Time course of insulin sensitivity and skeletal muscle glycogen synthase activity after a single bout of exercise in horses

2007 ◽  
Vol 103 (3) ◽  
pp. 1063-1069 ◽  
Author(s):  
Shannon E. Pratt ◽  
Raymond J. Geor ◽  
Lawrence L. Spriet ◽  
L. Jill McCutcheon
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Muscle Glycogen ◽  
Time Course ◽  
Glycogen Content ◽  
Activity Ratio ◽  
Glycogen Synthase ◽  
Muscle Glycogen Content ◽  
Skeletal Muscle Glycogen ◽  
Single Bout

The time course of insulin sensitivity, skeletal muscle glycogen and GLUT4 content, and glycogen synthase (GS) activity after a single bout of intense exercise was examined in eight horses. On separate days, a euglycemic-hyperinsulinemic clamp (EHC) was undertaken at 0.5, 4, or 24 h after exercise or after 48 h of rest [control (Con)]. There was no increase in mean glucose infusion rate (GIR) with exercise (0.5-, 4-, and 24-h trials), and GIR was significantly decreased at 0.5 h postexercise (GIR: 8.6 ± 2.7, 6.7 ± 2.0, 9.0 ± 2.0, and 10.6 ± 2.2 mg·kg−1·min−1 for Con and at 0.5, 4, and 24 h, respectively). Before each EHC, muscle glycogen content (mmol glucosyl units/kg dry muscle) was higher ( P < 0.05) for Con (565 ± 102) than for other treatments (317 ± 84, 362 ± 79, and 382 ± 74 for 0.5, 4, and 24 h, respectively) and muscle GLUT4 content was unchanged. Pre-EHC active-to-total GS activity ratio was higher ( P < 0.05) at 0.5, 4, and 24 h after exercise than in Con. Post-EHC active GS and GS activity ratio were higher ( P < 0.05) in Con and at 24 h. There was a significant inverse correlation ( r = −0.43, P = 0.02) between glycogen content and GS activity ratio but no relationship between GS activity and GIR. The lack of increase in insulin sensitivity, determined by EHC, after exercise that resulted in a significant reduction in muscle glycogen content is consistent with the slow rate of muscle glycogen resynthesis observed in equine studies.

scholarly journals Skeletal muscle glycogen content in patients with cirrhosis

Hepatology ◽  
1994 ◽  
Vol 20 (1) ◽  
pp. 135-141 ◽  
Author(s):  
Oliver Selberg ◽  
Eva Radoch ◽  
Gerhard Franz Walter ◽  
Manfred James Müller
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Muscle Glycogen Content ◽  
Skeletal Muscle Glycogen

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.

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

1992 ◽  
Vol 262 (4) ◽  
pp. E427-E433 ◽  
Author(s):  
L. Coderre ◽  
A. K. Srivastava ◽  
J. L. Chiasson
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Content ◽  
Activity Ratio ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Glycogen Metabolism ◽  
Dexamethasone Treatment ◽  
Muscle Glycogen Content ◽  
Glycogen Synthase Activity ◽  
Muscle Glycogen Concentration

The effects of hypercorticism on the regulation of glycogen metabolism by insulin in skeletal muscles was examined by using the hindlimb perfusion technique. Rats were injected daily with either saline or dexamethasone (0.4 mg.kg-1.day-1) for 14 days and were studied in the fed or fasted (24 h) state under saline or insulin (1 mU/ml) treatment. In fed controls, insulin resulted in glycogen synthase activation and in enhanced glycogen synthesis. In dexamethasone-treated animals, basal muscle glycogen concentration remained normal, but glycogen synthase activity ratio was decreased in white and red gastrocnemius and plantaris muscles. Furthermore, insulin failed to activate glycogen synthase and glycogen synthesis. In the controls, fasting was associated with decreased glycogen concentrations and with increased glycogen synthase activity ratio in all four groups of muscles (P less than 0.01). Dexamethasone treatment, however, completely abolished the decrease in muscle glycogen content as well as the augmented glycogen synthase activity ratio associated with fasting. Insulin infusion stimulated glycogen synthesis in fasted controls but not in dexamethasone-treated rats. These data therefore indicate that dexamethasone treatment inhibits the stimulatory effect of insulin on glycogen synthase activity and on glycogen synthesis. Furthermore, hypercorticism suppresses the decrease in muscle glycogen content associated with fasting.

