Effect of estradiol on tissue glycogen metabolism in exercised oophorectomized rats

1987 ◽  
Vol 63 (2) ◽  
pp. 492-496 ◽  
Author(s):  
Z. V. Kendrick ◽  
C. A. Steffen ◽  
W. L. Rumsey ◽  
D. I. Goldberg
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Sunflower Oil ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Glycogen Metabolism ◽  
Submaximal Exercise ◽  
Total Work ◽  
Glycogen Utilization ◽  
Glycogen Sparing

The effect of both physiological and pharmacological doses of estradiol on exercise performance and tissue glycogen utilization was determined in oophorectomized estradiol-replaced (ER) rats. Doses of beta-estradiol 3-benzoate (0.02, 0.04, 0.1, 0.2, 1, 2, 4, or 10 micrograms.0.1 ml of sunflower oil-1.100 g body wt-1) were injected 5 days/wk for 4 wk. Controls were sham injected (SI). After treatment, the animals were run to exhaustion on a motorized treadmill. ER animals receiving the 0.02-microgram dose ran significantly longer and completed more total work than the SI group. ER animals receiving doses of greater than or equal to 0.04 microgram ran longer and performed more work than the 0.02-microgram group. At exhaustion, myocardial glycogen content was significantly decreased in animals that were ER with less than or equal to 0.1 microgram, whereas those replaced with doses greater than 0.1 microgram utilized significantly less glycogen. With the 10-micrograms dose no significant decrease in heart glycogen content was observed at exhaustion. A submaximal 2-h run significantly reduced glycogen content in heart, red and white portions of the vastus lateralis, and the livers of SI animals. The latter effect was attenuated in skeletal muscle and liver, and there was no effect in the hearts of the ER animals receiving 2 micrograms. These data indicate that estradiol replacement in oophorectomized rats influenced myocardial glycogen utilization during exhaustive exercise and spared tissue glycogen during submaximal exercise. These glycogen sparing effects may have contributed to the significant improvements in exercise performance observed in this study.

Effect of estradiol on tissue glycogen metabolism and lipid availability in exercised male rats

1991 ◽  
Vol 71 (5) ◽  
pp. 1694-1699 ◽  
Author(s):  
Z. V. Kendrick ◽  
G. S. Ellis
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Exercise Performance ◽  
Glycogen Content ◽  
Day Treatment ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Male Rats ◽  
Plasma Lactate ◽  
Glycogen Utilization

The effect of 17 beta-estradiol 3-benzoate (10 micrograms.0.1 ml sunflower oil-1.100 g body wt-1) on exercise performance, tissue glycogen utilization, and lipid availability was determined in male rats. In experiment 1, estradiol or oil was administered 1 h or 1–6 days before a treadmill run to exhaustion. No differences in body weight between oil- and estradiol-administered animals were observed during the 6-day treatment. Animals receiving estradiol for 3–6 days ran significantly longer and completed more work than oil-administered animals. Significant degradation of red and white vastus muscle, myocardial, and liver glycogen was observed in all animals run to exhaustion. In experiment 2, animals were administered estradiol for 5 days and then run for 2 h. The submaximal run for 2 h significantly reduced tissue glycogen content in red and white vastus muscle, heart, and liver of oil-administered animals. The latter effect was attenuated in both vastus muscles, liver, and myocardial tissues in the estradiol-administered animals. Estradiol administration significantly increased plasma fatty acids and lowered plasma lactate during the submaximal run. These data indicate that when body weight remained constant between groups of male rats, estradiol administration for 3–6 days increased exercise performance. Furthermore, estradiol administration for 5 days resulted in greater lipid availability and less tissue glycogen utilization during submaximal running for 2 h.

