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.

Leucine metabolism in perfused rat skeletal muscle during contractions

1987 ◽  
Vol 253 (6) ◽  
pp. E636-E647 ◽  
Author(s):  
D. A. Hood ◽  
R. L. Terjung
Keyword(s):  
Skeletal Muscle ◽  
Whole Body ◽  
Muscle Preparation ◽  
Rat Skeletal Muscle ◽  
Leucine Metabolism ◽  
Leucine Oxidation ◽  
Leucine Uptake ◽  
Hindlimb Muscle ◽  
Red Muscle ◽  
Fast Twitch

An isolated single rat hindlimb muscle preparation was used to examine leucine metabolism during steady-state conditions as a function of metabolic rate (VO2) and leucine concentration. The rates of muscle leucine uptake and leucine oxidation (measured as alpha-decarboxylation) were dependent on leucine delivery. At a physiological leucine concentration (0.1 mM), leucine uptake and alpha-ketoisocaproic acid (KIC) release during rest was 12.8 +/- 0.4 and 1.86 +/- 0.06 nmol.min-1.g-1 g, respectively. Leucine oxidation was 2.35 +/- 0.11 nmol.min-1.g-1 (n = 24) and if fully oxidized could account for only 3-4% of the resting VO2. This fraction was reduced to approximately 1% during contractions. The rate of leucine oxidation progressively increased, up to two to three times above rest (6-7 nmol.min-1.g-1), during contractions of graded frequency (7.5, 15, 30, 45, and 60 tetani/min) in a manner related to the eightfold increase in VO2 of the mixed fiber muscle. The fraction of muscle leucine uptake that was transaminated (i.e., leucine decarboxylation + KIC release) increased from 33% at rest to approximately 60% during contractions. The increase in leucine oxidation during contractions was probably primarily due to the high oxidative fast-twitch, red muscle mass, whose VO2 was estimated to increase up to 24-fold above rest. On the basis of our observed rates of muscle leucine alpha-decarboxylation, it is reasonable to attribute the rates of whole-body leucine oxidation of nontrained individuals during exercise to leucine oxidation by the working muscle.

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.

Trioctanoin infusion increases in vivo leucine oxidation: a lesson in isotope modeling

1986 ◽  
Vol 251 (3) ◽  
pp. E343-E348 ◽  
Author(s):  
N. Rodriguez ◽  
W. F. Schwenk ◽  
B. Beaufrere ◽  
J. M. Miles ◽  
M. W. Haymond
Keyword(s):  
Conscious Dogs ◽  
Whole Body ◽  
Keto Acid ◽  
Leucine Metabolism ◽  
Leucine Oxidation ◽  
Potential Indicator ◽  
Direct Contrast ◽  
Specific Activities

We have reported that infusion of trioctanoin in conscious dogs had little effect on leucine oxidation but decreased the rate of appearance (Ra) and interconversion of leucine and its alpha-keto acid, alpha-ketoisocaproate (KIC). To verify that these conclusions were independent of the leucine tracers and isotope models employed, the studies were repeated using [1-14C]leucine and [4,5-3H]KIC rather than [1-14C]KIC and [4,5-3H]leucine. In the present study, leucine oxidation calculated using the plasma [14C]leucine or [14C]KIC specific activities (SA) increased nearly twofold (P less than 0.001) during trioctanoin infusion in direct contrast to our previous results. When the data from either study were analyzed using the plasma SA of the leucine moiety reciprocal to the infused tracer as a potential indicator of the intracellular leucine SA, similar conclusions were obtained from either study: trioctanoin infusion in conscious dogs appears to increase whole-body leucine oxidation and does not decrease proteolysis. These studies challenge the validity of previously used isotope models of leucine metabolism and suggest that the plasma KIC SA during infusion of labeled leucine may most accurately reflect changes in whole-body leucine metabolism.

Influence of thyroid hormones and catecholamines on myosin of swim-exercised rats

1990 ◽  
Vol 68 (3) ◽  
pp. 973-978 ◽  
Author(s):  
H. Rupp ◽  
R. Wahl
Keyword(s):  
Thyroid Hormones ◽  
The Body ◽  
Physiological Signals ◽  
Adrenergic System ◽  
Adrenergic Blockade ◽  
Serum Concentrations ◽  
Beta Adrenergic ◽  
Intermittent Access ◽  
Beta Blocking ◽  
Access To Food

To define the physiological signals involved in the redirection of myosin expression in the swim-exercised rat, the relative influence of thyroid hormones and beta-adrenergic blockade was determined. Swimming exercise resulted in an increased proportion of myosin V1 (60.9 +/- 9.7 vs. 38.0 +/- 4.1% of sedentary rats fed ad libitum) but did not increase serum concentrations of total and free thyroxine or triiodothyronine determined either 17-21 h or immediately after swimming. The proportion of V1 increased, although intermittently food-deprived rats with the body weight of swimming rats exhibited a reduced proportion of V1 (23.5 +/- 2.7). When swimming rats had only intermittent access to food, they had reduced concentrations of all thyroid hormones, but the proportion of V1 (51.5 +/- 7.6) was nonetheless increased. Thus the redirection of myosin expression cannot be attributed to an increased secretion of thyroid hormones. The influence of the adrenergic system was assessed by treating swimming rats with the beta-blocking drug atenolol. Because the proportion of V1 was reduced, but thyroid hormones were not affected, beta-adrenergic blockade seems to influence myosin expression independently of thyroid hormones.

