Hemodynamic response to graded exercise after chronic beta-adrenergic blockade

The effect of sustained beta-adrenergic blockade (BB) on the hemodynamic response to graded exercise has been studied in 31 patients with high blood pressure. Hemodynamic investigations were conducted during a control period and were repeated after 1 mo of BB. Similar readjustments were observed at rest and during submaximal and maximal exercise. No significant change occurred in maximal physical working capacity during beta blockade. This resulted from hemodynamic readjustments. Maximal exercise heart rate was reduced by 34%, and this was compensated for by a 31% enhancement in stroke index. Consequently cardiac index decreased by only 14%. In the Fick equation the decrease in cardiac index was further compensated by an increase of the total arteriovenous O2 difference of 8%, thereby maintaining O2 delivery to the tissues. At maximal exercise mean brachial artery pressure dropped 14.5%, while mean pulmonary artery pressure increased by 20%. It is concluded that the compensatory action of the stroke volume, resulting from the interaction of an increased preload and a decreased impedance, played a major role in the hemodynamic readjustments following chronic BB to maintain maximal working capacity.

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HEMODYNAMIC RESPONSE TO EXERCISE AFTER BETA-ADRENERGIC AND PARASYMPATHETIC BLOCKADE

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y67-096 ◽

1967 ◽

Vol 45 (5) ◽

pp. 813-819 ◽

Cited By ~ 8

Author(s):

Gordon R. Cumming ◽

W. Carr

Keyword(s):

Heart Rate ◽

Cardiac Index ◽

Left Ventricular ◽

Cardiac Response ◽

Exercise Heart Rate ◽

Stroke Index ◽

Beta Adrenergic ◽

The Mean ◽

Response To Exercise ◽

Control Exercise

Cardiac responses to supine bicycle exercise were studied in six normal subjects after the intravenous administration of 5 mg of propranolol and again after the additive effect of 0.03 mg/kg of atropine. Mean resting heart rate was decreased 15 beats/min by propranolol and then increased by 38 beats/min after atropine. Mean exercise heart rate was 157 for control exercise, 119 after propranolol and 143 after propranolol + atropine. The resting cardiac index was reduced 21% by propranolol and restored to control values after atropine. The mean control exercise cardiac index was 7.2 l/min per m2; this was reduced to 5.8 after propranolol and increased to 6.2 after atropine. The mean stroke index was not altered by control exercise, increased 3 ml/beat per m2 with exercise after propranolol and increased 6 ml/beat per m2 with exercise after propranolol + atropine. Resting pulmonary artery, aortic and left-ventricular end-diastolic pressures were not altered by propranolol or by propranolol + atropine. The mean control exercise left-ventricular end-diastolic pressure was 9 mm Hg, increased to 19 mm Hg after propranolol and fell to 12 mm Hg after propranolol + atropine. The mean exercise aortic systolic pressure was 10 mm Hg below the value for control exercise after propranolol and 8 mm Hg below control after propranolol + atropine. Atropine lessens the inhibition of the cardiac response to exercise with beta adrenergic inhibition, possibly by increasing the heart rate.

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High sodium intake alters the hemodynamic response to mental stress in normotensive subjects after systemic beta adrenergic blockade

The FASEB Journal ◽

10.1096/fasebj.24.1_supplement.1020.10 ◽

2010 ◽

Vol 24 (S1) ◽

Author(s):

Bruno Moreira Silva ◽

Rachel L. Elvebak ◽

Jean N. Knutson ◽

Nathaniel D. Warner ◽

Michael J. Joyner ◽

...

Keyword(s):

Mental Stress ◽

Sodium Intake ◽

Hemodynamic Response ◽

Adrenergic Blockade ◽

Beta Adrenergic ◽

High Sodium ◽

High Sodium Intake ◽

Normotensive Subjects

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Hemodynamic Response to Exercise after Beta-Adrenergic Blockade in Normal and Labile Hypertensive Patients

Cardiology ◽

10.1159/000169273 ◽

1970 ◽

Vol 55 (2) ◽

pp. 105-113 ◽

Cited By ~ 1

Author(s):

L.E. Folle ◽

J. Dighiero ◽

I. Sadi ◽

C. Pommerenck ◽

R. Elena

Keyword(s):

Hemodynamic Response ◽

Adrenergic Blockade ◽

Beta Adrenergic ◽

Hypertensive Patients ◽

Response To Exercise

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Effect of maximal exercise testing on serum cholesterol in healthy subjects undergoing exercise training and on beta-adrenergic blockade

