scholarly journals Effect of epinephrine on muscle glycogenolysis during exercise in trained men

1998 ◽  
Vol 84 (2) ◽  
pp. 465-470 ◽  
Author(s):  
M. A. Febbraio ◽  
D. L. Lambert ◽  
R. L. Starkie ◽  
J. Proietto ◽  
M. Hargreaves
Keyword(s):  
Oxygen Uptake ◽  
Muscle Glycogen ◽  
Respiratory Exchange Ratio ◽  
Peak Oxygen Uptake ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Glycogen Utilization ◽  
Muscle Glycogen Concentration ◽  
Epinephrine Concentration

Febbraio, M. A., D. L. Lambert, R. L. Starkie, J. Proietto, and M. Hargreaves. Effect of epinephrine on muscle glycogenolysis during exercise in trained men. J. Appl. Physiol. 84(2): 465–470, 1998.—To test the hypothesis that an elevation in circulating epinephrine increases intramuscular glycogen utilization, six endurance-trained men performed two 40-min cycling trials at 71 ± 2% of peak oxygen uptake in 20–22°C conditions. On the first occasion, subjects were infused with saline throughout exercise (Con). One week later, after determination of plasma epinephrine levels in Con, subjects performed the second trial (Epi) with an epinephrine infusion, which resulted in a twofold higher ( P < 0.01) plasma epinephrine concentration in Epi compared with Con. Although oxygen uptake was not different when the two trials were compared, respiratory exchange ratio was higher throughout exercise in Epi compared with Con (0.93 ± 0.01 vs. 0.89 ± 0.01; P < 0.05). Muscle glycogen concentration was not different when the trials were compared preexercise, but the postexercise value was lower ( P < 0.01) in Epi compared with Con. Thus net muscle glycogen utilization was greater during exercise with epinephrine infusion (224 ± 37 vs. 303 ± 30 mmol/kg for Con and Epi, respectively; P < 0.01). In addition, both muscle and plasma lactate and plasma glucose concentrations were higher ( P < 0.05) in Epi compared with Con. These data indicate that intramuscular glycogen utilization, glycolysis, and carbohydrate oxidation are augmented by elevated epinephrine during submaximal exercise in trained men.

Effect of infusing epinephrine on liver and muscle glycogenolysis during exercise in rats

1986 ◽  
Vol 250 (6) ◽  
pp. E641-E649 ◽  
Author(s):  
D. A. Arnall ◽  
J. C. Marker ◽  
R. K. Conlee ◽  
W. W. Winder
Keyword(s):  
Muscle Glycogen ◽  
Vastus Lateralis ◽  
Plasma Concentrations ◽  
Physiological Saline ◽  
Threshold Concentration ◽  
Plasma Epinephrine ◽  
Glycogen Depletion ◽  
Epinephrine Infusion ◽  
Liver Glycogenolysis ◽  
Epinephrine Concentration

To determine the possibility of a threshold concentration of plasma epinephrine that stimulates liver glycogenolysis during exercise, adrenodemedullated (ADM) and sham-operated (SHAM) rats were infused with saline or epinephrine at rates that produced plasma concentrations ranging between 0.01 ng/ml (0.06 nM) and 4.3 ng/ml (23.7 nM). During the infusion rats were run on a rodent treadmill for 0, 30, or 60 min at 21 m/min up a 15% grade. Liver glycogen decreased at similar rates in all exercising rats regardless of plasma epinephrine concentration. Epinephrine infusion stimulated significant muscle glycogen depletion in the soleus and red and white vastus lateralis muscles. ADM saline-infused animals exhibited the least muscle glycogen depletion. Blood glucose and lactate in exercising ADM rats increased as the epinephrine infusion concentration increased. During exercise, there was no epinephrine concentration that stimulated liver glycogenolysis more effectively than physiological saline.

