Document Detail


Age-associated declines in mitochondrial biogenesis and protein quality control factors are minimized by exercise training.
MedLine Citation:
PMID:  22573103     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial Vo(2max), reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome-c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.
Authors:
Erika Koltai; Nikolett Hart; Albert W Taylor; Sataro Goto; Jenny K Ngo; Kelvin J A Davies; Zsolt Radak
Related Documents :
9638963 - Comparison of endothelin-1 levels at rest and during exercise between patients with car...
2662743 - Comparison of atenolol and nifedipine in chronic stable angina pectoris.
16793333 - Plastic changes in the human h-reflex pathway at rest following skillful cycling training.
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-05-09
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  303     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-07-16     Completed Date:  2012-10-02     Revised Date:  2013-12-18    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R127-34     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / physiology
Aging / metabolism*
Animals
Male
Membrane Proteins / metabolism
Mitochondria, Muscle / metabolism*
Mitochondrial Proteins / metabolism*
Models, Animal
Muscle, Skeletal / metabolism*
Nuclear Respiratory Factor 1 / metabolism
Physical Conditioning, Animal*
Rats
Rats, Wistar
Transcription Factors / metabolism
Grant Support
ID/Acronym/Agency:
3R01-ES 003598-22S2/ES/NIEHS NIH HHS; R01 ES003598/ES/NIEHS NIH HHS; R01-ES003598/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Proteins; 0/Mitochondrial Proteins; 0/Nuclear Respiratory Factor 1; 0/Tfam protein, rat; 0/Transcription Factors; 0/Ttc11 protein, rat; 0/mitofusin 1 protein, rat
Comments/Corrections

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


Previous Document:  Protective effects of isothiocyanates on blood-CSF barrier disruption induced by oxidative stress.
Next Document:  Do mice selectively bred for high locomotor activity have a greater reliance on lipids to power subm...