Maximal exercise responses to acute and chronic beta-adrenergic blockade in healthy male subjects

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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Failure of chronic beta-adrenergic blockade to inhibit overfeeding-induced thermogenesis in humans

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.256.3.r653 ◽

1989 ◽

Vol 256 (3) ◽

pp. R653-R658 ◽

Cited By ~ 1

Author(s):

S. L. Welle ◽

K. S. Nair ◽

R. G. Campbell

Keyword(s):

Weight Maintenance ◽

Resting Metabolic Rate ◽

Control Group ◽

Adrenergic Blockade ◽

Beta Adrenergic ◽

Initial Reduction ◽

Adrenergic Antagonist ◽

Adrenergic Activity ◽

Propranolol Treatment ◽

Male Subjects

The effect of the beta-adrenergic antagonist propranolol on the increase in resting metabolic rate (RMR) induced by overfeeding was examined to determine whether increased beta-adrenergic activity contributes to this response. Six male subjects who were overfed with carbohydrate (1,600 excess kcal/day) for 10 days without drug treatment (control group) had increases (compared with values after 10 days of weight maintenance) in RMR after 6 days [0.24 +/- 0.06 kcal/min (22%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. Eight male subjects were given a weight-maintenance diet for 10 days with oral propranolol treatment (40-60 mg every 6 h) over the last 7 days of this period. Five of these subjects were then overfed for 10 days, and three remained on the weight-maintenance diet; propranolol treatment continued until the end of the study. Propranolol significantly reduced RMR (mean 9%) before the onset of overfeeding but did not prevent increases in RMR after 6 days [0.18 +/- 0.05 kcal/min (16%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. In the subjects who remained on the weight-maintenance diet throughout the study, there was no reversal of propranolol's initial reduction of RMR that would have falsely elevated the overfeeding effect. These data provide further evidence that the increase in RMR induced by overfeeding in humans is not mediated by increased beta-adrenergic activity.

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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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Upright posture and maximal exercise increase platelet aggregability and prostacyclin production in healthy male subjects

British Journal of Sports Medicine ◽

10.1136/bjsm.33.6.401 ◽

1999 ◽

Vol 33 (6) ◽

pp. 401-404 ◽

Cited By ~ 17

Author(s):

D. L. Feng ◽

J. Murillo ◽

P. Jadhav ◽

C. McKenna ◽

O. C. Gebara ◽

...

Keyword(s):

Maximal Exercise ◽

Upright Posture ◽

Healthy Male ◽

Platelet Aggregability ◽

Male Subjects ◽

Prostacyclin Production

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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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Acute response to submaximal and maximal exercise consequent to beta-adrenergic blockade: Implications for the prescription of exercise

The American Journal of Cardiology ◽

10.1016/0002-9149(85)91070-7 ◽

1985 ◽

Vol 55 (10) ◽

pp. D135-D141 ◽

Cited By ~ 42

Author(s):

Jack H. Wilmore ◽

Beau J. Freund ◽

Michael J. Joyner ◽

Gregory A. Hetrick ◽

Albert A. Hartzell ◽

...

Keyword(s):

Maximal Exercise ◽

Adrenergic Blockade ◽

Beta Adrenergic ◽

Acute Response

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Perceived exertion and gas exchange after calcium and beta-blockade in atrial fibrillation

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.1.97 ◽

1987 ◽

Vol 63 (1) ◽

pp. 97-104 ◽

Cited By ~ 19

Author(s):

J. Myers ◽

J. E. Atwood ◽

M. Sullivan ◽

S. Forbes ◽

R. Friis ◽

...

Keyword(s):

Atrial Fibrillation ◽

Blood Pressure ◽

Heart Rate ◽

Gas Exchange ◽

Perceived Exertion ◽

Maximal Exercise ◽

Adrenergic Blockade ◽

Channel Blockade ◽

Calcium Channel Blockade ◽

Beta Adrenergic

Nine male patients (mean age 65 yr) with chronic atrial fibrillation underwent maximal exercise testing during placebo, beta-adrenergic (celiprolol, 600 mg), or calcium (diltiazem, 30 or 60 mg four times daily) channel blockade. The results were analyzed to determine which factors most closely related to ratings of perceived exertion (RPE) during exercise. Heart rate (HR), blood pressure (BP), oxygen uptake (VO2), minute ventilation (VE), and carbon dioxide production (VCO2) were evaluated at rest, 3.0 mph/0% grade, the gas exchange anaerobic threshold (ATge), 80% of placebo maximal O2 uptake, and maximal exercise. Both beta-adrenergic and calcium channel blockade significantly reduced heart rate and systolic blood pressure relative to placebo; these effects were more profound during beta-adrenergic blockade and as exercise progressed. Correlation coefficients and estimates of slope were derived for changes in RPE during exercise vs. changes in HR, VO2, VE, and VCO2 during the three treatments (r = 0.76 to 0.92, P less than 0.001). Although RPE was significantly correlated with HR during placebo and diltiazem therapy (r = 0.45, P less than 0.01), this was not the case during beta-adrenergic blockade (r = 0.31, NS). Slope of the regression lines between RPE and VO2, VE, and VCO2 did not differ between the three treatments. Slope of the regression lines between RPE and HR differed only during calcium channel blockade. Because the presence of atrial fibrillation and beta-adrenergic blockade altered the associations between RPE, VO2, and HR, these results suggest that VE is more closely related to RPE than the other parameters.

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