Document Detail


Age is no barrier to muscle structural, biochemical and angiogenic adaptations to training up to 24 months in female rats.
MedLine Citation:
PMID:  15845588     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ageing is associated with reduced transport and utilization of O(2), diminishing exercise tolerance. Reductions may occur in cardiac output (delivery), and skeletal muscle oxidative capacity (utilization). To determine the reversibility of the declines in the muscular determinants of these limitations, skeletal muscle morphological, angiogenic and biochemical responses to acute exercise and endurance training were investigated in female Fischer 344 rats (n = 42; seven groups of six rats) aged 6 (Y) and 24 (O) months compared with resting untrained controls (Y(C), O(C)). Treadmill training lasted 8 weeks (10 deg incline, 1 h per day, 5 days per week). Two groups ran at maximum tolerated speeds (Y(TR), O(TR)), while an additional Y group (Y(TM)) trained at O(TR) speed. There was no effect of age on vascular endothelial growth factor gene expression in gastrocnemius muscles after acute exercise. Similarly, age did not impair the effects of training, with increases (P < 0.05; +/-s.e.m.) occurring in all of the following: 1 h exercise running speed (Y(TR) 92 +/- 4% versus O(TR) 140 +/- 25%); citrate synthase (Y(TR) 37 +/- 8% versus O(TR) 97 +/- 33%) and beta-hydroxyacyl-CoA-dehydrogenase (Y(TR) 31 +/- 7%, versus O(TR) 72 +/- 24%) activities; and capillary-to-fibre ratio (Y(TR) 5.2 +/- 0.2% versus O(TR) 8.1 +/- 0.2%). However, Y(TM) muscle was unchanged in each measure compared with Y(C). In conclusion, these muscular responses to training were (1) not reduced by ageing, but (2) dependent on relative and not absolute work rate, since, at the same speed, O(TR) rats showed greater changes than Y(TM). Therefore, increases in exercise tolerance and muscle adaptations are not impaired in female rats up to 24 months of age, and require a smaller absolute exercise stimulus (than young) to be manifest.
Authors:
H B Rossiter; R A Howlett; H H Holcombe; P L Entin; H E Wagner; P D Wagner
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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:  2005-04-21
Journal Detail:
Title:  The Journal of physiology     Volume:  565     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-06-24     Completed Date:  2005-09-12     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  993-1005     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Physiology, University of California, San Diego, La Jolla 92093-0623, USA. h.b.rossiter@leeds.ac.uk
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MeSH Terms
Descriptor/Qualifier:
3-Hydroxyacyl CoA Dehydrogenases / metabolism
Adaptation, Physiological / physiology*
Aging / physiology*
Animals
Citrate (si)-Synthase / metabolism
Female
Mitochondria / enzymology
Muscle Fibers, Skeletal / enzymology
Muscle, Skeletal / blood supply,  cytology,  physiology*
Neovascularization, Physiologic / physiology*
Physical Conditioning, Animal / physiology*
RNA, Messenger
Rats
Rats, Inbred F344
Running / physiology
Vascular Endothelial Growth Factor A / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
AR40155/AR/NIAMS NIH HHS; HL17731/HL/NHLBI NIH HHS; //Wellcome Trust
Chemical
Reg. No./Substance:
0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; EC 1.1.1.35/3-Hydroxyacyl CoA Dehydrogenases; EC 2.3.3.1/Citrate (si)-Synthase
Comments/Corrections

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