scholarly journals Hepatic and skeletal muscle glycogen content in rats treated with metformin and submitted to acute exercise by swimming

2018 ◽  
Vol 31 (2) ◽  
pp. 355
Author(s):  
Vitor Alexandre Pezolato ◽  
Marcos Almeida Marques ◽  
Fabio Marcos Abreu ◽  
Nataly Mendes Silva ◽  
Ronaldo Júlio Baganha ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Acute Exercise ◽  
Glycogen Content ◽  
Muscle Glycogen Content ◽  
Skeletal Muscle Glycogen

O objetivo deste estudo foi avaliar o comportamento das reservas glicogênicas de ratos, submetidos a uma condição de exercício agudo (50 minutos de natação na intensidade leve), após o tratamento com metformina. Quarenta ratos Wistar (180-200g) adultos foram divididos em quatro grupos (tratados ou não por quinze dias) e assim representados: Controle; Exercício agudo por natação (realizaram uma sessão de natação, sendo 50 minutos na intensidade leve); Tratado com metformina (receberam o fármaco metformina na dosagem de 1,4 mg/ml, durante o período experimental; Tratados com metformina e submetidos a condição exercício agudo por natação (receberam o fármaco metformina na dosagem de 1,4 mg/ml e realizaram uma sessão de natação, sendo 50 minutos na intensidade leve). O exercício agudo diminuiu as reservas glicogênicas, já os animais tratados com metformina, apresentaram um aumento em suas reservas glicogênicas musculares e hepáticas em relação ao grupo que realizou o exercício sem suplementação (p0,05). O tratamento com metformina promoveu melhora nas condições energéticas e menor resposta ao estresse, sugerindo ser uma importante ferramenta farmacológica para a potencialização da performance.

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.

scholarly journals Exercise training-induced adaptations associated with increases in skeletal muscle glycogen content

FEBS Journal ◽  
2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
Yasuko Manabe ◽  
Katja S. C. Gollisch ◽  
Laura Holton ◽  
Young-Bum Kim ◽  
Josef Brandauer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Muscle Glycogen Content ◽  
Skeletal Muscle Glycogen

scholarly journals Postmarathon paradox: insulin resistance in the face of glycogen depletion

1996 ◽  
Vol 270 (2) ◽  
pp. E336-E343 ◽  
Author(s):  
J. A. Tuominen ◽  
P. Ebeling ◽  
R. Bourey ◽  
L. Koranyi ◽  
A. Lamminen ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Lipid Oxidation ◽  
Muscle Glycogen ◽  
Glucose Oxidation ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Glucose Disposal ◽  
Glycogen Depletion ◽  
Muscle Glycogen Content ◽  
Control Study

Acute physical exercise enhances insulin sensitivity in healthy subjects. We examined the effect of a 42-km marathon run on insulin sensitivity and lipid oxidation in 19 male runners. In the morning after the marathon run, basal serum free fatty acid concentration was 2.2-fold higher, muscle glycogen content 37% lower (P < 0.01), glycogen synthase fractional activity 56% greater (P < 0.01), and glucose oxidation reduced by 43% (P < 0.01), whereas lipid oxidation was increased by 55% (P < 0.02) compared with the control study. During euglycemic-hyperinsulinemic clamp, whole body glucose disposal was decreased by 12% (P < 0.01) because of a 36% lower glucose oxidation rate (P < 0.05), whereas the rate of lipid oxidation was 10-fold greater (P < 0.02) than in the control study. After the marathon, muscle glycogen content correlated positively with lipid oxidation (r = 0.60, P < 0.05) and maximal aerobic power (Vo2peak; r = 0.61, P < 0.05). Vo2peak correlated positively with basal lipid oxidation (r = 0.57, P < 0.05). In conclusion, 1) after the marathon run, probably because of increased lipid oxidation, the insulin-stimulated glucose disposal is decreased despite muscle glycogen depletion and the activation of glycogen synthase; 2) the contribution of lipid oxidation in energy expenditure is increased in proportion to physical fitness; 3) these adaptations of fuel homeostasis may contribute to the maintenance of physical performance after prolonged exercise.

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