Effect of epinephrine on muscle glycogenolysis and insulin-stimulated muscle glycogen synthesis in humans

1998 ◽  
Vol 274 (1) ◽  
pp. E130-E138 ◽  
Author(s):  
Didier Laurent ◽  
Kitt Falk Petersen ◽  
Raymond R. Russell ◽  
Gary W. Cline ◽  
Gerald I. Shulman
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Synthesis ◽  
Whole Body ◽  
Synthesis Rate ◽  
Initial Increase ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Muscle Glycogen Synthesis ◽  
Epinephrine Concentration

To examine the effects of a physiological increase in plasma epinephrine concentration (∼800 pg/ml) on muscle glycogenolysis and insulin-stimulated glycogenesis, we infused epinephrine [1.2 μg ⋅ (m2 body surface)−1 ⋅ min−1] for 2 h and monitored muscle glycogen and glucose 6-phosphate (G-6- P) concentrations with13C/31P nuclear magnetic resonance (NMR) spectroscopy. Epinephrine caused an increase in plasma glucose (Δ ∼50 mg/dl), lactate (Δ ∼1.4 mM), free fatty acids (Δ ∼1,200 μM at peak), and whole body glucose oxidation (Δ ∼0.85 mg ⋅ kg−1 ⋅ min−1) compared with levels in a group of control subjects ( n = 4) in the presence of slight hyperinsulinemia (∼13 μU/ml, n = 8) or basal insulin (∼7 μU/ml, n = 7). However, epinephrine did not induce any detectable changes in glycogen or G-6- P concentrations, whereas muscle inorganic phosphate (Pi) decreased by 35%. Epinephrine infusion during a euglycemic-hyperinsulinemic clamp ( n = 8) caused a 45% decrease in the glucose infusion rate that could be mostly attributed to a 73% decrease in muscle glycogen synthesis rate. After an initial increase to ∼160% of basal values, G-6- Plevels decreased by ∼30% with initiation of the epinephrine infusion. We conclude that a physiological increase in plasma epinephrine concentration 1) has a negligible effect on muscle glycogenolysis at rest, 2) decreases muscle Pi, which may maintain phosphorylase activity at a low level, and 3) causes a major impairment in insulin-stimulated muscle glycogen synthesis, possibly due to inhibition of glucose transport-phosphorylation activity.

Substrate utilization in leg muscle of men after heat acclimation

1987 ◽  
Vol 63 (1) ◽  
pp. 31-35 ◽  
Author(s):  
J. P. Kirwan ◽  
D. L. Costill ◽  
H. Kuipers ◽  
M. J. Burrell ◽  
W. J. Fink ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Glycogen ◽  
Respiratory Exchange Ratio ◽  
Plasma Free Fatty Acid ◽  
Heat Acclimation ◽  
Substrate Utilization ◽  
Acclimation Period ◽  
Glycogen Utilization ◽  
Leg Muscle ◽  
Increased Blood Flow

Eight men were heat acclimated (39.6 degrees C and 29.2% rh) for 8 days to examine changes in substrate utilization. A heat exercise test (HET), (cycling for 60 min; 50% maximal O2 consumption) was performed before (UN-HET) and after (ACC-HET) the acclimation period. Muscle glycogen utilization (67.0 vs. 37.6 mmol/kg wet wt), respiratory exchange ratio (0.85 +/- 0.002 vs. 0.83 +/- 0.001), and calculated rate of carbohydrate oxidation (75.15 +/- 1.38 vs. 64.80 +/- 1.52 g/h) were significantly reduced (P less than 0.05) during the ACC-HET. Significantly lower (P less than 0.05) femoral venous glucose (15, 30, and 45 min) and lactate (15 min) levels were observed during the ACC-HET. No differences were observed in plasma free fatty acid (FFA) and glycerol concentrations or glucose, lactate and glycerol arteriovenous uptake/release between tests. A small but significant increase (P less than 0.05) above resting levels in FFA uptake was observed during the ACC-HET. Leg blood flow was slightly greater (P greater than 0.05) during the ACC-HET (4.64 +/- 0.13 vs. 4.80 +/- 0.13 l/min). These findings indicate a reduced use of muscle glycogen following heat acclimation. However, the decrease is not completely explained by a shift toward greater lipid oxidation or increased blood flow.

