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.

EFFECTS OF ALPHA-ADRENERGIC STIMULATION AND BLOCKADE ON PLASMA PARATHYROID HORMONE CONCENTRATIONS IN COWS

1978 ◽  
Vol 88 (3) ◽  
pp. 535-544 ◽  
Author(s):  
J. W. Blum ◽  
A. Guillebeau ◽  
U. Binswanger ◽  
P. Kunz ◽  
M. Da Prada ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Fatty Acid ◽  
Parathyroid Hormone ◽  
Free Fatty Acid ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Later Phase ◽  
Immunoreactive Parathyroid Hormone

ABSTRACT Experiments were designed to investigate responses of immunoreactive parathyroid hormone (PTH) during alpha-adrenergic stimulation and blockade in cows. Alpha-adrenergic agonists (methoxamine, phenylephrine and noradrenaline, the beta-adrenergic action of which was blocked by propranolol) did not change PTH and free fatty acid levels, whereas they characteristically increased the blood pressure and decreased the heart rate. In contrast, alpha-adrenergic blockade by phentolamine progressively increased PTH levels. The elevated PTH concentrations, associated with increased plasma noradrenaline and free fatty acid levels, rising heart rate and decreasing blood pressure, indicated that all these changes can be related to a beta-adrenergic stimulatory mechanism. Beta-adrenergic stimulation was presumably responsible for the initial elevation of PTH concentrations, whereas, during the later phase of the phentolamine infusions, a concomitant hypocalcaemia probably also produced a stimulatory effect.

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.

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.

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.

Effect of exercise on left ventricular-arterial coupling assessed in the pressure-volume plane

1993 ◽  
Vol 264 (5) ◽  
pp. H1629-H1633 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Adrenergic Blockade ◽  
Stroke Work ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Lv Volume ◽  
Left Ventricular Arterial Coupling

The left ventricle (LV) and arterial system are nearly optimally coupled to produce stroke work (SW) at rest. However, the effect of exercise on the coupling between the LV and arterial system has not been directly determined. We evaluated 11 dogs who were instrumented to determine LV volume from three diameters. The LV end-systolic pressure (Pes)-volume (Ves) relation was determined by transient caval occlusion at rest and while the animals ran at 5-7 mph on a treadmill. During exercise, the Pes-Ves relation was shifted toward the left and the slope [end-systolic elastance (Ees)] increased from 7.7 +/- 2.8 to 12.7 +/- 4.2 (SD) mmHg/ml (P < 0.05). The arterial end-systolic elastance (Ea), calculated as Pes divided by stroke volume, increased during exercise (8.8 +/- 3.0 to 10.9 +/- 4.7 mmHg/ml, P < 0.05). The ratio of Ees to Ea increased during exercise from 0.89 +/- 0.31 to 1.27 +/- 0.12 (P < 0.05). The portion of the pressure-volume area expressed as SW increased during exercise from 0.63 +/- 0.07 to 0.69 +/- 0.10 (P < 0.05). After adrenergic blockade, the Ees-to-Ea ratio was not significantly altered during exercise (0.90 +/- 0.24 vs. 0.83 +/- 0.15, P = NS). At rest and during exercise, both with intact reflexes and after beta-adrenergic blockade, the ratio of Ees to Ea remained within the range in which SW is > 95% of maximum. We conclude that during exercise, beta-adrenergic stimulation shifts the LV Pes-Ves relation to the left with an increased slope. This more than offsets the increase in Ea.(ABSTRACT TRUNCATED AT 250 WORDS)

β-Adrenergic blockade counteracts starvational ketosis, but aggravates post-exercise ketosis in non-athletes

1988 ◽  
Vol 119 (1) ◽  
pp. 167-171 ◽  
Author(s):  
Y. A. K. Vahed ◽  
J. H. Koeslag ◽  
J. de V. Lochner
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Body Mass ◽  
Blood Concentration ◽  
Adrenergic Blockade ◽  
Blood Concentrations ◽  
Post Exercise ◽  
Glucose Ingestion ◽  
Propranolol Administration ◽  
The Difference

