scholarly journals Relation of intrinsic heart rate and autonomic nervous tone to resting heart rate in the young and the adult of various domestic animals.

1989 ◽  
Vol 51 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Kanji MATSUI ◽  
Shigeru SUGANO
1987 ◽  
Vol 72 (2) ◽  
pp. 239-244 ◽  
Author(s):  
Benedito C. Maciel ◽  
Lourenco Gallo ◽  
José A. Marin Neto ◽  
Léa M. Z. Maciel ◽  
Maria L. D. Alves ◽  
...  

1. The mechanisms that control resting heart rate in hyperthyroidism were evaluated in six patients before and after treatment with propylthiouracil. 2. The patients were subjected to pharmacological blockade under resting conditions in two experimental sessions: first session, propranolol (0.2 mg/kg body weight); second session, atropine (0.04 mg/kg body weight) followed by propranolol (0.2 mg/kg body weight). All drugs were administered intravenously. 3. Resting heart rate was significantly reduced from 100 ± 6.5 beats/min to 72 ± 2.5 beats/min (P < 0.005) after clinical and laboratory control of the disease. After double blockade, intrinsic heart rate was reduced from 105 ± 6.8 beats/min before treatment to 98 ± 6.0 beats/min after treatment (P < 0.025). The reduction in heart rate caused by propranolol was not significantly different before (−13 ± 1.4 beats/min) and after (−9 ± 1.0 beats/min) propylthiouracil. In contrast, atropine induced a higher elevation of heart rate after treatment (45 ± 8.6 beats/min) than before treatment (26 ± 4.0 beats/min). 4. The present results suggest no appreciable participation of the sympathetic component of the autonomic nervous system in the tachycardia of hyperthyroidism, at least under the conditions of the present study. The small change observed in intrinsic heart rate, although significant, seems to indicate that this is not the most important mechanism involved in this tachycardia. 5. Our results suggest that an important reduction in the efferent activity of the parasympathetic component participates in the mechanisms that modify resting heart rate in hyperthyroidism.


1991 ◽  
Vol 35 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J.Gert van Dijk ◽  
Monique Koenderink ◽  
Aeilko H. Zwinderman ◽  
Joost Haan ◽  
Cor G.S. Kramer ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M D Flannery ◽  
F Sully ◽  
K Janssens ◽  
G Morris ◽  
J Kalman ◽  
...  

Abstract Background It is well known that athletes and in particular endurance athletes have lower resting heart rates than non-athletes. This has generally been considered a healthy adaptation. Traditionally this was thought be due to increased vagal tone. Several studies have shown that endurance athletes continue to have lower heart rates in the absence of autonomic influence suggesting bradycardia is due to intrinsic changes within the heart. A subset of endurance athletes have very low heart rates with Tour de France cyclists having described heart rates in the 30s. It is unclear whether in these elite athletes with very low heart rates the profound bradycardia is due to autonomic influence or intrinsic changes within the heart. Aim The aim of this study was to determine if extreme bradycardia in athletes is due to excess vagal tone or more profound intrinsic changes within the heart. Methods We recruited three cohorts for this study: non-athlete controls (NA), endurance athletes with a documented resting heart rate >40 (EA) and endurance athletes with a resting heart rate <40 (BA). All participants underwent baseline testing including ECG, echocardiography and VO2 max testing. All participants came back on a second occasion for treatment with dual autonomic blockade (DAB) to determine intrinsic heart rate in the following manner. After resting supine for five minutes resting heart rate was measured. Participants were then administered 0.04mg/kg of intravenous atropine. After five minutes participants were then administered 0.05mg/kg of intravenous metoprolol. This was repeated every five minutes until there was no further drop in heart rate or 0.2mg/kg had been administered. The resting heart rate at this stage was recorded as the intrinsic heart rate. Parasympathetic blockade was confirmed by lack of response to Valsalva manoeuvre and sympathetic blockade was confirmed by lack of response to metoprolol. VO2 max testing was then performed to determine maximum heart rate. Results 9 NA (7 male), 10 EA (8 male) and 5 BA (4 male) participated in this study. The average age was similar in all groups (NA 32.9y, EA 32.4y, BA 31.4y). The average resting heart rate was 71.7 in the NA group, 48.3 in the EA group and 41.6 in the BA group (p<0.05 for comparisons between all three groups). Following dual autonomic blockade resting heart rate was 86.0 in the NA group, 76.9 in the EA group and 64.4 in the BA group (p<0.05 for comparisons between all three groups). Maximum heart rate under DAB was 140.1 in the NA group, 138.0 in the EA group and 140.4 in the BA group. These differences were not significant. Conclusion In athletes with very low heart rates, bradycardia is due to more profound intrinsic changes within the heart. Acknowledgement/Funding NHMRC Project Grant


1996 ◽  
Vol 199 (7) ◽  
pp. 1563-1568 ◽  
Author(s):  
P E Signore ◽  
D R Jones

Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.


