Autonomic mechanisms in the initial heart rate response to standing

1980 ◽  
Vol 49 (5) ◽  
pp. 809-814 ◽  
Author(s):  
D. J. Ewing ◽  
L. Hume ◽  
I. W. Campbell ◽  
A. Murray ◽  
J. M. Neilson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Response Pattern ◽  
Heart Rate Response ◽  
Muscular Activity ◽  
Normal Subjects ◽  
Quiet Standing ◽  
Rate Variation ◽  
Normal Pattern ◽  
Vagal Control ◽  
Standing Up

Autonomic mechanisms underlying the initial heart rate response to standing were analyzed in nine normal subjects. The normal pattern of response was altered by atropine to a small and gradual R-R interval shortening over 30 beats, with no rebound R-R interval lengthening. With additional propranolol, R-R interval shortening was even less and confined to the first 15-20 beats, whereas propranolol alone did not affect the normal response pattern, showing that this is under vagal control with increased cardiac sympathetic activity occurring only if the vagus is blocked. The response was reproducible in 23 normal subjects. Heart rate variation during quiet standing was almost completely abolished by atropine, but unaffected by propranolol, confirming that it is also under vagal control. In four normal subjects no rebound R-R interval lengthening occurred during either "fast" or "slow" tilt, whereas it was present during both "slow" and "fast" standing. The rebound R-R interval lengthening is determined by the muscular activity involved in standing up, rather than by the speed of the maneuver.

Autonomic Control of the Immediate Heart Rate Response to Lying Down

1982 ◽  
Vol 62 (1) ◽  
pp. 57-64 ◽  
Author(s):  
F. Bellavere ◽  
D. J. Ewing
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Normal Subjects ◽  
Muscular Exercise ◽  
Diabetic Patients ◽  
Normal Pattern ◽  
Sympathetic Control ◽  
The Third ◽  
Steady Level ◽  
Lying Down

1. The initial heart rate response to lying down was analysed in 18 younger (23–36 years) and 10 older (48–67 years) normal subjects, and consisted of an immediate shortening of the R—R interval reaching a maximum around the third or fourth beat after lying, followed by a lengthening beyond the resting value to reach a steady level around beats 25–30. In six diabetic patients with autonomic neuropathy, no cardiac acceleration occurred and the deceleration was markedly diminished. 2. In eight young normal subjects the pattern of response was altered by atropine, which abolished the initial shortening of the R—R interval over the first 10 beats. Thereafter slow but steady lengthening of the R—R interval occurred. With additional propranolol the later part of the response was further attenuated. Propranolol alone did not affect the normal pattern of response. 3. Six young normal subjects performed short periods of muscular exercise, lying, sitting and standing, and the heart rate patterns were compared with that after lying down. After both manoeuvres R—R interval shortened and then lengthened back to the resting level within 10–15 beats. Thereafter it remained steady after muscular exercise, but continued to lengthen after lying down. 4. In four young normal subjects, no initial R—R interval shortening occurred during fast or slow ‘passive’ tilting from the 80° head-up position to horizontal, whereas shortening was seen both with fast and slow ‘active’ lying down. 5. It is concluded that the immediate part of the heart rate response to lying down (during the first 10 beats) is under vagal control and the later part predominantly under sympathetic control. The first part of the response is probably due to a ‘muscle—heart’ reflex which occurs during the change in posture.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

scholarly journals Dynamic Modelling of Heart Rate Response Under Different Exercise Intensity

2010 ◽  
Vol 4 (1) ◽  
pp. 81-85 ◽  
Author(s):  
Steven W Su ◽  
Weidong Chen ◽  
Dongdong Liu ◽  
Yi Fang ◽  
Weijun Kuang ◽  
...  
Keyword(s):  
Heart Rate ◽  
Time Constant ◽  
Heart Rate Response ◽  
Cardiovascular Response ◽  
Dynamic Modelling ◽  
Healthy Male Subject ◽  
Step Response ◽  
Rate Variation ◽  
Response Dynamics ◽  
Non Invasive

Heart rate is one of the major indications of human cardiovascular response to exercises. This study investigates human heart rate response dynamics to moderate exercise. A healthy male subject has been asked to walk on a motorised treadmill under a predefined exercise protocol. ECG, body movements, and oxygen saturation (SpO2) have been reliably monitored and recorded by using non-invasive portable sensors. To reduce heart rate variation caused by the influence of various internal or external factors, the designed step response protocol has been repeated three times. Experimental results show that both steady state gain and time constant of heart rate response are not invariant when walking speed is faster than 3 miles/hour, and time constant of offset exercise is noticeably longer than that of onset exercise.

