Exercise gas exchange in asthmatics after beta-adrenergic blockade

1983 ◽  
Vol 55 (2) ◽  
pp. 529-533 ◽  
Author(s):  
D. Y. Sue ◽  
L. R. Van Meter ◽  
J. E. Hansen ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Cardiovascular Response ◽  
Minute Ventilation ◽  
Work Rate ◽  
Incremental Exercise ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist

Pharmacologic beta-adrenergic blockade reduces maximal heart rate (HR) during exercise but variable results have been reported for minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2). A total group of 19 subjects with mild asthma was studied. We studied 16 subjects from the group who received placebo or pindolol, a beta-adrenergic antagonist, during 1-min incremental exercise on a cycle ergometer. During incremental exercise, HR, VE, VCO2, and VO2 were less after beta-blockade than after placebo at the same work rate below the anaerobic threshold. Maximal HR, VE, VO2, VCO2, and work rate were significantly less after beta-blockade. In addition, we studied six subjects from the group, including three who had also performed incremental exercise, during the steady state of constant-work cycling exercise. We found no difference in VE, VCO2, or VO2 although HR was less after beta-blockade. We conclude that beta-adrenergic blockade affects gas exchange by delaying the normal cardiovascular response to exercise. Decreased VE during incremental exercise is due to slowed delivery of CO2 load to the lungs rather than alterations in substrate, lung function, or ventilatory control.

Effects of beta-adrenergic blockade on ventilation and gas exchange during exercise in humans

1983 ◽  
Vol 54 (5) ◽  
pp. 1306-1313 ◽  
Author(s):  
E. S. Petersen ◽  
B. J. Whipp ◽  
J. A. Davis ◽  
D. J. Huntsman ◽  
H. V. Brown ◽  
...  
Keyword(s):  
Heart Rate ◽  
Gas Exchange ◽  
Time Constant ◽  
Minute Ventilation ◽  
Work Rate ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
O2 Uptake ◽  
Beta Adrenergic ◽  
Co2 Partial Pressure

The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.

Ventilatory and hyperkalemic responses to incremental exercise after propranolol treatment

1994 ◽  
Vol 77 (4) ◽  
pp. 1907-1912 ◽  
Author(s):  
D. A. Schneider ◽  
M. T. McEniery ◽  
C. Solomon ◽  
J. Jurimae ◽  
M. S. Wehr
Keyword(s):  
Minute Ventilation ◽  
Plasma Potassium ◽  
Muscle Afferents ◽  
Incremental Exercise ◽  
Co2 Production ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Propranolol Treatment ◽  
Positive Correlations ◽  
And Control

The purpose of the present study was to examine the relationship of plasma potassium (K+) and minute ventilation (VE) during incremental cycling (20 W/2 min) under conditions of beta-adrenergic blockade (80 mg of propranolol) and placebo in six untrained male subjects. No significant differences existed between treatments in O2 uptake, CO2 production, blood lactate, pH, or VE during the submaximal work stages of incremental exercise common to both treatments (20–220 W). During exercise with beta-blockade, plasma K+ concentrations were found to be significantly elevated compared with control levels at every work stage except 20 W. Significant positive correlations between VE and plasma K+ were found during both beta-blockade (r = 0.99) and control conditions (r = 1.00). Although the high correlation between VE and K+ was not altered with beta-blockade, propranolol treatment resulted in a significant reduction in the slope of this relationship during incremental exercise (P < 0.01). These findings suggest that 1) beta-blockade decreases the VE-K+ relationship observed during exercise and 2) K+ stimulation of muscle afferents is not an important signal in the control of exercise ventilation.

Effect of beta-blockade on the drift in O2 consumption during prolonged exercise

1988 ◽  
Vol 64 (2) ◽  
pp. 753-758 ◽  
Author(s):  
J. K. Kalis ◽  
B. J. Freund ◽  
M. J. Joyner ◽  
S. M. Jilka ◽  
J. Nittolo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Minute Ventilation ◽  
Cycle Ergometer ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
O2 Consumption ◽  
Double Blind ◽  
Cycle Ergometer Test ◽  
Ergometer Test

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)

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

1983 ◽  
Vol 54 (4) ◽  
pp. 901-905 ◽  
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.