505 EFFECT OF STRENGTH TRAINING AND GROWTH HORMONE ADMINIS. TRATION ON WHOLE BODY AND SKELETAL MUSCLE LEUCINE METABOLISM

1990 ◽  
Vol 22 (2) ◽  
pp. S85 ◽  
Author(s):  
K. E. YARASHESKI ◽  
J. A. CAMPBELL ◽  
M. J. RENNIE ◽  
J. O. HOLLOSZY ◽  
D. M. BIER
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Strength Training ◽  
Whole Body ◽  
Leucine Metabolism

Effect of endurance training on leucine metabolism in perfused rat skeletal muscle

1987 ◽  
Vol 253 (6) ◽  
pp. E648-E656 ◽  
Author(s):  
D. A. Hood ◽  
R. L. Terjung
Keyword(s):  
Steady State ◽  
Citrate Synthase ◽  
Whole Body ◽  
Trained Group ◽  
Leucine Metabolism ◽  
Leucine Oxidation ◽  
Hindlimb Muscle ◽  
Branched Chain ◽  
And Control

An isolated single rat hindlimb muscle preparation was used to examine the influence of exercise training on leucine metabolism during steady-state conditions at rest and during isometric contractions. Treadmill training increased the activity of citrate synthase in the hindlimb muscle by 40-45%. Leucine oxidation, measured as the rate of alpha-decarboxylation, was not different between trained (2.28 +/- 0.15 nmol.min-1.g-1, n = 9) and control (2.57 +/- 0.20, n = 9) muscle at rest. In addition, successive 40-min contraction periods at 15 and 45 tetani/min induced similar increases (50 and 100%, respectively) in leucine oxidation in both groups. However, trained muscle maintained a greater tension output (P less than 0.05) during contractions and exhibited a greater oxygen consumption (VO2) (P less than 0.05) during 45 tetani/min. Thus the rate of leucine oxidation, relative to VO2, was less (P less than 0.05) in the trained group. This response was probably related to differences in intracellular factors modulating branched-chain alpha-keto acid dehydrogenase, the rate-limiting step in leucine oxidation. Although our observed rates of muscle leucine alpha-decarboxylation can reasonably account for the rates of whole-body leucine alpha-decarboxylation of nontrained individuals found during steady-state tracer studies in vivo, this is less reasonably the case for the trained group. This suggests that a greater rate of leucine oxidation by nonmuscle tissues (e.g., liver) may occur in trained compared with nontrained individuals.

Relation between plasma and tissue parameters of leucine metabolism in fed and starved rats

1986 ◽  
Vol 250 (6) ◽  
pp. E615-E621 ◽  
Author(s):  
J. A. Vazquez ◽  
H. S. Paul ◽  
S. A. Adibi
Keyword(s):  
Continuous Infusion ◽  
Total Protein ◽  
Specific Activity ◽  
Whole Body ◽  
Leucine Incorporation ◽  
Body Protein ◽  
Leucine Metabolism ◽  
Leucine Oxidation ◽  
The Difference ◽  
Plasma Leucine

By use of a primed continuous infusion of [1-14C]leucine, we investigated parameters of leucine metabolism in plasma, expired air, and tissues of fed and 48-h starved rats. The ratios of muscle to plasma specific activity of alpha-ketoisocaproate (KIC) in fed and starved rats were not significantly different from 1. The ratio of muscle to plasma specific activity of leucine was also not significantly different from 1 in fed rats, but was significantly lower than 1 in starved rats. The rate of leucine oxidation was 28-34% higher when calculation was based on plasma KIC rather than leucine specific activity. However, starvation significantly increased the rate of leucine oxidation with either specific activity. The rates of leucine incorporation into whole-body protein, calculated as the difference between plasma leucine turnover and oxidation, were unaffected by starvation, but the incorporations into total protein measured directly were significantly decreased in liver and muscle. We conclude that leucine or KIC specific activity in muscle is better predicted by plasma KIC than leucine specific activity, and the difference between rates of plasma leucine turnover and oxidation does not appear to be a valid measurement of leucine incorporation into whole-body protein.

Beta-adrenergic blockade in ponies with recurrent obstructive pulmonary disease

1988 ◽  
Vol 64 (6) ◽  
pp. 2324-2328 ◽  
Author(s):  
J. S. Scott ◽  
R. V. Broadstone ◽  
F. J. Derksen ◽  
N. E. Robinson
Keyword(s):  
Airway Obstruction ◽  
Clinical Remission ◽  
Dynamic Compliance ◽  
Airway Responsiveness ◽  
Adrenergic System ◽  
Adrenergic Blockade ◽  
Recurrent Airway Obstruction ◽  
Beta Adrenergic ◽  
Obstructive Pulmonary Disease ◽  
Airway Caliber

Ponies with recurrent airway obstruction have hyperresponsive airways during acute disease exacerbations but not during clinical remission. We examined the effect of beta-adrenergic blockade with propranolol on airway responsiveness to aerosol histamine in six ponies with recurrent airway obstruction and six age- and gender-matched controls. Measurements were made with principal ponies in clinical remission (period A) and during an acute period of airway obstruction (period B). beta-Adrenergic blockade did not change airway responsiveness, dynamic compliance (Cdyn), or pulmonary resistance (RL) in either group of ponies at period A or in the control ponies at period B. In principal ponies at period B, propranolol significantly increased RL but was without effect on Cdyn or airway responsiveness. We conclude that the beta-adrenergic system is involved in the control of central airway caliber in principal ponies at period B but that this system does not seem to be involved in the mechanism of airway hyperresponsiveness to histamine.

Effect of beta-adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation

1975 ◽  
Vol 229 (3) ◽  
pp. 731-736 ◽  
Author(s):  
RJ Anderson ◽  
MS Taher ◽  
RE Cronin ◽  
KM McDonald ◽  
RW Schrier
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Blocking Agent ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Renal Autoregulation ◽  
Beta Receptor ◽  
Adrenergic Blocking

The role of the renin-angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin ii, [1-sarcosine, 8-glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta-adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70-90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.

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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