Propranolol does not impair exercise oxygen uptake in normal men at high altitude

1986 ◽  
Vol 61 (5) ◽  
pp. 1935-1941 ◽  
Author(s):  
L. G. Moore ◽  
A. Cymerman ◽  
S. Y. Huang ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
...  
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Hemoglobin Concentration ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
O2 Uptake ◽  
Compensatory Mechanisms ◽  
Beta Adrenergic ◽  
Propranolol Treatment ◽  
Normal Men

Decreased maximal O2 uptake (VO2max) and stimulation of the sympathetic nervous system have been previously shown to occur at high altitude. We hypothesized that tachycardia mediated by beta-adrenergic stimulation acted to defend VO2max at high altitude. Propranolol treatment beginning before high-altitude (4,300 m) ascent reduced heart rate during maximal and submaximal exercise in six healthy men treated with propranolol (80 mg three times daily) compared with five healthy subjects receiving placebo (lactose). Compared with sea-level values, the VO2max fell on day 2 at high altitude, but the magnitude of fall was similar in the placebo and propranolol treatment groups (26 +/- 6 vs. 32 +/- 5%, P = NS) and VO2max remained similar at high altitude in both groups once treatment was discontinued. During 30 min of submaximal (80% of VO2max) exercise, propranolol-treated subjects maintained O2 uptake levels that were as large as those in placebo subjects. The maintenance of maximal or submaximal levels of O2 uptake in propranolol-treated subjects at 4,300 m could not be attributed to increased minute ventilation, arterial O2 saturation, or hemoglobin concentration. Rather, it appeared that propranolol-treated subjects maintained O2 uptake by transporting a greater proportion of the O2 uptake with each heartbeat. Thus, contrary to our hypothesis, beta-adrenergic blockade did not impair maximal or submaximal O2 uptake at high altitude due perhaps to compensatory mechanisms acting to maintain stroke volume and cardiac output.

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.

Effect of short- and long-term beta-adrenergic blockade on lipolysis during fasting in humans

1989 ◽  
Vol 257 (1) ◽  
pp. E65-E73 ◽  
Author(s):  
S. Klein ◽  
E. J. Peters ◽  
O. B. Holland ◽  
R. R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Lean Body Mass ◽  
Body Mass ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Healthy Human ◽  
Beta Adrenergic ◽  
Triglyceride Fatty Acid ◽  
Propranolol Treatment ◽  
Oral Propranolol

Stable isotope tracers and indirect calorimetry were used to evaluate the importance of beta-adrenergic stimulation of lipolysis and triglyceride-fatty acid cycling during fasting in healthy human volunteers. Each subject was studied after 12 and 84 h of fasting both with and without propranolol infusion (protocol 1) and when oral propranolol treatment was given throughout fasting (protocol 2). In protocol 1, the rates of appearance of glycerol and palmitic acid increased from 3.04 +/- 0.19 and 1.78 +/- 0.17 mumol.kg lean body mass-1.min-1, respectively, after 12 h of fasting to 5.28 +/- 0.31 and 3.47 +/- 0.15 mumol.kg lean body mass-1.min-1, respectively, after 84 h of fasting (P less than 0.005). The rate of triglyceride-fatty acid cycling increased from 97 +/- 8 to 169 +/- 5 mumol/min (P less than 0.005). Intravenous propranolol infusion decreased the rate of lipolysis after both 12 and 84 h of fasting, but the magnitude of the antilipolytic effect was much greater after 84 h (P less than 0.005). In protocol 2, the rate of lipolysis and triglyceride-fatty acid cycling was still increased by fasting despite beta-adrenergic blockade with oral propranolol. This study demonstrates that beta-adrenergic stimulation contributes to the mobilization of fat during fasting. However, other mechanism(s) can increase lipolysis and triglyceride-fatty acid cycling when beta-adrenergic receptors are continuously blocked.

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.

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.

scholarly journals Mice and Rats Display Different Ventilatory, Hematological, and Metabolic Features of Acclimatization to Hypoxia

2021 ◽  
Vol 12 ◽  
Author(s):  
Christian Arias-Reyes ◽  
Jorge Soliz ◽  
Vincent Joseph
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Rattus Rattus ◽  
Hemoglobin Concentration ◽  
Whole Body ◽  
Ecological Niches ◽  
House Mice ◽  
Sprague Dawley ◽  
Mitochondrial Oxygen Consumption ◽  
Sd Rats

