Hypoxia increases exercise heart rate despite combined inhibition of β-adrenergic and muscarinic receptors

2015 ◽  
Vol 308 (12) ◽  
pp. H1540-H1546 ◽  
Author(s):  
C. Siebenmann ◽  
P. Rasmussen ◽  
H. Sørensen ◽  
T. C. Bonne ◽  
M. Zaar ◽  
...  

Hypoxia increases the heart rate response to exercise, but the mechanism(s) remains unclear. We tested the hypothesis that the tachycardic effect of hypoxia persists during separate, but not combined, inhibition of β-adrenergic and muscarinic receptors. Nine subjects performed incremental exercise to exhaustion in normoxia and hypoxia (fraction of inspired O2 = 12%) after intravenous administration of 1) no drugs (Cont), 2) propranolol (Prop), 3) glycopyrrolate (Glyc), or 4) Prop + Glyc. HR increased with exercise in all drug conditions ( P < 0.001) but was always higher at a given workload in hypoxia than normoxia ( P < 0.001). Averaged over all workloads, the difference between hypoxia and normoxia was 19.8 ± 13.8 beats/min during Cont and similar (17.2 ± 7.7 beats/min, P = 0.95) during Prop but smaller ( P < 0.001) during Glyc and Prop + Glyc (9.8 ± 9.6 and 8.1 ± 7.6 beats/min, respectively). Cardiac output was enhanced by hypoxia ( P < 0.002) to an extent that was similar between Cont, Glyc, and Prop + Glyc (2.3 ± 1.9, 1.7 ± 1.8, and 2.3 ± 1.2 l/min, respectively, P > 0.4) but larger during Prop (3.4 ± 1.6 l/min, P = 0.004). Our results demonstrate that the tachycardic effect of hypoxia during exercise partially relies on vagal withdrawal. Conversely, sympathoexcitation either does not contribute or increases heart rate through mechanisms other than β-adrenergic transmission. A potential candidate is α-adrenergic transmission, which could also explain why a tachycardic effect of hypoxia persists during combined β-adrenergic and muscarinic receptor inhibition.

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.


1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.


2018 ◽  
pp. 437-445
Author(s):  
Gregory S. Thomas

The chapter Heart Rate Response to Exercise reviews the studies performed to estimate a patient’s maximum predicted heart rate. While the commonly used formula (220 – age), developed in 1971, is easy to remember, it underestimates the actual maximum heart rate in older persons. Studies of large sample size have found the maximum heart rate to be relatively independent of sex and physical fitness but to incrementally decline with age. The decrease with age is less than 1 beat per minute per year, however. A more accurate and recommended formula is [(208) – (0.7)(age)] as developed by Tanaka and colleagues.


2020 ◽  
Vol 11 (3) ◽  
pp. 31-36
Author(s):  
Satyajit Bagudai ◽  
Hari Prasad Upadhyay

Introduction: Studies have reported that off springs of hypertensive parents are more likely to develop hypertension. Affection of target organ starts even before the diagnosis of hypertension. Autonomic dysfunction may be the initial cardiac effects in the pathogenesis of hypertension. Till now very few studies have been done to find the early outcomes in the cardiac autonomic functions in the normotensive siblings of hypertensive patients. Heart rate recovery after exercise is a useful marker for cardiac autonomic function. Since the etio-pathogenesis of hypertension is expected to affect the autonomic cardiovascular parameters even before the prehypertensive stage, the following study was carried out to analyze the heart rate recovery, in the descendent non- hypertensive young adults with and without parental history of hypertension. Aim and objective: This research study was aimed to study the quantify and compare the difference (if any) of heart rate recovery in response to 3minute step test between non hypertensive children of non- hypertensive and hypertensive parents within an age group of 18-22 years. Material &Methods: A total of 63 normotensive students were divided into one hypertensive parents(HP) group containing students with parental history of hypertension) and one non hypertensive parents group (NHP) having students without parental history of hypertension). Each student was subjected to 3 minute Master step test. Recordings of heart rate were made before and after exercise. Heart rate recovery index (HRRI) of 1minute (HRRI1), as well as in 2, 3 and 4 minute (HRRI2, HRRI3, HRRI4) were calculated and analyzed. Results: The resting (basal) heart rate as well as 1st minute heart rate recovery index (HRRI1) was not significantly different in the two groups. Likewise, the 2nd minute (HRRI2), 3rd minute (HRRI3), and 4th minute HRRI (HRR4) respectively were also not significantly different between the two groups. Conclusion: This study concluded that there is no significant difference in heart rate recovery among non-hypertensive young adults, with and without parental history of hypertension.