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

1987 ◽  
Vol 62 (5) ◽  
pp. 1819-1825 ◽  
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.

Effect of beta-adrenergic blockade on lactate turnover in exercising dogs

1984 ◽  
Vol 57 (6) ◽  
pp. 1754-1759 ◽  
Author(s):  
B. Issekutz
Keyword(s):  
Plasma Glucose ◽  
Lactate Production ◽  
Hormonal Control ◽  
Glucose Turnover ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Metabolic Clearance ◽  
Beta Adrenergic ◽  
Indwelling Catheters ◽  
Lactate Turnover

Dogs with indwelling catheters in the jugular vein and in the carotid artery ran on the treadmill (slope: 15%, speed: 133 m/min). Lactate turnover and glucose turnover were measured using [U-14C]lactate and [3-3H]glucose as tracers, according to the primed constant-rate infusion method. In addition, the participation of plasma glucose in lactate production (Ra-L) was measured with [U-14C]glucose. Propranolol was given either (A) before exercise (250 micrograms/kg, iv) or (B) in form of a primed infusion administered to the dog running at a steady rate. Measurements of plasma propranolol concentration showed that in type A experiments plasma propranolol fell in 45 min below the lower limit of the complete beta-blockade. In the first 15 min of work Ra-L rose rapidly; then it fell below that of the control (exercise) values. During steady exercise, the elevated Ra-L was decreased by propranolol infusion close to resting values. beta-Blockade doubled the response of glucose production, utilization, and metabolic clearance rate to exercise. In exercising dogs approximately 40-50% of Ra-L arises from plasma glucose. This value was increased by the blockade to 85-90%. It is concluded that glycogenolysis in the working muscle has a dual control: 1) an intracellular control operating at the beginning of exercise, and 2) a hormonal control involving epinephrine and the beta-adrenergic receptors.

Beta-adrenergic blockade alters whole-body leucine metabolism in humans

1989 ◽  
Vol 67 (1) ◽  
pp. 221-225 ◽  
Author(s):  
L. S. Lamont ◽  
D. G. Patel ◽  
S. C. Kalhan
Keyword(s):  
Skeletal Muscle ◽  
Blocking Agent ◽  
Whole Body ◽  
Beta Blockade ◽  
Adrenergic System ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Leucine Metabolism ◽  
Leucine Oxidation ◽  
Tracer Dilution

This study examined the effects of a nonselective beta-blocking agent on whole-body leucine metabolism in humans. Five normal, healthy subjects (4 male, 1 female) underwent a 6-h primed, constant-rate infusion of L-[1–13C]leucine after 5 days of twice daily oral use of 80 mg propranolol and a placebo. Leucine turnover was determined by tracer dilution and leucine oxidation by 13C enrichment of the expired CO2. Propranolol decreased the total daily energy expenditure from 1,945 +/- 177.5 to 1,619 +/- 92.5 kcal/day (P less than 0.05). A fasting associated decrease in blood glucose and an attenuated rise in free fatty acids and ketones were observed during beta-blockade. Propranolol also increased plasma leucine concentrations (73.1 +/- 8.7 to 103.4 +/- 7.3 mumol/l; P less than 0.05) and leucine oxidation (13.2 +/- 1.2 to 17.1 +/- 1.3 mumol.kg-1.h-1; P less than 0.05), although leucine turnover was not significantly altered (100.5 +/- 7.3 vs. 126.0 +/- 12.3 mumol.kg-1.h-1). In addition, the urinary urea nitrogen-to-creatinine ratio was greater during propranolol administration (0.24 +/- 0.04 vs. 0.34 +/- 0.02 mol/g; P less than 0.05). These data suggest that the beta-adrenergic system plays a role in the modulation of whole-body leucine metabolism in humans. Whether these changes are the result of a direct effect on skeletal muscle or an indirect effect mediated by altering the fuel supply to skeletal muscle cannot be discriminated by the present study.