Verification phase as a useful tool in the determination of the maximal oxygen uptake of distance runners

2006 ◽  
Vol 31 (5) ◽  
pp. 541-548 ◽  
Author(s):  
Adrian W. Midgley ◽  
Lars R. McNaughton ◽  
Sean Carroll
Keyword(s):  
Heart Rate ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Peak Oxygen Uptake ◽  
Treadmill Running ◽  
Distance Runners ◽  
Peak Heart Rate ◽  
Incremental Test ◽  
Volitional Exhaustion

This study investigated the utility of a verification phase for increasing confidence that a “true” maximal oxygen uptake had been elicited in 16 male distance runners (mean age (±SD), 38.7  (± 7.5 y)) during an incremental treadmill running test continued to volitional exhaustion. After the incremental test subjects performed a 10 min recovery walk and a verification phase performed to volitional exhaustion at a running speed 0.5 km·h–1 higher than that attained during the last completed stage of the incremental phase. Verification criteria were a verification phase peak oxygen uptake ≤ 2% higher than the incremental phase value and peak heart rate values within 2 beats·min–1 of each other. Of the 32 tests, 26 satisfied the oxygen uptake verification criterion and 23 satisfied the heart rate verification criterion. Peak heart rate was lower (p = 0.001) during the verification phase than during the incremental phase, suggesting that the verification protocol was inadequate in eliciting maximal values in some runners. This was further supported by the fact that 7 tests exhibited peak oxygen uptake values over 100 mL·min–1 (≥ 3%) lower than the peak values attained in the incremental phase. Further research is required to improve the verification procedure before its utility can be confirmed.

Epinephrine inhibits exogenous glucose utilization in exercising horses

2000 ◽  
Vol 88 (5) ◽  
pp. 1777-1790 ◽  
Author(s):  
Raymond J. Geor ◽  
Kenneth W. Hinchcliff ◽  
Laura Jill McCutcheon ◽  
Richard A. Sams
Keyword(s):  
Muscle Glycogen ◽  
Glucose Utilization ◽  
Treadmill Exercise ◽  
Moderate Intensity ◽  
Oral Glucose ◽  
Moderate Intensity Exercise ◽  
Epinephrine Infusion ◽  
Glucose Administration ◽  
Exogenous Glucose ◽  
Glycogen Utilization

This study examined the effects of preexercise glucose administration, with and without epinephrine infusion, on carbohydrate metabolism in horses during exercise. Six horses completed 60 min of treadmill exercise at 55 ± 1% maximum O2 uptake 1) 1 h after oral administration of glucose (2 g/kg; G trial); 2) 1 h after oral glucose and with an intravenous infusion of epinephrine (0.2 μmol ⋅ kg− 1 ⋅ min− 1; GE trial) during exercise, and 3) 1 h after water only (F trial). Glucose administration (G and GE) caused hyperinsulinemia and hyperglycemia (∼8 mM). In GE, plasma epinephrine concentrations were three- to fourfold higher than in the other trials. Compared with F, the glucose rate of appearance was ∼50% and ∼33% higher in G and GE, respectively, during exercise. The glucose rate of disappearance was ∼100% higher in G than in F, but epinephrine infusion completely inhibited the increase in glucose uptake associated with glucose administration. Muscle glycogen utilization was higher in GE [349 ± 44 mmol/kg dry muscle (dm)] than in F (218 ± 28 mmol/kg dm) and G (201 ± 35 mmol/kg dm). We conclude that 1) preexercise glucose augments utilization of plasma glucose in horses during moderate-intensity exercise but does not alter muscle glycogen usage and 2) increased circulating epinephrine inhibits the increase in glucose rate of disappearance associated with preexercise glucose administration and increases reliance on muscle glycogen for energy transduction.