Phylogeographic studies showed that house mice (Mus musculus) originated in the Himalayan region, while common rats (Rattus rattus and Rattus norvegicus) come from the lowlands of China and India. Accordingly, it has been proposed that its origins gave mice, but not rats, the ability to invade ecological niches at high altitudes (pre-adaptation). This proposal is strongly supported by the fact that house mice are distributed throughout the world, while common rats are practically absent above 2,500 m. Considering that the ability of mammals to colonize high-altitude environments (&gt;2,500 m) is limited by their capability to tolerate reduced oxygen availability, in this work, we hypothesize that divergences in the ventilatory, hematological, and metabolic phenotypes of mice and rats establish during the process of acclimatization to hypoxia (Hx). To test this hypothesis male FVB mice and Sprague-Dawley (SD) rats were exposed to Hx (12% O2) for 0 h (normoxic controls), 6 h, 1, 7, and 21 days. We assessed changes in ventilatory [minute ventilation (VE), respiratory frequency (fR), and tidal volume (VT)], hematological (hematocrit and hemoglobin concentration), and metabolic [whole-body O2 consumption (VO2) and CO2 production (VCO2), and liver mitochondrial oxygen consumption rate (OCR) parameters]. Compared to rats, results in mice show increased ventilatory, metabolic, and mitochondrial response. In contrast, rats showed quicker and higher hematological response than mice and only minor ventilatory and metabolic adjustments. Our findings may explain, at least in part, why mice, but not rats, were able to colonize high-altitude habitats.

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.

Effects of erythrocyte infusion on VO2max at high altitude

1996 ◽  
Vol 81 (1) ◽  
pp. 252-259 ◽  
Author(s):  
A. J. Young ◽  
M. N. Sawka ◽  
S. R. Muza ◽  
R. Boushel ◽  
T. Lyons ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Treadmill Running ◽  
Control Group ◽  
O2 Uptake ◽  
Control Subjects ◽  
And Control ◽  
Experimental Group

This study investigated whether autologous erythrocyte infusion would ameliorate the decrement in maximal O2 uptake (VO2max) experienced by lowlanders when they ascend to high altitude. VO2max was measured in 16 men (treadmill running) at sea level (SL) and on the 1st (HA1) and 9th (HA9) days of high-altitude (4,300 m) residence. After VO2max was measured at SL, subjects were divided into two matched groups (n = 8). Twenty-four hours before ascent to high altitude, the experimental group received a 700-ml infusion of autologous erythrocytes and saline (42% hematocrit), whereas the control group received only saline. The VO2max of erythrocyte-infused [54 +/- 1 (SE) ml.kg-1.min-1] and control subjects (52 +/- 2 ml.kg-1.min-1) did not differ at SL before infusion. The decrement in VO2max on HA1 did not differ between groups, averaging 26% overall, despite higher (P < 0.01) arterial hematocrit, hemoglobin concentration, and arterial O2 content in the erythrocyte-infused subjects. By HA9, there were no longer any differences in hematocrit, hemoglobin concentration, or arterial O2 content between groups. No change in VO2max occurred between HA1 and HA9 for either group. Thus, despite increasing arterial O2-carrying capacity, autologous erythrocyte infusion did not ameliorate the decrement in VO2max at 4,300-m altitude.

Function of canine diaphragm with hypovolemic shock and beta-adrenergic blockade

1984 ◽  
Vol 56 (3) ◽  
pp. 648-655 ◽  
Author(s):  
S. M. Scharf ◽  
H. Bark
Keyword(s):  
Function Analysis ◽  
Force Generation ◽  
Pleural Pressure ◽  
Adrenergic Blockade ◽  
Sympathetic Stimulation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Transdiaphragmatic Pressure ◽  
Diaphragm Function ◽  
Gastric Pressure

In anesthetized mongrel dogs we investigated the effects of hypovolemia and beta-adrenergic stimulation on the decrease in force generation by the diaphragm [transdiaphragmatic pressure (Pdi)] during electrical stimulation of the phrenic nerves for 1 h. In seven normovolemic dogs with arterial pressure (Pa) of approximately 125 Torr, Pdi fell approximately 48% from an initial value of 35 +/- 4.8 Torr. In dogs made moderately hypovolemic, Pdi was actually higher than with normovolemia (P less than 0.01). In dogs made severely hypovolemic, Pa approximately 50 Torr, Pdi at the start of pacing was less than with normovolemia (25 +/- 1.5 Torr) and remained so during phrenic nerve stimulation. When beta-adrenergic blockade with propranolol was added to moderate hypovolemia, the values of Pdi became similar to those of severe hypovolemia. Analysis of the relative contributions of gastric pressure and pleural pressure revealed that the factor responsible for maintaining Pdi with moderate hypovolemia was pleural pressure. Changes in thoracic gas volume and chest wall configuration did not explain the changes we saw in diaphragm function. Analysis of the relationship between rib cage motion and pleural pressure confirmed our finding of the greater pleural pressure generation with sympathetic stimulation that accompanies hypovolemia. These studies demonstrated that 1) severe hypovolemia impaired diaphragm function, 2) diaphragm function was maintained with moderate hypovolemia by beta-adrenergic stimulation, and 3) with hypovolemia-associated sympathetic stimulation there was an increase in force generation by the intercostal muscles.

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