The American Journal of Cardiology ◽

10.1016/0002-9149(88)90985-x ◽

1988 ◽

Vol 62 (7) ◽

pp. 478-480 ◽

Cited By ~ 1

Author(s):

Gerald F. Fletcher ◽

Barbara J. Fletcher ◽

Andrew Marshall

Keyword(s):

Exercise Training ◽

Serum Cholesterol ◽

Exercise Testing ◽

Healthy Subjects ◽

Maximal Exercise ◽

Adrenergic Blockade ◽

Beta Adrenergic

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Effects of beta-adrenergic blockade on O2 uptake during submaximal and maximal exercise

Journal of Applied Physiology ◽

10.1152/jappl.1983.54.4.901 ◽

1983 ◽

Vol 54 (4) ◽

pp. 901-905 ◽

Cited By ~ 39

Author(s):

P. A. Tesch ◽

P. Kaiser

Keyword(s):

Heart Rate ◽

Maximal Exercise ◽

Pulmonary Ventilation ◽

Submaximal Exercise ◽

Beta Blockade ◽

Adrenergic Blockade ◽

Maximal Heart Rate ◽

O2 Consumption ◽

O2 Uptake ◽

Beta Adrenergic

Changes in cardiorespiratory variables and perceived rate of exertion (RPE) were studied in 13 trained men performing cycling exercise before and after beta-adrenergic blockade. Propranolol (Inderal, 80 mg) was administered orally 2 h prior to standardized maximal and submaximal exercises. Muscle biopsies were obtained from vastus lateralis at rest for subsequent histochemical analyses of muscle fiber type distribution and capillary supply. During submaximal exercise O2 consumption decreased from 2.76 to 2.59 l . min-1 following blockade (P less than 0.01), whereas heart rate decreased from 157 to 113 beats . min-1 (P less than 0.001). Maximal O2 uptake was lowered from 3.79 to 3.26 l . min-1 (P less than 0.001) and maximal heart rate was reduced from 192 to 142 beats . min-1 (P less than 0.001) as a result of the blockade. Pulmonary ventilation was unaltered in both exercise conditions. “Local” RPE was higher (P less than 0.001) than “central” RPE after beta-blockade in both submaximal and maximal exercise. During normal condition this difference did not appear. Changes in both local and central RPE during submaximal exercise were positively correlated to changes in O2 uptake. Individual variations in the metabolic profile of the exercising muscle had no influence on beta-blockade-induced changes in O2 uptake. It is concluded that blockade of beta-adrenergic receptors reduces O2 consumption during submaximal (approximately 73% maximal O2 uptake) and maximal exercise in habitually trained men.

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Plasma catecholamine responses to exercise after training with beta-adrenergic blockade

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.2.586 ◽

1990 ◽

Vol 68 (2) ◽

pp. 586-593 ◽

Cited By ~ 8

Author(s):

E. E. Wolfel ◽

W. R. Hiatt ◽

H. L. Brammell ◽

V. Travis ◽

L. D. Horwitz

Keyword(s):

Exercise Training ◽

Maximal Exercise ◽

Submaximal Exercise ◽

Plasma Norepinephrine ◽

Plasma Catecholamine ◽

Adrenergic Blockade ◽

Absolute Level ◽

Beta Adrenergic ◽

Exercise Training Program ◽

Induced Changes

Exercise training has been shown to decrease plasma norepinephrine (NE) and epinephrine (EPI) levels during absolute levels of submaximal exercise, which may reflect alterations in sympathetic tone as a result of training. To determine if beta-adrenergic blockade altered these changes in the plasma concentration of catecholamines with exercise conditioning, we studied the effects of beta-adrenergic blockade on NE and EPI at rest and during exercise in 24 healthy, male subjects after a 6-wk exercise training program. The subjects were randomized to placebo (P), atenolol 50 mg twice daily (A), and nadolol 40 mg twice daily (N). There were no changes in resting NE and EPI compared with pretraining values in any subject group. During the same absolute level of submaximal exercise NE decreased in P and A but was unchanged in N, whereas EPI decreased only in P. At maximal exercise all three groups developed significant increases in NE after training that paralleled increases in systolic blood pressure. EPI at maximal exercise increased after training with N but was unchanged with P or A. These training-induced changes in plasma catecholamine levels were masked or blunted when the A and N groups were studied while still on medication after training. Thus beta-adrenergic blockade has important effects on adaptations of the sympathetic nervous system to training, especially during submaximal exercise.

