Epinephrine is unessential for stimulation of liver glycogenolysis during exercise

1985 ◽  
Vol 58 (2) ◽  
pp. 544-548 ◽  
Author(s):  
K. I. Carlson ◽  
J. C. Marker ◽  
D. A. Arnall ◽  
M. L. Terry ◽  
H. T. Yang ◽  
...  
Keyword(s):  
Pancreatic Beta Cells ◽  
Liver Glycogen ◽  
Plasma Glucagon ◽  
Lateral Gastrocnemius ◽  
White Region ◽  
Exercise Induced ◽  
Fast Twitch ◽  
Liver Glycogenolysis ◽  
Stimulation Of

To determine the role of adrenal medullary hormones in controlling the rate of liver glycogenolysis during exercise, adrenodemedullated (ADM) and sham-operated (SO) rats were run on a rodent treadmill at 21 m/min up a 15% grade for 0, 30, or 60 min. Rats were anesthetized by intravenous injection of pentobarbital sodium, and liver, muscle, and blood were collected and frozen. Liver glycogen decreased at similar rates in ADM and SO rats. Hepatic adenosine 3′,5′-cyclic monophosphate (cAMP), plasma glucagon, and plasma free fatty acids increased to the same extent in both ADM and SO rats. The adrenodemedullation caused a reduction in glycogenolysis in the fast-twitch white region of the quadriceps, soleus, and lateral gastrocnemius during exercise. The normal exercise-induced increase in blood glucose and lactate and the decline in plasma insulin were not observed in the demedullated rats. During submaximal exercise the principal targets for epinephrine released from the adrenal medulla appear to be pancreatic beta-cells and skeletal muscle and not the liver.

Role of plasma epinephrine in fasted exercising rats

1985 ◽  
Vol 248 (3) ◽  
pp. R302-R307 ◽  
Author(s):  
W. W. Winder ◽  
M. L. Terry ◽  
V. M. Mitchell
Keyword(s):  
Physiological Role ◽  
Quadriceps Muscle ◽  
Type I ◽  
Type Ii ◽  
Plasma Epinephrine ◽  
Lateral Gastrocnemius ◽  
White Region ◽  
Gastrocnemius Muscles ◽  
Fast Twitch

We have investigated the physiological role of the marked increase in plasma epinephrine that occurs in fasted exercising rats. Fasted adrenodemedullated (ADM) rats show a marked reduction in endurance run times compared with sham-operated (SO) controls. After running for 30 min at 21 m/min up a 10% grade, ADM rats' blood glucose was 2.9 +/- 0.1 mM vs. 4.3 +/- 0.2 mM in SO rats. At the same time, blood lactate was 3.0 +/- 0.2 mM in SO rats compared with 1.0 +/- 0.1 mM in ADM rats. Glycogenolysis was impaired in ADM rats in the fast-twitch white region of the quadriceps, lateral gastrocnemius, and soleus muscles but not in the fast-twitch red region of the quadriceps muscle. Hepatic adenosine 3',-5'-cyclic monophosphate was increased to the same extent in ADM and SO rats during exercise. Infusion of epinephrine into ADM rats during exercise corrected the hypoglycemia, restored lactate to normal, and stimulated glycogenolysis in soleus, white quadriceps, and lateral gastrocnemius muscles. Epinephrine-dependent glycogenolysis in contracting type I and noncontracting type II muscle fibers apparently provides essential quantities of lactate for hepatic gluconeogenesis in fasted exercising rats.

Effect of adrenodemedullation on metabolic responses to high-intensity exercise

1986 ◽  
Vol 251 (3) ◽  
pp. R552-R559
Author(s):  
J. C. Marker ◽  
D. A. Arnall ◽  
R. K. Conlee ◽  
W. W. Winder
Keyword(s):  
Soleus Muscle ◽  
High Intensity ◽  
Liver Glycogen ◽  
High Intensity Exercise ◽  
Metabolic Responses ◽  
Intense Exercise ◽  
Pentobarbital Sodium ◽  
Exercise Induced ◽  
Liver Glycogenolysis

To determine the role of epinephrine in glycogenolysis during high-intensity exercise, rats were adrenodemedullated (ADM) or sham operated (SHAM) and run for either 30 min at 38 m/min or for 5 min at 27, 38, or 48 m/min up a 15% grade. At the end of exercise the rats were anesthetized by intravenous injection of pentobarbital sodium. Liver, blood, and muscle samples were obtained. Plasma epinephrine values were 5.9 and 0.3 nM for SHAM and ADM animals, respectively, after 30 min of exercise. Liver glycogen decreased by 16 and 21 mg/g in the SHAM and ADM groups, respectively, and liver cAMP increased significantly in both groups. Glycogen in the soleus muscle decreased 80% in the SHAM but only 43% in the ADM animals after 30 min of exercise. The exercise-induced hyperglycemia observed in the SHAM animals was not present in the ADM animals. The responses of cyclic AMP, soleus glycogen, and blood glucose were similar in both the 5- and 30-min exercise groups. During intense exercise, epinephrine is unessential for stimulating liver glycogenolysis but does play an important role in stimulating glycogenolysis in the soleus muscle and in establishing exercise-induced hyperglycemia.

