Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress

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) produ...

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Vydané v:Journal of applied physiology (1985) Ročník 111; číslo 5; s. 1477
Hlavní autori: Bouitbir, Jamal, Charles, Anne-Laure, Rasseneur, Laurence, Dufour, Stéphane, Piquard, François, Geny, Bernard, Zoll, Joffrey
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.11.2011
Predmet:
Animals
Atorvastatin Calcium
Cell Respiration - drug effects
Cholesterol - blood
Creatine Kinase - blood
Glucose Transporter Type 4 - genetics
Glucose Transporter Type 4 - metabolism
Glycogen - metabolism
Heptanoic Acids - pharmacology
Male
Mitochondria - drug effects
Mitochondria - physiology
Muscle, Skeletal - drug effects
Muscle, Skeletal - metabolism
Oxidative Stress - drug effects
Oxidative Stress - physiology
Physical Conditioning, Animal - physiology
Physical Endurance - drug effects
Pyrroles - pharmacology
Rats
Rats, Wistar
Reactive Oxygen Species - metabolism
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
ISSN:1522-1601, 1522-1601
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Shrnutí: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.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1522-1601
1522-1601
DOI:10.1152/japplphysiol.00107.2011