Effect of inhaled nitric oxide on pulmonary hemodynamics after acute lung injury in dogs

1994 ◽  
Vol 76 (3) ◽  
pp. 1356-1362 ◽  
Author(s):  
J. A. Romand ◽  
M. R. Pinsky ◽  
L. Firestone ◽  
H. A. Zar ◽  
J. R. Lancaster
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Dead Space ◽  
Left Ventricular ◽  
Right Atrial ◽  
Adrenergic Blockade ◽  
Pulmonary Hemodynamics ◽  
Beta Adrenergic

Increased pulmonary vascular resistance (PVR) and mismatch in ventilation-to-perfusion ratio characterize acute lung injury (ALI). Pulmonary arterial pressure (Ppa) decreases when nitric oxide (NO) is inhaled during hypoxic pulmonary vasoconstriction (HPV); thus NO inhalation may reduce PVR and improve gas exchange in ALI. We studied the hemodynamic and gas exchange effects of NO inhalation during HPV and then ALI in eight anesthetized open-chest mechanically ventilated dogs. Right atrial pressure, Ppa, and left ventricular and arterial pressures were measured, and cardiac output was estimated by an aortic flow probe. Shunt and dead space were also estimated. The effect of 5-min exposures to 0, 17, 28, 47, and 0 ppm inhaled NO was recorded during hyperoxia, hypoxia, and oleic acid-induced ALI. During ALI, partial beta-adrenergic blockade (propranolol, 0.15 mg/kg i.v.) was induced and 74 ppm NO was inhaled. Nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) levels were measured. During hyperoxia, NO inhalation had no measurable effects. Hypoxia increased Ppa (from 19.8 +/- 6.1 to 28.3 +/- 8.7 mmHg, P < 0.01) and calculated PVR (from 437 +/- 139 to 720 +/- 264 dyn.s.cm-5, P < 0.01), both of which decreased with 17 ppm NO. ALI decreased arterial PO2 and increased airway pressure, shunt, and dead space ventilation. Ppa (19.8 +/- 6.1 vs. 23.4 +/- 7.7 mmHg) and PVR (437 +/- 139 vs. 695 +/- 359 dyn.s.cm-5, P < 0.05) were greater during ALI than during hyperoxia. No inhalation had no measureable effect during ALI before or after beta-adrenergic blockade. MetHb remained low, and NO-Hb was unmeasurable. Bolus infusion of nitroglycerin (15 micrograms) induced an immediate decrease in Ppa and PVR during ALI.(ABSTRACT TRUNCATED AT 250 WORDS)

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

1989 ◽  
Vol 256 (3) ◽  
pp. R653-R658 ◽  
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.

Influence of beta-adrenergic blockade on the control of sweating in humans

1986 ◽  
Vol 61 (5) ◽  
pp. 1701-1705 ◽  
Author(s):  
G. W. Mack ◽  
L. M. Shannon ◽  
E. R. Nadel
Keyword(s):  
Skin Temperature ◽  
Sweat Rate ◽  
Energy Balance Equation ◽  
Cycle Ergometer ◽  
Beta Blockade ◽  
Evaporative Heat Loss ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Local Skin ◽  
Ergometer Exercise

To evaluate the role of beta-adrenergic receptors in the control of human sweating, we studied six subjects during 40 min of cycle-ergometer exercise (60% maximal O2 consumption) at 22 degrees C 2 h after oral administration of placebo or nonselective beta-blockade (BB, 80 mg propranolol). Internal temperature (esophageal temperature, Tes), mean skin temperature (Tsk), local chest temperature (Tch), and local chest sweat rate (msw) were continuously recorded. The control of sweating was best described by the slope of the linear relationship between msw and Tes and the threshold Tes for the onset of sweating. The slope of the msw-Tes relationship decreased 27% (P less than 0.01), from 1.80 to 1.30 mg X cm-2 X min-1 X degree C-1 during BB. The Tes threshold for sweating (36.8 degrees C) was not altered as the result of BB. These data suggest that BB modified the control of sweating via some peripheral interaction. Since Tsk was significantly (P less than 0.05) reduced during BB exercise, from a control value of 32.8 to 32.2 degrees C, we evaluated the influence of the reduction in local skin temperature (Tsk) in the altered control of sweating. Reductions in Tch accounted for only 45% of the decrease in the slope of the msw-Tes relationship during BB. Since evaporative heat loss requirement during exercise with BB, as estimated from the energy balance equation, was also reduced 18%, compared with control exercise, we concluded that during BB the reduction in sweating at any Tes is the consequence of both a decrease in local Tsk and a direct effect on sweat gland.

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