Document Detail

Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress.
MedLine Citation:
PMID:  21852406     Owner:  NLM     Status:  MEDLINE    
Physical exercise exacerbates the cytotoxic effects of statins in skeletal muscle. Mitochondrial impairments may play an important role in the development of muscular symptoms following statin treatment. Our objective was to characterize mitochondrial function and reactive oxygen species (ROS) production in skeletal muscle after exhaustive exercise in atorvastatin-treated rats. The animals were divided into four groups: resting control (CONT; n = 8) and exercise rats (CONT+EXE; n = 8) as well as resting (ATO; n = 10) and exercise (ATO+EXE; n = 8) rats that were treated with atorvastatin (10 mg·kg(-1)·day(-1) for 2 wk). Exhaustive exercise showed that the distance that was covered by treated animals was reduced (P < 0.05). Using dihydroethidium staining, we showed that the ROS level was increased by 60% in the plantaris muscle of ATO compared with CONT rats and was highly increased in ATO+EXE (226%) compared with that in CONT+EXE rats. The maximal mitochondrial respiration (V(max)) was decreased in ATO rats compared with that in CONT rats (P < 0.01). In CONT+EXE rats, V(max) significantly increased compared with those in CONT rats (P < 0.05). V(max) was significantly lower in ATO+EXE rats (-39%) compared with that in CONT+EXE rats (P < 0.001). The distance that was covered by rats significantly correlated with V(max) (r = 0.62, P < 0.01). The glycogen content was decreased in ATO, CONT+EXE, and ATO+EXE rats compared with that in CONT rats (P < 0.05). GLUT-4 mRNA expression was higher after exhaustive exercise in CONT+EXE rats compared with the other groups (P < 0.05). Our results show that exhaustive exercise exacerbated metabolic perturbations and ROS production in skeletal muscle, which may reduce the exercise capacity and promote the muscular symptoms in sedentary atorvastatin-treated animals.
Jamal Bouitbir; Anne-Laure Charles; Laurence Rasseneur; Stéphane Dufour; François Piquard; Bernard Geny; Joffrey Zoll
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Publication Detail:
Type:  Journal Article     Date:  2011-08-18
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  111     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-18     Completed Date:  2012-06-05     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:  1477-83     Citation Subset:  IM    
Université de Strasbourg, EA3072, Faculté de Médecine & Faculté des Sciences du Sport, Strasbourg, France.
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MeSH Terms
Cell Respiration / drug effects
Cholesterol / blood
Creatine Kinase / blood
Glucose Transporter Type 4 / genetics,  metabolism
Glycogen / metabolism
Heptanoic Acids / pharmacology*
Mitochondria / drug effects*,  physiology
Muscle, Skeletal / drug effects,  metabolism
Oxidative Stress / drug effects*,  physiology
Physical Conditioning, Animal / physiology*
Physical Endurance / drug effects
Pyrroles / pharmacology*
RNA, Messenger / biosynthesis,  genetics
Rats, Wistar
Reactive Oxygen Species / metabolism
Reg. No./Substance:
0/Glucose Transporter Type 4; 0/Heptanoic Acids; 0/Pyrroles; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/Slc2a4 protein, rat; 57-88-5/Cholesterol; 9005-79-2/Glycogen; A0JWA85V8F/atorvastatin; EC Kinase

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

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