5′‐AMP‐activated protein kinase regulates skeletal muscle glycogen content and ergogenics

2005 ◽  
Vol 19 (7) ◽  
pp. 771-779 ◽  
Author(s):  
Brian R. Barnes ◽  
Stephan Glund ◽  
Yun Chau Long ◽  
Göran Hjälm ◽  
Leif Andersson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Muscle Glycogen Content ◽  
Skeletal Muscle Glycogen ◽  
Amp Activated Protein Kinase

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

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 The roles of IL-6 in the regulation of glucose homeostasis

2009 ◽  
Vol 34 (1) ◽  
pp. 83-84
Author(s):  
Jenny E. Gusba
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Muscle Contraction ◽  
Glucose Transport ◽  
Glucose Homeostasis ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Glycogen Resynthesis ◽  
Muscle Glycogen Content ◽  
Tnf Α

This thesis examined the roles of interleukin (IL)-6 in the regulation of glucose homeostasis, with a specific focus on skeletal muscle. Study 1 sought to determine whether muscle glycogen content is a stimulus for the production of IL-6, examining the periods during and after exercise. The relationship between IL-6 and muscle glycogen content was measured during similar bouts of exhaustive exercise on 2 occasions that resulted in large increases in muscle messenger (m)RNA for IL-6 and circulating levels of IL-6. On 1 occasion, subjects received carbohydrate during recovery to facilitate rates of glycogen resynthesis. During exercise, subjects performed similar bouts of exercise, such that differences in an individual’s glycogen levels between trials could be compared with differences in IL-6. No correlation was detected between the net change in glycogen content and the net change in plasma IL-6 or IL-6 mRNA from rest to exhaustion. Moreover, when the difference within subjects at exhaustion in IL-6 and glycogen was compared, there was no correlation between the 2 variables. During recovery, although carbohydrate intake significantly increased glycogen resynthesis, there was no change in postexercise IL-6 mRNA level or plasma IL-6 concentration. Therefore, glycogen was not the sole regulator of IL-6 production in skeletal muscle. Study 2 examined the direct effect of IL-6 and tumor necrosis factor (TNF)-α on glucose transport and the phosphorylation of key signalling proteins with or without insulin and during rodent muscle contraction. Under basal conditions, IL-6 increased glucose transport in association with an increase in 5′AMP-activated protein kinase (AMPK) and AS160 phosphorylation, but IL-6 decreased insulin-stimulated glucose transport via a reduction in phosphorylation of calcium–calmodulin-dependent protein kinase (CaMK)II and AS160. A novel finding generated from these experiments was the direct involvement of IL-6 in contraction-mediated glucose transport. In the case of muscle contraction, IL-6 was found to increase the phosphorylation of CaMKII and AS160. This research suggests that the activation of CaMKII is involved in the actions of IL-6 under insulin-stimulated and contraction-mediated conditions. Furthermore, AS160 was identified as a common signalling intermediate, influenced by IL-6. It also suggests that AS160 may be a point of convergence for multiple signalling pathways. Finally, the actions of TNF-α mimicked those of IL-6, except during contraction, where TNF-α had no significant effect on glucose transport and attenuated the effects of IL-6.

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

Genetic model for the chronic activation of skeletal muscle AMP-activated protein kinase leads to glycogen accumulation

2007 ◽  
Vol 292 (3) ◽  
pp. E802-E811 ◽  
Author(s):  
Laura Barré ◽  
Christine Richardson ◽  
Michael F. Hirshman ◽  
Joseph Brozinick ◽  
Steven Fiering ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Genetic Model ◽  
Glycogen Synthase ◽  
Dominant Negative ◽  
Α Subunit ◽  
Chronic Activation ◽  
Amp Activated Protein Kinase

The AMP-activated protein kinase (AMPK) is an important metabolic sensor/effector that coordinates many of the changes in mammalian tissues during variations in energy availability. We have sought to create an in vivo genetic model of chronic AMPK activation, selecting murine skeletal muscle as a representative tissue where AMPK plays important roles. Muscle-selective expression of a mutant noncatalytic γ1 subunit (R70Qγ) of AMPK activates AMPK and increases muscle glycogen content. The increase in glycogen content requires the presence of the endogenous AMPK catalytic α-subunit, since the offspring of cross-breeding of these mice with mice expressing a dominant negative AMPKα subunit have normal glycogen content. In R70Qγ1-expressing mice, there is a small, but significant, increase in muscle glycogen synthase (GSY) activity associated with an increase in the muscle expression of the liver isoform GSY2. The increase in glycogen content is accompanied, as might be expected, by an increase in exercise capacity. Transgene expression of this mutant AMPKγ1 subunit may provide a useful model for the chronic activation of AMPK in other tissues to clarify its multiple roles in the regulation of metabolism and other physiological processes.

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