scholarly journals Intravenous adenosine and dyspnea in humans

2005 ◽  
Vol 98 (1) ◽  
pp. 180-185 ◽  
Author(s):  
Nausherwan K. Burki ◽  
Wheeler J. Dale ◽  
Lu-Yuan Lee
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Peripheral Chemoreceptor ◽  
C Fibers ◽  
Group Data ◽  
Lung Resistance ◽  
Time Latency ◽  
Stimulation Of

Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm and dyspnea and to increase ventilation in humans, but these effects have not been systematically studied. We therefore compared the effects of 10 mg of intravenous adenosine with placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea, and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change ( P > 0.1) in lung resistance as measured by the interrupter technique. There were significant increases ( P < 0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in every subject, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analyzed (18.9 ± 5.8, 20.3 ± 5.5, and 19.7 ± 4.5 s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared with the normoxic state, the intensity of the dyspneic response was significantly ( P < 0.05) reduced, whereas the heart rate response increased significantly ( P < 0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.

Propranolol and the Ventilatory Response to Hypoxia and Hypercapnia in Normal Man

1978 ◽  
Vol 55 (5) ◽  
pp. 491-497 ◽  
Author(s):  
J. M. Patrick ◽  
Janice Tutty ◽  
S. B. Pearson
Keyword(s):  
Heart Rate ◽  
Chemical Control ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Control Of Breathing ◽  
Maximal Expiratory Flow ◽  
Progressive Exercise ◽  
Normal Man ◽  
Ventilatory Response To Hypoxia

1. The effect on respiration of a single dose of propranolol has been studied in normal subjects. 2. The degree of β-adrenoreceptor blockade was assessed in terms of the impaired heart-rate response to progressive exercise and the plasma propranolol concentration. 3. No effect of propranolol was demonstrated on either the ventilatory response to rebreathing CO2 in hyperoxia, or the response to progressive isocapnic hypoxia. Simple indices of maximal expiratory flow (FEV1.0% and PEFR) were also unchanged. 4. The absence of any effect of propranolol on the chemical control of breathing in man is discussed in relation to the conflicting literature.

Role of the carotid bodies in the heart rate response to breath holding in man

1976 ◽  
Vol 41 (3) ◽  
pp. 336-340 ◽  
Author(s):  
P. M. Gross ◽  
B. J. Whipp ◽  
J. T. Davidson ◽  
S. N. Koyal ◽  
K. Wasserman
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Normal Subjects ◽  
The Other ◽  
Breath Holding ◽  
Asthmatic Patients ◽  
Carotid Bodies ◽  
Normal Man

To investigate the role of the carotid bodies in regulating the bradycardia of breath holding in man, we studied heart rate (HR) responses to prolonged breath holding (BH) in five asymptomatic asthmatic patients whose carotid bodies had been resected (CBR). Seven normal subjects served as controls. BH experiments were randomly initiated with single breaths of 100%, 21%,or 12% 92. During BH with 21% O2, normal subjects displayed the typical bradycardia; this response, however, was attenuated with the other O2 concentrations. In contrast, the CBR subjects manifested BH tachycardia which was inversely proportional to the O2 tension. HR increased in be CBR group by 5%, 31%, and 45% during BH with 100%, 21%, and 12% O2, respectively. These results demonstrate that the bradycardia of BH in normal man is under the influence of the carotid bodies. During BH and in the absence of carotid bodies, an O2 tension-dependent tachycardia is unveiled.

Blood Pressure and Heart Rate Response to Isometric Exercise and Mental Arithmetic in Normotensive and Hypertensive Subjects

1976 ◽  
Vol 51 (s3) ◽  
pp. 681s-685s ◽  
Author(s):  
G. Nyberg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Response ◽  
Mental Arithmetic ◽  
Isometric Exercise ◽  
Systolic Pressure ◽  
Normal Subjects ◽  
Repeated Testing ◽  
Hand Grip ◽  
Repeated Exercise

1. Sustained hand-grip exercise and mental arithmetic were performed by normal and hypertensive subjects. Blood pressure and heart rate were recorded with a device which allows blind and unbiased measurements, based on the conventional cuff method. 2. Both stimuli caused increases in heart rate and systolic and diastolic blood pressure, which were greater for isometric exercise than for mental arithmetic. 3. Normal females had a greater response to repeated exercise, and had a smaller systolic pressure elevation during mental arithmetic than the other groups. 4. Repeated testing showed good reproducibility in normal subjects.

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