Catecholamines and exercise-induced glucagon and fatty acid mobilization in the rat

1975 ◽  
Vol 229 (2) ◽  
pp. 376-383 ◽  
Author(s):  
AS Luyckx ◽  
A Dresse ◽  
A Cession-Fossion ◽  
PJ Lefebvre
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Adrenergic Receptors ◽  
Sympathetic Stimulation ◽  
Plasma Glucagon ◽  
Beta Adrenergic Receptors ◽  
Adipose Cell ◽  
Exercise Induced ◽  
Fatty Acid Mobilization ◽  
Stimulation Of

Physical exercise in rats provokes an increase in plasma glucagon and free fatty acid concentrations. The persistence of exercise-induced glucagon stimulation in adrenodemedullated animals and conversely, its inhibition by immunosympathectomy, (-)-ropranolol, and pindolol substantiate the conclusion that stimulation of the alpha2 cells in exercise involves sympathetic stimulation of the beta-adrenergic receptors. The reduction of free fatty acid mobilization by immunosympathectomy and (-)-propranolol and its persistence after adrenodemedullation suggest that it is similarly mediated, at least in part, by adipose cell beta-sympathetic receptors.

Metabolic role of the exercise-induced increment in epinephrine in the dog

1988 ◽  
Vol 255 (4) ◽  
pp. E428-E436 ◽  
Author(s):  
J. M. Moates ◽  
D. B. Lacy ◽  
R. E. Goldstein ◽  
A. D. Cherrington ◽  
D. H. Wasserman
Keyword(s):  
Glucose Production ◽  
Plasma Glucagon ◽  
Metabolic Role ◽  
Exercise Period ◽  
Exercise Induced ◽  
Glucagon And Insulin ◽  
Induced Changes ◽  
Response To Exercise ◽  
Rest And Exercise

The role of the exercise-induced increment in epinephrine was studied in five adrenalectomized (ADX) and in six normal dogs (C). Experiments consisted of an 80-min equilibration period, a 40-min basal period, and a 150-min exercise period. ADX were studied with epinephrine replaced to basal levels during rest and to increased levels during exercise to simulate its normal rise (HE) and on a separate day with epinephrine maintained at basal levels throughout the study (BE). Cortisol was replaced during rest and exercise in ADX so as to simulate the levels seen in C. Glucose was infused as needed in ADX to maintain the glycemia evident during exercise in C. Glucose production (Ra) and utilization (Rd) were assessed isotopically. In C, epinephrine had risen by 95 +/- 25 pg/ml by the end of exercise. In HE, the increment in epinephrine (117 +/- 29 pg/ml) was similar to that seen in C, whereas in BE epinephrine fell by 18 +/- 9 pg/ml. Basal norepinephrine levels were 139 +/- 9, 260 +/- 25, and 313 +/- 33 pg/ml in C, HE, and BE, respectively. In response to exercise, norepinephrine increased by nearly twofold in all protocols. Basal and exercise-induced changes in plasma glucagon and insulin were similar in C and ADX. Ra increased similarly in C (5.3 +/- 0.6 mg.kg-1.min-1) and HE (4.9 +/- 0.6 mg.kg-1.min-1). In BE, Ra rose normally for the initial 90 min but then declined resulting in a rise of only 2.9 +/- 0.5 mg.kg-1.min-1 after 150 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Liver glycogenolysis during exercise in adrenodemedullated male and female rats

1986 ◽  
Vol 251 (6) ◽  
pp. R1151-R1155
Author(s):  
W. W. Winder ◽  
S. F. Loy ◽  
D. S. Burke ◽  
S. J. Hawkes
Keyword(s):  
Adrenergic Receptor ◽  
Mature Female ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Epinephrine ◽  
Male And Female ◽  
Male And Female Rats ◽  
Liver Glycogenolysis ◽  
Stimulation Of

Previous studies have shown that adrenodemedullation has no effect on the rate of liver glycogenolysis during exercise in male rats. Mature female rats have been reported to have a higher hepatic beta-adrenergic receptor activity than do male rats of the same age. The present study was undertaken to determine the role of plasma epinephrine in stimulating liver glycogenolysis during exercise in female rats. Both male and female rats were adrenodemedullated or sham operated. Three weeks later rats were run for 60 min at 21 m/min up a 15% grade. The rate of liver glycogenolysis during exercise was not affected by adrenodemedullation in either female rats or male rats. Hepatic adenosine 3',5'-cyclic monophosphate increased to approximately the same extent in sham operated as in adrenodemedullated female rats during exercise. Adrenodemedullation caused a significant reduction in the amount of glycogen utilized by the soleus muscle and in the degree of hyperglycemia during exercise. We conclude that epinephrine is unessential for stimulation of liver glycogenolysis during exercise in either male or female rats.