ABSTRACT Post-exercise ketosis is not abolished by glucose ingestion immediately after exercise but is counteracted by simultaneous β-adrenergic blockade. To investigate the effect of β-adrenergic blockade on post-exercise ketosis without the ingestion of glucose, we administered propranolol (1 mg/kg body mass) to 15 carbohydrate-starved people, of whom five had just walked 9 km in 2 h. There were 43 control subjects (no propranolol). The blood concentration of 3-hydroxybutyrate rose from 0·18 ± 0·02 (s.e.m.) mmol/l at 07.00 h to 0·35 ±0 04 mmol/l at 09.00 h whether the subjects had exercised during those 2 h or not (d.f. = 57). The blood concentration of 3-hydroxybutyrate at 15.00 h in the groups not treated with propranolol was not affected by exercise (0·95 ± 0·90 mmol/l; d.f. = 42). Propranolol significantly raised the concentration of 3-hydroxybutyrate at 15.00 h to 1·68 ±0·26 mmol/l when given after exercise (d.f. = 4), but lowered it to 0·46 ±0·07 mmol/l in the non-exercised group (d.f. = 9). This was not accompanied by significant differences in the blood concentrations of glucose, free fatty acid, insulin or glucagon. The difference in response to propranolol administration is probably determined by the alanine and lactate flux from muscle for hepatic oxaloacetate synthesis. J. Endocr. (1988) 119, 167–171

Free fatty acid and glucose metabolism in human aging: evidence for operation of the Randle cycle

1994 ◽  
Vol 266 (3) ◽  
pp. E501-E509 ◽  
Author(s):  
R. C. Bonadonna ◽  
L. C. Groop ◽  
D. C. Simonson ◽  
R. A. DeFronzo
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Metabolism ◽  
Lipid Oxidation ◽  
Lean Body Mass ◽  
Body Mass ◽  
Total Lipid ◽  
The Elderly ◽  
Glucose Turnover ◽  
Plasma Ffa

We assessed insulin effects on plasma free fatty acid (FFA) and glucose metabolism in seven elderly (71 +/- 2 yr) and in seven younger (21 +/- 1 yr) subjects matched for body weight and body mass index but not for percent body fat (32.4 +/- 3.8% in elderly vs. 20.4 +/- 3.5% in young, P < 0.05), by performing sequential euglycemic clamps at five insulin doses (0.6, 1.5, 3, 6, and 15 pmol.min-1.kg-1) in combination with indirect calorimetry and [1-14C]palmitate plus [3-3H]glucose infusion. At baseline, plasma FFA concentration, turnover infusion. At baseline, plasma FFA concentration, turnover and oxidation, and total lipid oxidation were all increased in the elderly (897 +/- 107 vs. 412 +/- 50 mumol/l and 11.2 +/- 1.4 vs. 5.14 +/- 0.86, 3.45 +/- 0.65 vs. 1.37 +/- 0.25, and 4.63 +/- 0.72 vs. 3.01 +/- 0.33 mumol.min-1.kg-1 lean body mass, P < 0.05 for all comparisons), whereas glucose turnover was similar as a result of decreased glucose oxidation (8.2 +/- 1.4 vs. 13 +/- 1.9 mumol.min-1.kg-1 lean body mass, P < 0.05) and increased glucose storage (6.6 +/- 1.4 vs. 1.7 +/- 1.3 mmol.min-1.kg-1 lean body mass, P < 0.05). At all insulin infusions, plasma FFA concentration, turnover and oxidation, and total lipid oxidation were higher in the elderly than in the younger group (P < 0.05). However, if normalized per fat mass, all FFA and lipid metabolic fluxes, both in the postabsorptive state and during hyperinsulinemia, were comparable in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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