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Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress.
J Appl Physiol (1985). 2011 Nov; 111(5):1477-83.JA

Abstract

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.

Authors+Show Affiliations

Université de Strasbourg, EA3072, Faculté de Médecine & Faculté des Sciences du Sport, Strasbourg, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

21852406

Citation

Bouitbir, Jamal, et al. "Atorvastatin Treatment Reduces Exercise Capacities in Rats: Involvement of Mitochondrial Impairments and Oxidative Stress." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 111, no. 5, 2011, pp. 1477-83.
Bouitbir J, Charles AL, Rasseneur L, et al. Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress. J Appl Physiol (1985). 2011;111(5):1477-83.
Bouitbir, J., Charles, A. L., Rasseneur, L., Dufour, S., Piquard, F., Geny, B., & Zoll, J. (2011). Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress. Journal of Applied Physiology (Bethesda, Md. : 1985), 111(5), 1477-83. https://doi.org/10.1152/japplphysiol.00107.2011
Bouitbir J, et al. Atorvastatin Treatment Reduces Exercise Capacities in Rats: Involvement of Mitochondrial Impairments and Oxidative Stress. J Appl Physiol (1985). 2011;111(5):1477-83. PubMed PMID: 21852406.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress. AU - Bouitbir,Jamal, AU - Charles,Anne-Laure, AU - Rasseneur,Laurence, AU - Dufour,Stéphane, AU - Piquard,François, AU - Geny,Bernard, AU - Zoll,Joffrey, Y1 - 2011/08/18/ PY - 2011/8/20/entrez PY - 2011/8/20/pubmed PY - 2012/6/6/medline SP - 1477 EP - 83 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J Appl Physiol (1985) VL - 111 IS - 5 N2 - 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. SN - 1522-1601 UR - https://www.unboundmedicine.com/medline/citation/21852406/Atorvastatin_treatment_reduces_exercise_capacities_in_rats:_involvement_of_mitochondrial_impairments_and_oxidative_stress_ L2 - https://journals.physiology.org/doi/10.1152/japplphysiol.00107.2011?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -