aliya Z. Kulikova

The article contains a literature review devoted to research on the influence of odours on physiological, emotional, and cognitive aspects of human health. The following databases were used at literature search execution: Pubmed, Scopus, Web of Science, MedLine, Global Health, Russian Research Citation Index. A total amount of 60 sources was analyzed for 1983-2019. The experimental research results aimed at studying the influence of odours on such physiological indices a: heart rate, heart rate variability, arterial blood pressure, respiratory rate, skin conductibility reaction, sleep, are described, and emotional and cognitive characteristics of the test subjects. The response to odours exposure was shown to depend on their intensity, hedonistic tone, the chemical structure of the odorant, as well as individual peculiarities of the test subjects, including their past experiences with smelling. In most cases, exposure to unpleasant odours activates the sympathetic nervous system, therefore heart rate, respiratory rate, skin blood circulation and its conductivity increase. Attention concentration increases at the deterioration of cognitive functions. Anger and repulsion reactions are noted at the emotional level; a feeling of discomfort with a motivation to escape appears. The exposure of pleasant odours leads to parasympathetic nervous system activation, heart rate, respiratory rate, skin conductibility, and blood circulation decrease. Cognitive functions improve, the quality of problem-solving increases, attention concentration decreases. A person’s mood gets better; the sensation of happiness appears. At that literature analysis has revealed most of the studies on the human to have significant restrictions: standard exposure methods absence, the difficulty of execution blind experiments that were deemed to be ignorant by test subjects as well as the influence of individual preferences and previous personal experience on the effects generated by the odour. The authors proposed recommendations on the current restrictions prevention and optimization of conducting the experimental research on the influence of odours on humans.


2013 ◽  
Vol 13 (1) ◽  
pp. 5-13 ◽  
Author(s):  
Zuzana Visnovcova ◽  
A. Calkovska ◽  
I. Tonhajzerova

Abstract The autonomic nervous system (ANS) is a principal regulatory system for maintaining homeostasis, adaptability and physiological flexibility of the organism at rest as well as in response to stress. In the aspect of autonomic regulatory inputs on the cardiovascular system, recent research is focused on the study of exaggerated/diminished cardiovascular reactivity in response to mental stress as a risk factor for health complications, e.g. hypertension. Thus, the analysis of biological signals reflecting a physiological shift in sympathovagal balance during stress in the manner of vagal withdrawal associated with sympathetic overactivity is important. The heart rate variability, i.e. “beat-to-beat” oscillations of heart rate around its mean value, reflects mainly complex neurocardiac parasympathetic control. The electrodermal activity could represent “antagonistic” sympathetic activity, the so-called “sympathetic arousal” in response to stress. The detailed study of the physiological parameters under various stressful stimuli and in recovery phase using traditional and novel mathematical analyses could reveal discrete alterations in sympathovagal balance. This article summarizes the importance of heart rate variability and electrodermal activity assessment as the potential noninvasive indices indicating autonomic nervous system activity in response to mental stress.


1996 ◽  
Vol 271 (3) ◽  
pp. R641-R646 ◽  
Author(s):  
D. S. O'Leary ◽  
D. J. Woodbury

The objective of this study was to determine the role of cardiac output in mediating spontaneous fluctuations in mean arterial pressure (MAP) conscious dogs. Dogs were chronically instrumented to monitor MAP and cardiac output. Atrioventricular (AV) block was induced, and left ventricular and right atrial electrodes were implanted. After recovery, MAP was observed for 5 min under two conditions: 1) normal variation in heart rate and cardiac output via triggering the ventricular stimulator with each atrial depolarization (effectively reversing the AV block, AV-linked stimulation) and 2) computer control of ventricular rate to maintain cardiac output constant on a by-beat basis at the same level as observed during normal variations in heart rate and cardiac output. When cardiac output was held constant, large-amplitude, low-frequency oscillations in MAP were readily apparent. Spectral analysis by fast Fourier transform revealed that during constant cardiac output the power observed at low frequencies in the MAP spectrum represented 95.0 +/- 2.7% of the total power compared with 75.5 +/- 4.6% during normal variations in heart rate and cardiac output (P < 0.05). In addition, when cardiac output was held constant, the power observed at higher frequencies markedly decreased from 24.5 +/- 4.6% of total power during AV-linked stimulation to only 5.0 +/- 2.7% of total power during constant cardiac output (P < 0.05). We conclude that low-frequency oscillations in MAP are due to changes in peripheral resistance, whereas a significant amount of high-frequency changes in MAP stems from spontaneous changes in cardiac output.


1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.


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