scholarly journals Protective role of extracellular chloride in fatigue of isolated mammalian skeletal muscle

2004 ◽  
Vol 287 (3) ◽  
pp. C762-C770 ◽  
Author(s):  
Simeon P. Cairns ◽  
Vladimir Ruzhynsky ◽  
Jean-Marc Renaud
Keyword(s):  
Protective Role ◽  
Mammalian Skeletal Muscle ◽  
Tetanic Stimulation ◽  
Tetanic Force ◽  
Mammalian Muscle ◽  
Force Depression ◽  
Slow Twitch ◽  
Exercise Induced ◽  
Fast Twitch

A possible role of extracellular Cl− concentration ([Cl−]o) in fatigue was investigated in isolated skeletal muscles of the mouse. When [Cl−]o was lowered from 128 to 10 mM, peak tetanic force was unchanged, fade was exacerbated (wire stimulation electrodes), and a hump appeared during tetanic relaxation in both nonfatigued slow-twitch soleus and fast-twitch extensor digitorum longus (EDL) muscles. Low [Cl−]o increased the rate of fatigue 1) with prolonged, continuous tetanic stimulation in soleus, 2) with repeated intermittent tetanic stimulation in soleus or EDL, and 3) to a greater extent with repeated tetanic stimulation when wire stimulation electrodes were used rather than plate stimulation electrodes in soleus. In nonfatigued soleus muscles, application of 9 mM K+ with low [Cl−]o caused more rapid and greater tetanic force depression, along with greater depolarization, than was evident at normal [Cl−]o. These effects of raised [K+]o and low [Cl−]o were synergistic. From these data, we suggest that normal [Cl−]o provides protection against fatigue involving high-intensity contractions in both fast- and slow-twitch mammalian muscle. This phenomenon possibly involves attenuation of the depolarization caused by stimulation- or exercise-induced run-down of the transsarcolemmal K+ gradient.

Liver glycogenolysis during exercise without a significant increase in cAMP

1979 ◽  
Vol 237 (3) ◽  
pp. R147-R152
Author(s):  
W. W. Winder ◽  
J. Boullier ◽  
R. D. Fell
Keyword(s):  
Blood Glucose ◽  
Liver Glycogen ◽  
Plasma Glucagon ◽  
Major Increase ◽  
Induced Changes ◽  
Liver Glycogenolysis

Liver glycogenolysis may be controlled by glucagon or catecholamine-induced changes in cAMP or by cAMP-independent mechanisms. The purpose of these experiments was to determine whether an increase in liver cAMP occurs during exercise at a time when the rate of liver glycogenolysis is greatly accelerated. Rats were taught to run on a treadmill 10 min/day for 6 wk. They were then run continuously for periods of time ranging from 0 to 120 min at 0.8 mph up a 15% grade. Liver glycogen was depleted by the end of 90 min in fed animals and by 20 min in overnight-fasted animals. Liver cAMP was not significantly increased in fed animals during the first 60 min of exercise. The major increase in liver cAMP occurred after liver glycogen was depleted, at which time the rat must rely entirely on gluconeogenesis for maintenance of blood glucose. This increase in cAMP corresponded to large increases in plasma glucagon and catecholamines. We conclude that liver glycogenolysis in the rat can occur during exercise independently from significant detectable increases in cAMP concentrations.

Importance of glucagon in mediating epinephrine-induced hyperglycemia in alloxan-diabetic dogs

1981 ◽  
Vol 241 (4) ◽  
pp. E328-E335 ◽  
Author(s):  
G. Perez ◽  
F. W. Kemmer ◽  
H. L. Lickley ◽  
M. Vranic
Keyword(s):  
Glucose Concentration ◽  
Glucose Production ◽  
Plasma Glucagon ◽  
Marginal Increase ◽  
Lipolytic Effect ◽  
Diabetic Dogs ◽  
Stimulation Of

In normal dogs epinephrine stimulates glucose production (Ra) independently of glucagon. To investigate the role of this interaction in diabetes, epinephrine (0.1 micrograms . kg-1 . min-1) was infused for 90 min in five alloxan-diabetic dogs in the presence or absence of somatostatin (0.1 micrograms . kg-1 . min-1). In response to epinephrine, glycemia rose by 40% reflecting a near maximal (122%) increase in Ra. Plasma glucagon (IRG) rose to 953 pg/ml, whereas insulin (IRI) increased minimally. When somatostatin was infused with epinephrine to prevent the rise of IRG and IRI, there was only a marginal increase of glucose concentration (12%) and production (38%). The effect of somatostatin was reversed by infusing glucagon (10 ng . kg-1 . min-1) together with epinephrine and somatostatin into five additional alloxan-diabetic dogs. Increments in IRG, glycemia, and Ra were fully reestablished. A 100% FFA increase was observed in all three groups, indicating that the lipolytic effect of epinephrine was independent of glucagon. In conclusion, in diabetic dogs, in contrast to normal dogs, epinephrine induced a marked and prolonged increase in glucose concentration and production mostly through a stimulation of IRG secretion.

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