Document Detail


Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle.
MedLine Citation:
PMID:  15879168     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 (approximately 174 or approximately 591 mmol/kg dry wt) preexercise muscle glycogen content. Muscle biopsies were taken from the vastus lateralis before, approximately 20 s after, and 10 min after exercise. ERK1/2 and p90 ribosomal S6 kinase phosphorylation increased (P < or = 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.
Authors:
Andrew Creer; Philip Gallagher; Dustin Slivka; Bozena Jemiolo; William Fink; Scott Trappe
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Publication Detail:
Type:  Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.     Date:  2005-05-05
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  99     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-08-16     Completed Date:  2005-10-27     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  950-6     Citation Subset:  IM    
Affiliation:
Human Performance Laboratory, Ball State Univ., Muncie, IN 47306, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Dietary Carbohydrates / metabolism
Glycogen / metabolism*
Humans
Knee Joint / physiology
Male
Mitogen-Activated Protein Kinase 1 / metabolism*
Mitogen-Activated Protein Kinase 3 / metabolism*
Muscle Contraction / physiology*
Muscle, Skeletal / physiology*
Physical Endurance / physiology*
Protein-Serine-Threonine Kinases / metabolism*
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-akt
Signal Transduction / physiology*
Grant Support
ID/Acronym/Agency:
AG-18409/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Carbohydrates; 0/Proto-Oncogene Proteins; 9005-79-2/Glycogen; EC 2.7.11.1/AKT1 protein, human; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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