Effect of epinephrine on alveolar liquid clearance in the rat

1999 ◽  
Vol 87 (2) ◽  
pp. 611-618 ◽  
Author(s):  
Paul D. Charron ◽  
J. Phillip Fawley ◽  
Michael B. Maron
Keyword(s):  
Pulmonary Edema ◽  
Mass Balance ◽  
Sodium Transport ◽  
No Reduction ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Baseline Values ◽  
Alveolar Liquid Clearance ◽  
Epinephrine Concentration ◽  
Alveolar Liquid

Endogenous epinephrine has been found to increase alveolar liquid clearance (ALC) in several pulmonary edema models. In this study, we infused epinephrine intravenously for 1 h in anesthetized rats to produce plasma epinephrine concentrations commonly observed in this species under stressful conditions and measured ALC by mass balance. Epinephrine increased ALC from 31.5 ± 3.2 to 48.9 ± 1.1 (SE)% of the instilled volume ( P < 0.05). The increased ALC was prevented by either propranolol or amiloride. To determine whether ALC returns to normal after plasma epinephrine concentration normalizes, we measured ALC 2 h after stopping an initial 1-h epinephrine infusion and found ALC to be at baseline values. Finally, to determine whether desensitization of the liquid clearance response occurs, we evaluated the effects of both repeated 1-h infusions and a continuous 4-h infusion of epinephrine on ALC and found no reduction in ALC under either condition. We conclude that epinephrine increases ALC by stimulating β-adrenoceptors and sodium transport, that the increase is reversible once plasma epinephrine concentration normalizes, and that desensitization of the ALC response does not appear to occur after 4 h of continuous epinephrine exposure.

scholarly journals A kinetic model of the circulatory regulation of tissue plasminogen activator during exercise, epinephrine infusion, and endurance training

Blood ◽  
1993 ◽  
Vol 81 (12) ◽  
pp. 3293-3302
Author(s):  
WL Chandler ◽  
WC Levy ◽  
RC Veith ◽  
JR Stratton
Keyword(s):  
Blood Flow ◽  
Endurance Training ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Hepatic Blood Flow ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Tissue Plasminogen ◽  
Pai 1 ◽  
Epinephrine Concentration

A computer simulation of the circulatory system was used to kinetically model secretion, inhibition, and clearance of tissue plasminogen activator (t-PA) during three different processes that increase active t-PA levels: epinephrine infusion, exercise, and endurance training. Infusion of epinephrine stimulated an increase in t-PA secretion that was proportional to the plasma epinephrine concentration. In addition, epinephrine infusion increased hepatic blood flow and t-PA clearance, thus slowing the increase of plasma t-PA levels. During exercise, t-PA levels increased due both to increased t-PA secretion and to decreased clearance secondary to reduced hepatic blood flow. The increase in t-PA secretion during exercise was directly proportional to the epinephrine concentration in blood with the same ratio of t-PA secretion to epinephrine as found during epinephrine infusion, suggesting that increased plasma epinephrine during exercise was the primary stimulus for t-PA secretion. Lastly, the simulation predicted that 6 months of endurance training produced a decrease in resting plasminogen activator inhibitor type 1 (PAI-1) secretion, resulting in less t-PA inhibition and an overall increase in active t-PA after training. Accurate analysis of the regulation of active t-PA levels in blood required simultaneous modeling of t-PA and PAI-1 secretion, hepatic clearance, and inhibition of t-PA by PAI-1.

Preexercise muscle glycogen content affects metabolism during exercise despite maintenance of hyperglycemia

1998 ◽  
Vol 274 (1) ◽  
pp. E83-E88 ◽  
Author(s):  
Sandra M. Weltan ◽  
Andrew N. Bosch ◽  
Steven C. Dennis ◽  
Timothy D. Noakes
Keyword(s):  
Muscle Glycogen ◽  
Glucose Oxidation ◽  
Glycogen Content ◽  
Respiratory Exchange Ratio ◽  
Glucose Infusion ◽  
Muscle Glycogen Content ◽  
Hyperglycemic Clamp ◽  
Upper Limit ◽  
Glycogen Utilization ◽  
Total Glucose