1959 ◽  
Vol 196 (4) ◽  
pp. 745-750 ◽  
Author(s):  
Robert F. Rushmer

Diastolic and systolic dimensions of the left ventricle and the free wall of the right ventricle in intact dogs are affected little by spontaneous exercise. The concept that stroke volume and heart rate in normal man increase by about the same relative amounts was derived from estimations of cardiac output, particularly in athletes, based upon indirect measurements using foreign gases or CO2. Data for man obtained with the modern cardiac catheterization or indicator dilution techniques confirm the impression derived from intact dogs that increased stroke volume is neither an essential nor a characteristic feature of the normal cardiac response to exercise. Stroke volume undoubtedly increases whenever cardiac output is increased with little change in heart rate (e.g. in athletes or in patients with chronic volume loads on the heart). Tachycardia produced experimentally with an artificial pacemaker in a resting dog causes a marked reduction in diastolic and systolic dimensions and in the stroke change of dimensions. The factors generally postulated to increase stroke volume during normal exercise may prevent the reduction in stroke volume accompanying tachycardia.


1992 ◽  
Vol 85 (Supplement) ◽  
pp. 3S-45
Author(s):  
Allen F. Bowyer ◽  
Rosemary A. Thomas

1988 ◽  
Vol 255 (5) ◽  
pp. E636-E641 ◽  
Author(s):  
B. E. Zola ◽  
B. Miller ◽  
G. L. Stiles ◽  
P. S. Rao ◽  
E. H. Sonnenblick ◽  
...  

To study the effects of chronic diabetes on heart rate and adrenergic responsiveness we compared unanesthetized diabetic rabbits, 10-13 mo after alloxan monohydrate injection, to age-matched controls. There were no significant differences found between groups for body or heart weight. Both resting and intrinsic heart rate (the latter obtained after atropine sulfate and propranolol HCl) were similar. In addition, serum and left ventricular epinephrine and norepinephrine concentrations as well as left ventricular beta-receptor density and affinity were unchanged in diabetic animals. Heart rate responses to isoproterenol were blunted in diabetics at the three highest doses. Base-line mean blood pressure was modestly lower in diabetic rabbits, and parallel declines in pressure for both groups were observed in response to isoproterenol. The diminished heart rate response to isoproterenol in diabetic rabbits may be due to diminished myocardial sensitivity to catecholamines, possibly combined with altered baroreceptor reflexes. These experiments may provide an explanation for the blunted heart rate response to exercise described in human diabetics.


1984 ◽  
Vol 108 (2) ◽  
pp. 316-326 ◽  
Author(s):  
Iwao Sato ◽  
Katsuro Shimomura ◽  
Yasuhiro Hasegawa ◽  
Tohru Ohe ◽  
Mokuo Matsuhisa ◽  
...  

Heart & Lung ◽  
2015 ◽  
Vol 44 (3) ◽  
pp. 246-250 ◽  
Author(s):  
Hilary F. Armstrong ◽  
Jose Gonzalez-Costello ◽  
Wilawan Thirapatarapong ◽  
Ulrich P. Jorde ◽  
Matthew N. Bartels

Sign in / Sign up

Export Citation Format

Share Document