Human Skeletal Muscle Glycogen Branching Enzyme Activities with Exercise and Training

1974 ◽  
Vol 52 (1) ◽  
pp. 119-122 ◽  
Author(s):  
A. W. Taylor ◽  
J. Stothart ◽  
M. A. Booth ◽  
R. Thayer ◽  
S. Rao
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Enzyme Activities ◽  
Vastus Lateralis ◽  
Submaximal Exercise ◽  
Relative Fitness ◽  
Vastus Lateralis Muscle ◽  
Branching Enzyme ◽  
Skeletal Muscle Glycogen ◽  
Glycogen Branching Enzyme

Sixteen healthy male subjects classified as sedentary (8) or active (8), exercised to exhaustion on a bicycle ergometer at a load requiring 70% of their maximal aerobic capacity. Biopsy samples of the vastus lateralis muscle were taken at rest and at the time of fatigue. A 12 week training program increased skeletal muscle glycogen content and branching enzyme activities twofold. The exhaustive submaximal exercise reduced the glycogen levels of the trained group to values similar to the fatigue levels of the non-trained subjects. Skeletal muscle glycogen branching enzyme activities decreased with submaximal exercise to fatigue in all groups. Maximal exercise to fatigue resulted in small increases in the activities of the enzyme. The results of the present study and a previous study (Taylor et al. 1972. Can. J. Physiol. Pharmacol. 50, 411–415) indicate that the activities of the glycogen synthesizing enzymes are highly correlated with the skeletal muscle resting glycogen concentration and the relative fitness of the subjects.

Progressive increase in human skeletal muscle AMPKα2 activity and ACC phosphorylation during exercise

2002 ◽  
Vol 282 (3) ◽  
pp. E688-E694 ◽  
Author(s):  
T. J. Stephens ◽  
Z.-P. Chen ◽  
B. J. Canny ◽  
B. J. Michell ◽  
B. E. Kemp ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Western Blots ◽  
Muscle Glycogen Content ◽  
Muscle Creatine

The effect of prolonged moderate-intensity exercise on human skeletal muscle AMP-activated protein kinase (AMPK)α1 and -α2 activity and acetyl-CoA carboxylase (ACCβ) and neuronal nitric oxide synthase (nNOSμ) phosphorylation was investigated. Seven active healthy individuals cycled for 30 min at a workload requiring 62.8 ± 1.3% of peak O2consumption (V˙o 2 peak) with muscle biopsies obtained from the vastus lateralis at rest and at 5 and 30 min of exercise. AMPKα1 activity was not altered by exercise; however, AMPKα2 activity was significantly ( P < 0.05) elevated after 5 min (∼2-fold), and further elevated ( P < 0.05) after 30 min (∼3-fold) of exercise. ACCβ phosphorylation was increased ( P < 0.05) after 5 min (∼18-fold compared with rest) and increased ( P< 0.05) further after 30 min of exercise (∼36-fold compared with rest). Increases in AMPKα2 activity were significantly correlated with both increases in ACCβ phosphorylation and reductions in muscle glycogen content. Fat oxidation tended ( P = 0.058) to increase progressively during exercise. Muscle creatine phosphate was lower ( P < 0.05), and muscle creatine, calculated free AMP, and free AMP-to-ATP ratio were higher ( P < 0.05) at both 5 and 30 min of exercise compared with those at rest. At 30 min of exercise, the values of these metabolites were not significantly different from those at 5 min of exercise. Phosphorylation of nNOSμ was variable, and despite the mean doubling with exercise, statistically significance was not achieved ( P = 0.304). Western blots indicated that AMPKα2 was associated with both nNOSμ and ACCβ consistent with them both being substrates of AMPKα2 in vivo. In conclusion, AMPKα2 activity and ACCβ phosphorylation increase progressively during moderate exercise at ∼60% of V˙o 2 peak in humans, with these responses more closely coupled to muscle glycogen content than muscle AMP/ATP ratio.

