Document Detail


Exercise early in life in rats born small does not normalize reductions in skeletal muscle PGC-1α in adulthood.
MedLine Citation:
PMID:  22354784     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have previously shown that 4 wk of exercise training early in life normalizes the otherwise greatly reduced pancreatic β-cell mass in adult male rats born small. The aim of the current study was to determine whether a similar normalization in adulthood of reduced skeletal muscle mitochondrial biogenesis markers and alterations in skeletal muscle lipids of growth-restricted male rats occurs following early exercise training. Bilateral uterine vessel ligation performed on day 18 of gestation resulted in Restricted offspring born small (P < 0.05) compared with both sham-operated Controls and a sham-operated Reduced litter group. Offspring remained sedentary or underwent treadmill running from 5-9 (early exercise) or 20-24 (later exercise) wk of age. At 24 wk of age, Restricted and Reduced litter offspring had lower (P < 0.05) skeletal muscle peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein expression compared with Control offspring. Early exercise training had the expected effect of increasing skeletal muscle markers of mitochondrial biogenesis, but, at this early age (9 wk), there was no deficit in Restricted and Reduced litter skeletal muscle mitochondrial biogenesis. Unlike our previous observations in pancreatic β-cell mass, there was no "reprogramming" effect of early exercise on adult skeletal muscle such that PGC-1α was lower in adult Restricted and Reduced litter offspring irrespective of exercise training. Later exercise training increased mitochondrial biogenesis in all groups. In conclusion, although the response to exercise training remains intact, early exercise training in rats born small does not have a reprogramming effect to prevent deficits in skeletal muscle markers of mitochondrial biogenesis in adulthood.
Authors:
Rhianna C Laker; Mary E Wlodek; Glenn D Wadley; Linda A Gallo; Peter J Meikle; Glenn K McConell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-02-21
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  302     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-16     Completed Date:  2012-07-17     Revised Date:  2012-08-30    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1221-30     Citation Subset:  IM    
Affiliation:
Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / anatomy & histology,  physiology
Age Factors
Animals
Birth Weight / physiology*
Citrate (si)-Synthase / metabolism
Disease Models, Animal
Female
Fetal Growth Retardation / physiopathology*
Male
Mitochondria / metabolism
Muscle, Skeletal / anatomy & histology,  physiology*
Organ Size
Physical Conditioning, Animal / physiology*
Pregnancy
Prenatal Exposure Delayed Effects / physiopathology*
Rats
Rats, Inbred WKY
Trans-Activators / deficiency,  metabolism*
Triglycerides / metabolism
Chemical
Reg. No./Substance:
0/Ppargc1a protein, mouse; 0/Trans-Activators; 0/Triglycerides; EC 2.3.3.1/Citrate (si)-Synthase

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