Document Detail


Loaded wheel running and muscle adaptation in the mouse.
MedLine Citation:
PMID:  15734890     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Voluntary cage wheel exercise has been used extensively to determine the physiological adaptation of cardiac and skeletal muscle in mice. In this study, we tested the effect of different loading conditions on voluntary cage wheel performance and muscle adaptation. Male C57Bl/6 mice were exposed to a cage wheel with no-resistance (NR), low-resistance (LR), or high-resistance (HR) loads for 7 wk. Power output was elevated (3-fold) under increased loading (LR and HR) conditions compared with unloaded (NR) exercise training. Only unloaded (NR) exercise induced an increase in heart mass, whereas only loaded (LR and HR) exercise training induced an increase in skeletal (soleus) muscle mass. Moreover, unloaded and loaded exercise training had a differential impact on the cross-sectional area of muscle fibers, depending on the type of myosin heavy chain expressed by each fiber. The biochemical adaptation of the heart was characterized by a decrease in genes associated with pathological (but not physiological) cardiac hypertrophy and a decrease in calcineurin expression in all exercise groups. In addition, transcriptional activity of myocyte enhancer factor-2 (MEF-2) was significantly decreased in the hearts of the LR group as determined by a MEF-2-dependent transgene driving the expression of beta-galactosidase. Phosphorylation of glycogen synthase kinase-3beta, protein kinase B (Akt), and p70 S6 kinase was increased only in the hearts of the NR group, consistent with the significant increase in cardiac mass. In conclusion, unloaded and loaded cage wheel exercise have a differential impact on cage wheel performance and muscle (cardiac and skeletal) adaptation.
Authors:
John P Konhilas; Ulrika Widegren; David L Allen; Angelika C Paul; Allison Cleary; Leslie A Leinwand
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2005-02-25
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  289     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-06-17     Completed Date:  2005-08-11     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H455-65     Citation Subset:  IM; S    
Affiliation:
Dept. of Molecular, Cellular, and Developmental Biology, Univ. of Colorado, Campus Box 347, Boulder, CO 80309-0347, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological*
Animals
Calcineurin / metabolism
DNA-Binding Proteins / metabolism
Glycogen Synthase Kinase 3 / metabolism
Heart / physiology
Male
Mice
Mice, Inbred C57BL
Motor Activity / physiology*
Muscle, Skeletal / physiology*
Myocardium / metabolism
Myogenic Regulatory Factors
Phosphorylation
Physical Exertion / physiology*
Protein-Serine-Threonine Kinases / metabolism
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-akt
RNA, Messenger / metabolism
Ribosomal Protein S6 Kinases, 70-kDa / metabolism
Signal Transduction
Transcription Factors / metabolism
Grant Support
ID/Acronym/Agency:
F32 HL-70509/HL/NHLBI NIH HHS; HL-56510/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Myogenic Regulatory Factors; 0/Proto-Oncogene Proteins; 0/RNA, Messenger; 0/Transcription Factors; 0/myocyte-specific enhancer-binding factor 2; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.26/Glycogen Synthase Kinase 3; EC 3.1.3.16/Calcineurin

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


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