Human skeletal muscle malonyl-CoA at rest and during prolonged submaximal exercise

1996 ◽  
Vol 270 (3) ◽  
pp. E541-E544 ◽  
Author(s):  
L. M. Odland ◽  
G. J. Heigenhauser ◽  
G. D. Lopaschuk ◽  
L. L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
High Performance ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Submaximal Exercise ◽  
Acid Oxidation ◽  
Vastus Lateralis Muscle ◽  
Malonyl Coa

Previous literature has indicated that contraction-induced decreases in malonyl-CoA are instrumental in the regulation of fatty acid oxidation during prolonged submaximal exercise. This study was designed to measure malonyl-CoA in human vastus lateralis muscle at rest and during submaximal exercise. Eight males and one female cycled for 70 min (10 min at 40% and 60 min at 65% maximal O2 uptake). Needle biopsies were obtained at rest and at 10 min, 20 min, and 70 min of exercise. Malonyl-CoA content in preexercise biopsy samples determined by high-performance liquid chromatography (HPLC) was 1.53 +/- 0.18 micromol/kg dry mass (dm). Malonyl-CoA content did not change significantly during exercise (1.39 +/- 0.21 at 10 min, 1.46 +/- 0.14 at 20 min, and 1.22 +/- 0.15 micromol/kg dm at 70 min). In contrast, malonyl-CoA content determined by HPLC in perfused rat red gastrocnemius muscle decreased significantly during 20 min of stimulation at 0.7 Hz [3.44 +/- 0.54 to 1.64 +/- 0.23 nmol/g dm, (n=9)]. We conclude that human skeletal muscle malonyl-CoA content 1) is less than reported in rat skeletal muscle at rest, 2) does not decrease with prolonged submaximal exercise, and 3) is not predictive of increased fatty acid oxidation during exercise.

Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle

2005 ◽  
Vol 99 (3) ◽  
pp. 950-956 ◽  
Author(s):  
Andrew Creer ◽  
Philip Gallagher ◽  
Dustin Slivka ◽  
Bozena Jemiolo ◽  
William Fink ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Akt Signaling ◽  
Cellular Growth ◽  
Muscle Glycogen Content ◽  
Ribosomal S6 Kinase

Two pathways that have been implicated for cellular growth and development in response to muscle contraction are the extracellular signal-regulated kinase (ERK1/2) and Akt signaling pathways. Although these pathways are readily stimulated after exercise, little is known about how nutritional status may affect stimulation of these pathways in response to resistance exercise in human skeletal muscle. To investigate this, experienced cyclists performed 30 repetitions of knee extension exercise at 70% of one repetition maximum after a low (2%) or high (77%) carbohydrate (LCHO or HCHO) diet, which resulted in low or high (∼174 or ∼591 mmol/kg dry wt) preexercise muscle glycogen content. Muscle biopsies were taken from the vastus lateralis before, ∼20 s after, and 10 min after exercise. ERK1/2 and p90 ribosomal S6 kinase phosphorylation increased ( P ≤ 0.05) 10 min after exercise, regardless of muscle glycogen availability. Akt phosphorylation was elevated ( P < 0.05) 10 min after exercise in the HCHO trial but was unaffected after exercise in the LCHO trial. Mammalian target of rapamycin phosphorylation was similar to that of Akt during each trial; however, change or lack of change was not significant. In conclusion, the ERK1/2 pathway appears to be unaffected by muscle glycogen content. However, muscle glycogen availability appears to contribute to regulation of the Akt pathway, which may influence cellular growth and adaptation in response to resistance exercise in a low-glycogen state.

Liver and peripheral tissue glycogen metabolism in obese mice: effect of a mixed meal

1993 ◽  
Vol 265 (5) ◽  
pp. E743-E751
Author(s):  
C. Chen ◽  
P. F. Williams ◽  
I. D. Caterson
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Cardiac Muscle ◽  
White Adipose Tissue ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Glycogen Storage ◽  
Obese Mice ◽  
Entire Study

Glycogen metabolism in the liver, skeletal muscle, cardiac muscle, and white adipose tissue was studied in gold thioglucose (GTG) obese mice after fasting and during refeeding. Prolonged (48 h) fasted control and GTG mice were refed with standard laboratory diet for 24 h. During fasting and refeeding, the changes in glycogen content and the activity of glycogen synthase I and R and phosphorylase alpha in the liver were similar in lean and GTG mice. However, the glycogen storage in the livers from GTG mice was always greater than that in lean animals. In GTG mice the activity of liver glycogen synthase I and R was significantly higher than that in lean animals 3 and 6 h after refeeding. The activity of liver phosphorylase alpha in GTG mice was higher than that in lean mice after refeeding. There were no significant differences in the glycogen content of white adipose tissue, cardiac muscle, and skeletal muscle from lean and GTG mice during the entire study. The results of this study suggest that increased glycogen storage in the liver is a major alteration in nonoxidative glucose metabolism and contributes to the development of insulin resistance and glucose intolerance in GTG obese mice.

