Effect of β-Adrenoceptor Blockade on Exercise-Induced Plasma Catecholamine Concentration-Heart Rate Response Relationship

1987 ◽  
Vol 10 (6) ◽  
pp. 667-674 ◽  
Author(s):  
Akihiro Ohnishi ◽  
Akemi Minegishi ◽  
Takashi Ishizaki
Author(s):  
Sri Sumartiningsih ◽  
Hsin-Fu Lin ◽  
Jung-Charng Lin

This study aimed to examine the exercise-induced heart rate response (HRR) and heart rate variability (HRV) in subjects caused by inhaling smoke from tobacco cigarettes (TC) and aerosolized vapor from electronic nicotine dispensing systems (ENDS) (commonly referred to as e-cigarettes (EC)). A randomized crossover study recruited 24 young adult male smokers with an average age of 23 years and with a smoking habit of at least two years. Heart rate response was recorded after a maximal multistage shuttle 20 m run test (MMST) under three different levels of nicotine: Control 0 mg nicotine of EC (C), 3 mg nicotine of EC (3EC), and 3 mg nicotine of TC (3TC). HRV was evaluated based on the beat-to-beat time interval during the running test. The results showed no statistically significant differences in the run time to exhaustion under the three conditions (C: 398 ± 151 s; 3EC: 399 ± 160 s; 3TC: 381 ± 150 s). Exercise-induced HRR was significantly attenuated under the TC condition (p < 0.05). Intriguingly, the HRV standard deviation of normal-to-normal intervals (SDNN) during exercise significantly increased under 3EC and 3TC. The results showed that a significant acute autonomic cardiac modulation during exercise is induced by an acute episode of EC and TC smoking.


2015 ◽  
Vol 17 (S1) ◽  
Author(s):  
Alice Lighton ◽  
Marinos Koulouroudias ◽  
Filip Zemrak ◽  
Charlotte Manisty ◽  
James Moon ◽  
...  

2013 ◽  
Vol 35 (05) ◽  
pp. 371-378
Author(s):  
E. Ciolac ◽  
C. Roberts ◽  
J. Rodrigues da Silva ◽  
G. Guimarães

2005 ◽  
Vol 109 (6) ◽  
pp. 493-501 ◽  
Author(s):  
Lysander W. J. Bogert ◽  
Ayten Erol-Yilmaz ◽  
Raymond Tukkie ◽  
Johannes J. Van Lieshout

Cerebral blood flow increases upon the transition from rest to moderate exercise, but becomes affected when the ability to raise CO (cardiac output) is limited. HR (heart rate) is considered to contribute significantly to the increase in CO in the early stages of dynamic exercise. The aim of the present study was to test whether manipulation of the HR response in patients dependent on permanent rate-responsive ventricular pacing contributes to the increase in CO, MCA Vmean [mean MCA (middle cerebral artery) velocity] and work capacity during exercise. The effect of setting the pacemaker to DSS (‘default’ sensor setting) compared with OSS (‘optimized’ sensor setting) on blood pressure, CO, SV (stroke volume) and MCA Vmean was evaluated during ergometry cycling. From rest to exercise at 75 W, the rise in HR in OSS [from 73 (65–87) to 116 (73–152) beats/min; P<0.05] compared with DSS [70 (60–76) to 97 (67–117) beats/min; P<0.05] was larger. There was an increase in SV during exercise with DSS, but not with OSS, such that, at all workloads, SVs were greater during DSS than OSS. The slope of the HR–CO relationship was larger with DSS than OSS (P<0.05). From rest to exercise, MCA Vsys (systolic MCA velocity) increased in OSS and DSS, and MCA Vdias (diastolic MCA velocity) was reduced with DSS. No changes were observed in MCA Vmean. Manipulation of the pacemaker setting had no effect on the maximal workload [133 (100–225) W in OSS compared with 129 (75–200) W in DSS]. The results indicate that, in pacemaker-dependent subjects with complete heart block and preserved myocardial function, enhancing the HR response to exercise neither augments CO by a proportional offset of the exercise-induced increase in SV nor improves cerebral perfusion.


1982 ◽  
Vol 243 (5) ◽  
pp. H676-H681 ◽  
Author(s):  
C. Borst ◽  
W. Wieling ◽  
J. F. van Brederode ◽  
A. Hond ◽  
L. G. de Rijk ◽  
...  

We explored in 43 healthy subjects the afferent mechanisms of the initial heart rate response to standing by comparing free standing, 70 degrees head-up tilt, handgrip, and contraction of abdominal and leg muscles. The results indicate the following. 1) Standing evokes an immediate, large, bimodal increase of heart rate (HR) of about 20 s duration that far exceeds the gradual HR rise induced by 70 degrees head-up tilt. 2) The immediate HR increase with active standing is due to the exercise reflex and results in a first peak about 3 s after standing briskly. 3) The secondary, more gradual HR increase after 5 s of standing and the subsequent rapid decrease of HR between about 12 and 20 s corresponds through the baroreceptor reflex with a striking fall, recovery, and sometimes overshoot of arterial pressure. 4) The maximum HR increase found after about 12 s of standing is augmented and delayed after rest. 5) The time course of the initial HR response is not modified by physical training. We conclude that active and passive changes of posture result in fundamentally different cardiovascular effects for about 20 s and that "central command," muscle receptors, high-pressure receptors, low-pressure receptors, and the plasma catecholamine level are probably all involved in the initial HR response to standing.


1957 ◽  
Author(s):  
Philip J. Bersh ◽  
Joseph M. Notterman ◽  
William N. Schoenfeld

1995 ◽  
Vol 133 (6) ◽  
pp. 723-728 ◽  
Author(s):  
Ettore C degli Uberti ◽  
Maria R Ambrosio ◽  
Marta Bondanelli ◽  
Giorgio Transforini ◽  
Alberto Valentini ◽  
...  

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643 Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function. Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy


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