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Effects of chronic beta-adrenergic blockade on exercise training in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.5.1960 ◽

1988 ◽

Vol 64 (5) ◽

pp. 1960-1967 ◽

Cited By ~ 1

Author(s):

E. E. Wolfel ◽

J. Lindenfeld ◽

J. Smoak ◽

L. D. Horwitz

Keyword(s):

Heart Rate ◽

Submaximal Exercise ◽

Peak Exercise ◽

Exercise Heart Rate ◽

Adrenergic Blockade ◽

Adrenergic Stimulation ◽

Beta Adrenergic ◽

Exercise Time ◽

Adrenergic Blocker

To assess the role of beta-adrenergic stimulation in cardiovascular conditioning we examined the effects of a beta-adrenergic blocker, propranolol, in mongrel dogs during an 8-wk treadmill-training program. Seven dogs were trained without a drug (NP), six were trained on propranolol 10 mg.kg-1.day-1 (P), and five served as caged controls (C). Effective beta-adrenergic blockade was documented by a decrease in peak exercise heart rate of 54 +/- 11 (SE) beats/min (P less than 0.05) and a one-log magnitude of increase in the isoproterenol-heart rate dose-response curve. Testing was performed before drug treatment or training and again after training without the drug for 5 days. Submaximal exercise heart rate decreased similarly in both NP and P (-26 +/- 4 NP vs. -25 +/- 9 beats/min P, P less than 0.05 for both) but peak heart rate decreased only with NP (-33 +/- 9 beats/min, P less than 0.05). Treadmill exercise time increased similarly in both groups: 3.4 +/- 0.6 min in NP and 3.0 +/- 0.2 min in P (both P less than 0.05). Blood volume also increased after training in both groups: 605 +/- 250 ml (26%) in NP and 377 +/- 140 ml (17%) in P (both P less than 0.05). Submaximal exercise arterial lactates were reduced similarly in both groups but peak exercise lactate was reduced more in NP (-1.4 +/- 0.3 NP vs -0.3 +/- 0.12 mmol/l P, P less than 0.05). Lactate threshold increased in both groups but the increase was greater in NP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.5.1819 ◽

1987 ◽

Vol 62 (5) ◽

pp. 1819-1825 ◽

Cited By ~ 19

Author(s):

M. J. Joyner ◽

S. M. Jilka ◽

J. A. Taylor ◽

J. K. Kalis ◽

J. Nittolo ◽

...

Keyword(s):

Tidal Volume ◽

Maximal Exercise ◽

Minute Ventilation ◽

Co2 Production ◽

Beta Blockade ◽

Adrenergic Blockade ◽

Respiratory Drive ◽

Heavy Exercise ◽

Beta Adrenergic ◽

Beta 2

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.

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Effects of Labetalol on Systemic and Pulmonary Haemodynamics at Rest and during Exercise in Hypertensive Patients

Clinical Science ◽

10.1042/cs055279s ◽

1978 ◽

Vol 55 (s4) ◽

pp. 279s-281s

Author(s):

R. Fagard ◽

A. Amery ◽

T. Reybrouck ◽

P. Lijnen ◽

L. Billiet

Keyword(s):

Heart Rate ◽

Brachial Artery ◽

Maximal Exercise ◽

Peripheral Resistance ◽

Plasma Renin ◽

Exercise Heart Rate ◽

Plasma Aldosterone Concentration ◽

Hypertensive Patients ◽

Artery Pressure ◽

Pulmonary Haemodynamics

1. Labetalol was administered to 18 hypertensive patients for an average duration of 2·44 weeks, with an average final daily dose of 1·65 g. 2. Labetalol decreased resting heart rate by 16% and maximal exercise heart rate by 21%; the phenylephrine-induced rise of systolic brachial artery pressure was reduced by 36%. 3. During labetalol brachial artery pressure was lowered by 29/15 mmHg in the recumbent position, by 41/23 mmHg at rest sitting, and by 53/23 mmHg at maximal exercise; total peripheral resistance was not significantly affected at rest recumbent, but was reduced at sitting and at exercise; cardiac output decreased in all conditions. 4. Labetalol reduced mean pulmonary artery and capillary wedge pressures only in the sitting position. Pulmonary vascular resistance remained unchanged. 5. The drug produced significant decreases of plasma renin activity and of plasma aldosterone concentration.

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