Effect of hypercorticism on regulation of skeletal muscle glycogen metabolism by epinephrine

1992 ◽  
Vol 262 (4) ◽  
pp. E434-E439 ◽  
Author(s):  
L. Coderre ◽  
A. K. Srivastava ◽  
J. L. Chiasson
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Activity Ratio ◽  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Dexamethasone Treatment ◽  
Fed State ◽  
Glycogen Concentration ◽  
Glycogen Synthase Activity

The effect of hypercorticism on the regulation of glycogen metabolism by epinephrine was examined in skeletal muscles using a hindlimb perfusion technique. Rats were injected with either saline or dexamethasone (0.4 mg.kg-1.day-1) for 14 days and were studied in the fed and fasted (24 h) states under saline or epinephrine (10(-7) M) treatment. In the fed state, dexamethasone administration did not affect basal glycogen concentration but decreased glycogen synthase activity ratio in white and red gastrocnemius muscles. Epinephrine failed to decrease glycogen content despite the expected activation of glycogen phosphorylase in the fed dexamethasone-treated rats. Dexamethasone treatment resulted in a threefold increase in the level of muscle adenosine, a phosphorylase a inhibitor. In control rats, fasting was associated with a decrease in muscle glycogen concentration (P less than 0.01) and with an increase in the glycogen synthase activity ratio. Dexamethasone treatment, however, totally abolished both the decreased muscle glycogen content and glycogen synthase activation observed in fasting controls. In the dexamethasone-treated group, fasting restored the glycogenolytic effect of epinephrine. Interestingly, it was associated with decreased muscle adenosine concentrations. These data indicate that, in the fed state, dexamethasone treatment inhibits skeletal muscle glycogenolysis in response to epinephrine despite phosphorylase activation and glycogen synthase inactivation. It is suggested that this abnormality could be due to the inhibition of phosphorylase a by increased muscle adenosine levels.

Skeletal muscle GLUT-4 and glucose uptake during exercise in humans

1994 ◽  
Vol 77 (3) ◽  
pp. 1565-1568 ◽  
Author(s):  
G. McConell ◽  
M. McCoy ◽  
J. Proietto ◽  
M. Hargreaves
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Muscle Glycogen ◽  
Protein Level ◽  
Glycogen Content ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Muscle Glycogen Content ◽  
Glut 4

The present study examined the relationship between total skeletal muscle GLUT-4 protein level and glucose uptake during exercise. Eight active non-endurance-trained men cycled at 72 +/- 1% peak pulmonary oxygen consumption for 40 min, with rates of glucose appearance and disappearance (Rd) determined by utilizing a primed continuous infusion of [3–3H]glucose commencing 2 h before exercise. Muscle glycogen content and utilization, citrate synthase activity, and total GLUT-4 protein were measured on muscle biopsy samples obtained from the vastus lateralis. A direct relationship existed between preexercise muscle glycogen content and glycogen utilization during exercise (r = 0.76, P < 0.05). Citrate synthase activity and glucose Rd at the end of exercise averaged 21.9 +/- 3.0 mumol.min-1.g-1 and 27.3 +/- 2.5 mumol.kg-1.min-1, respectively. There was a direct correlation between citrate synthase activity and GLUT-4 protein (r = 0.78, P < 0.05); however, at the end of exercise, glucose Rd was inversely related to both GLUT-4 (r = -0.89, P < 0.01) and citrate synthase activity (r = -0.72, P < 0.05). Plasma insulin, which decreased during exercise, was not related to glucose Rd. In conclusion, glucose uptake during 40 min of exercise at 72% peak pulmonary oxygen consumption was inversely related to the total muscle GLUT-4 protein level. This suggests that factors other than the total GLUT-4 protein level are important in the regulation of glucose uptake during exercise.