2018 ◽  
Vol 56 (211) ◽  
pp. 670-673 ◽  
Author(s):  
Reena Kumari Jha ◽  
Amrita Acharya ◽  
Ojashwi Nepal

Introduction: The Autonomic nervous system is responsible for regulation and integration of visceral functions. Disturbance of autonomic nervous system play crucial role in pathogenesis and clinical course of many diseases. In the present study deep breathing test and valsalva maneuver have been described to monitor parasympathetic function genderwise. Methods: A cross-sectional study was conducted among 100 subjects, aged 18-25 years, from May to November 2017, in exercise physiology laboratory, Kathmandu University School of Medical Sciences, Chaukot, Kavre. Electrocardiograph recorded by AD instrument was used to calculate the resting heart rate and the heart rate response to deep breathing test and valsalva maneuver. Results: Heart rate response to deep breathing test (31.69±14.79 Vs. 36.08±18.65, P=0.195) and valsalva ratio (1.59±0.39 Vs. 1.69±0.54, P=0.314) tend to be higher in female than male subjects but not significant. The resting heart rate of females was significantly higher than that of males (84.37 ± 11.08 Vs. 78.43 ± 12.06, P<0.05). Heart rate was significantly increased during and decreased after valsalva maneuver in both male and female subjects. Conclusions: This study concludes that both deep breathing test and valsalva maneuver activates parasympathetic system inhealthy subjects. And also dominant parasympathetic activity was found in female comparison to male subjects.


1992 ◽  
Vol 167 (1) ◽  
pp. 179-201 ◽  
Author(s):  
M. Axelsson ◽  
W. Davison ◽  
M. E. Forster ◽  
A. P. Farrell

The aim of this study was to investigate cardiac performance and cardiovascular control in two red-blooded nototheniid species of antarctic fishes, Pagothenia bernacchii (a benthic fish) and P. borchgrevinki (a cryopelagic fish), and to make comparisons with existing information on haemoglobin-free antarctic teleosts. In quiescent P. bernacchii at 0 degrees C ventral aortic pressure (PVA) was 3.09 kPa and cardiac output (Q) was 17.6 ml min-1 kg-1, with a heart rate (fH) of 10.5 beats min-1 and stroke volume of 1.56 ml kg-1. Following atropine treatment, Q was maintained but heart rate increased and stroke volume decreased. Resting heart rate resulted from an inhibitory cholinergic tone of 80.4% and an excitatory adrenergic tone of 27.5%. The intrinsic heart rate was 21.7 beats min-1 at 0 degrees C. In quiescent P. borchgrevinki at 0 degrees C, PVA was 3.6 kPa, Q was 29.6 ml min-1 kg-1 and stroke volume was 2.16 ml kg-1. The resting heart rate in P. borchgrevinki of 11.3 beats min-1 resulted from an inhibitory cholinergic tone of 54.5% and an excitatory adrenergic tone of 3.2%. The intrinsic heart rate was 23.3 beats min-1. P. bernacchii maintained Q during a progressive decrease in water oxygen tension from 20 to 6.7 kPa, but fH was increased significantly. Thus, although there is cholinergic control of the heart, no hypoxic bradycardia was observed. Recovery from hypoxia was associated with increases in Q and fH; stroke volume returned to control values. PVA declined in recovery as total vascular resistance decreased. Hypoxic exposure following atropine treatment resulted in progressive increases in PVA, Q and stroke volume; fH decreased during the recovery period. Hypoxic exposure in P. borchgrevinki produced similar cardiovascular responses to those observed in P. bernacchii. During an acute increase in water temperature from 0 to 5 degrees C, P. bernacchii regulated Q and total vascular resistance. Stroke volume decreased as fH increased. The intrinsic heart rate had a Q10 of 1.96 over this temperature range. P. bernacchii maintained chronotropic inhibition up to a temperature of 2.5-3.0 degrees C. However, by 5 degrees C this chronotropic inhibition of the heart rate was lost. Infusion of adrenaline into the ventral aorta of P. bernacchii resulted in significant increases in Q, fH, PVA and total vascular resistance. Infusion of adrenaline after atropine treatment caused similar cardiovascular changes without the change in fH. P. borchgrevinki could sustain swimming in a water tunnel at approximately 1 body length per second for 6–10 min.(ABSTRACT TRUNCATED AT 400 WORDS)


1986 ◽  
Vol 48 (4) ◽  
pp. 703-709 ◽  
Author(s):  
Masayoshi KUWAHARA ◽  
Min Do HUH ◽  
Hisashi HIROSE ◽  
Shigeru SUGANO

1990 ◽  
Vol 61 (11) ◽  
pp. 1028-1032
Author(s):  
Naoto ISHIKAWA ◽  
Atsushi TAJIMA ◽  
Yukio LANAI ◽  
Hideya HOMMA ◽  
P. BUNYAVEJCHEWIN ◽  
...  

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