Trained cyclists with low muscle glycogen (LGH; n = 8) or normal glycogen (NGH; n = 5) exercised for 145 min at 70% of maximal oxygen uptake during a hyperglycemic clamp. Respiratory exchange ratio was higher in NGH than LGH, and free fatty acid concentrations were lower in NGH than LGH. Areas under the curve for insulin and lactate were lower in LGH than NGH. Total glucose infusion and total glucose oxidation were not different between NGH and LGH, and total glucose oxidation amounted to 65 and 66% of total glucose infusion in NGH and LGH, respectively. Rates of glucose oxidation rose during exercise, reaching peaks of 9.2 ± 1.7 and 8.3 ± 1.1 mmol/min in NGH and LGH, respectively. Muscle glycogen disappearance was greater in NGH than LGH. Thus 1) low muscle glycogen content does not cause increased glucose oxidation, even during hyperglycemia; instead there is an increase in fat oxidation, 2) there is an upper limit to the rate of glucose oxidation during exercise with hyperglycemia irrespective of muscle glycogen status, and 3) net muscle glycogen utilization is determined by muscle glycogen content at the start of exercise, even during hyperglycemia.

Effect of graded epinephrine infusion on blood lactate response to exercise

1995 ◽  
Vol 79 (4) ◽  
pp. 1206-1211 ◽  
Author(s):  
M. J. Turner ◽  
E. T. Howley ◽  
H. Tanaka ◽  
M. Ashraf ◽  
D. R. Bassett ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Blood Lactate ◽  
Random Order ◽  
Peak Oxygen Uptake ◽  
Sudden Increase ◽  
Control Test ◽  
Epinephrine Infusion ◽  
Exercise Tests ◽  
Ergometer Exercise ◽  
Graded Exercise

In an attempt to determine whether the lactate threshold (LT) is the result of a sudden increase in plasma epinephrine (Epi), eight healthy college-aged males (22.4 +/- 0.4 yr) were recruited to perform three cycle ergometer exercise tests. Each subject performed a graded exercise test (GXT) to determine LT, Epi threshold, and norepinephrine threshold (64.6 +/- 2.4, 62.5 +/- 2.4, and 60.8 +/- 4.3% peak oxygen uptake, respectively). Each subject also completed, in random order, two 30-min submaximal (20% peak oxygen uptake below LT) exercise tests. During one test, graded Epi infusions were carried out at rates of 0.02–0.12 micrograms.kg-1.min-1; the other served as a control test. Infusion resulted in plasma Epi concentrations similar to those observed during GXT. The increase in blood lactate with Epi infusion was significantly greater than that during the control test (3.0 +/- 0.3 vs. 1.4 +/- 0.1 mmol/l at minute 30) but did not approach levels exhibited during GXT. We suggest an interaction of the increasing plasma Epi with other factors may be responsible for the sudden increase in blood lactate during graded exercise.

scholarly journals A kinetic model of the circulatory regulation of tissue plasminogen activator during exercise, epinephrine infusion, and endurance training

Blood ◽  
1993 ◽  
Vol 81 (12) ◽  
pp. 3293-3302 ◽  
Author(s):  
WL Chandler ◽  
WC Levy ◽  
RC Veith ◽  
JR Stratton
Keyword(s):  
Blood Flow ◽  
Endurance Training ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Hepatic Blood Flow ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Tissue Plasminogen ◽  
Pai 1 ◽  
Epinephrine Concentration

Abstract A computer simulation of the circulatory system was used to kinetically model secretion, inhibition, and clearance of tissue plasminogen activator (t-PA) during three different processes that increase active t-PA levels: epinephrine infusion, exercise, and endurance training. Infusion of epinephrine stimulated an increase in t-PA secretion that was proportional to the plasma epinephrine concentration. In addition, epinephrine infusion increased hepatic blood flow and t-PA clearance, thus slowing the increase of plasma t-PA levels. During exercise, t-PA levels increased due both to increased t-PA secretion and to decreased clearance secondary to reduced hepatic blood flow. The increase in t-PA secretion during exercise was directly proportional to the epinephrine concentration in blood with the same ratio of t-PA secretion to epinephrine as found during epinephrine infusion, suggesting that increased plasma epinephrine during exercise was the primary stimulus for t-PA secretion. Lastly, the simulation predicted that 6 months of endurance training produced a decrease in resting plasminogen activator inhibitor type 1 (PAI-1) secretion, resulting in less t-PA inhibition and an overall increase in active t-PA after training. Accurate analysis of the regulation of active t-PA levels in blood required simultaneous modeling of t-PA and PAI-1 secretion, hepatic clearance, and inhibition of t-PA by PAI-1.

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