scholarly journals Effect of ginger extract ingestion on skeletal muscle glycogen contents and endurance exercise in male rats

2021 ◽  
Vol 25 (2) ◽  
pp. 15-19
Author(s):  
Satoshi Hattori ◽  
Naomi Omi ◽  
Zhou Yang ◽  
Moeka Nakamura ◽  
Masahiro Ikemoto
Keyword(s):  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Muscle Glycogen ◽  
Exercise Performance ◽  
Glycogen Content ◽  
Intermittent Exercise ◽  
Endurance Capacity ◽  
Ginger Extract ◽  
Muscle Glycogen Content ◽  
Skeletal Muscle Glycogen

[Purpose] Skeletal muscle glycogen is a determinant of endurance capacity for some athletes. Ginger is well known to possess nutritional effects, such as anti-diabetic effects. We hypothesized that ginger extract (GE) ingestion increases skeletal muscle glycogen by enhancing fat oxidation. Thus, we investigated the effect of GE ingestion on exercise capacity, skeletal muscle glycogen, and certain blood metabolites in exercised rats. [Methods] First, we evaluated the influence of GE ingestion on body weight and elevation of exercise performance in rats fed with different volumes of GE. Next, we measured the skeletal muscle glycogen content and free fatty acid (FFA) levels in GE-fed rats. Finally, we demonstrated that GE ingestion contributes to endurance capacity during intermittent exercise to exhaustion. [Results] We confirmed that GE ingestion increased exercise performance (p<0.05) and elevated the skeletal muscle glycogen content compared to the non- GE-fed (CE, control exercise) group before exercise (Soleus: p<0.01, Plantaris: p<0.01, Gastrocnemius: p<0.05). Blood FFA levels in the GE group were significantly higher than those in the CE group after exercise (p<0.05). Moreover, we demonstrated that exercise capacity was maintained in the CE group during intermittent exercise (p<0.05). [Conclusion] These findings indicate that GE ingestion increases skeletal muscle glycogen content and exercise performance through the upregulation of fat oxidation.

Interaction between clenbuterol and run training: effects on exercise performance and MLC isoform content

1996 ◽  
Vol 80 (3) ◽  
pp. 795-801 ◽  
Author(s):  
C. P. Ingalls ◽  
W. S. Barnes ◽  
S. B. Smith
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Myosin Light Chain ◽  
Polyacrylamide Gel Electrophoresis ◽  
Interval Training ◽  
Myofibrillar Protein ◽  
Total Work ◽  
Treadmill Test ◽  
Running Performance ◽  
Treatment Groups

The purpose of this study was to determine the separate and combined effects of clenbuterol (CB) administration and interval training on running performance and myosin light-chain (MLC) isoform expression in mouse skeletal muscle. Mice were randomly assigned to one of four treatment groups: 1) control (Con), 2) exercise (Ex), 3) drug (CB), or 4) exercise + drug (Ex + CB). CB and Ex + CB mice were given CB (1.6 mg/kg) orally 4 days/wk. Ex and Ex + CB mice were trained 4 days/wk on a motorized treadmill (3 sets of 3 min, 36-40 m/min, 10-17% grade, 30-s recovery). After 8 wk of treatment, exercise conditioning increased total work performed 58% in the Ex group during a run-to-exhaustion treadmill test, whereas CB decreased total work by 25% in the CB group; in combination with exercise training, CB treatment eliminated the Ex-induced increase in work. Polyacrylamide gel electrophoresis indicated that run training, CB treatment, or a combination did not (P = 0.01) promote changes in fast and slow MLC isoforms in the soleus, gastrocnemius, or tibialis anterior muscles. Although not different from each other after 8 wk, CB and Ex + CB treatments produced significantly greater values than Con and Ex for the following variables: muscle mass (17-46%), total protein (22-50%), and myofibrillar protein (19-53%). It was concluded that CB decreases exercise performance and that the combination of Ex and CB have antagonistic effects on running performance; the two treatments do not interact to diminish the anabolic effects of CB on skeletal muscle and do not alter MLC isoform profiles.

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