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Exercise Training Protects against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats.
J Clin Med. 2020 Jul 19; 9(7)JC

Abstract

Statins are used to prevent and treat atherosclerotic cardiovascular disease, but they also induce myopathy and mitochondrial dysfunction. Here, we investigated whether exercise training prevents glucose intolerance, muscle impairment, and mitochondrial dysfunction in the skeletal muscles of Wistar rats treated with atorvastatin (5 mg kg-1 day-1) for 12 weeks. The rats were assigned to the following three groups: the control (CON), atorvastatin-treated (ATO), and ATO plus aerobic exercise training groups (ATO+EXE). The ATO+EXE group exhibited higher glucose tolerance and forelimb strength and lower creatine kinase levels than the other groups. Mitochondrial respiratory and Ca2+ retention capacity was significantly lower in the ATO group than in the other groups, but exercise training protected against atorvastatin-induced impairment in both the soleus and white gastrocnemius muscles. The mitochondrial H2O2 emission rate was relatively higher in the ATO group and lower in the ATO+EXE group, in both the soleus and white gastrocnemius muscles, than in the CON group. In the soleus muscle, the Bcl-2, SOD1, SOD2, Akt, and AMPK phosphorylation levels were significantly higher in the ATO+EXE group than in the ATO group. In the white gastrocnemius muscle, the SOD2, Akt, and AMPK phosphorylation levels were significantly higher in the ATO+EXE group than in the ATO group. Therefore, exercise training might regulate atorvastatin-induced muscle damage, muscle fatigue, and mitochondrial dysfunction in the skeletal muscles.

Authors+Show Affiliations

Department of Physiology, National Research Laboratory for Mitochondrial Signaling, BK21 Plus Project Team, College of Medicine, Smart Marine Therapeutics Center, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea.Department of Kinesiology, Inha University, Incheon 22212, Korea.Department of Kinesiology, Inha University, Incheon 22212, Korea.Department of Kinesiology, Inha University, Incheon 22212, Korea.Department of Physiology, National Research Laboratory for Mitochondrial Signaling, BK21 Plus Project Team, College of Medicine, Smart Marine Therapeutics Center, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea.Department of Kinesiology, Inha University, Incheon 22212, Korea.Department of Pharmacology and Medicinal Toxicology Research Center, Inha University School of Medicine, Incheon 22212, Korea.Department of Physiology, College of Medicine, Kyung Hee University, Seoul 02447, Korea.Department of Leisure Sports, Seoil University, Seoul 02192, Korea.Department of Physiology, National Research Laboratory for Mitochondrial Signaling, BK21 Plus Project Team, College of Medicine, Smart Marine Therapeutics Center, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea.Department of Kinesiology, Inha University, Incheon 22212, Korea.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32707695

Citation

Seo, Dae Yun, et al. "Exercise Training Protects Against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats." Journal of Clinical Medicine, vol. 9, no. 7, 2020.
Seo DY, Heo JW, No MH, et al. Exercise Training Protects against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats. J Clin Med. 2020;9(7).
Seo, D. Y., Heo, J. W., No, M. H., Yoo, S. Z., Ko, J. R., Park, D. H., Kang, J. H., Kim, C. J., Jung, S. J., Han, J., & Kwak, H. B. (2020). Exercise Training Protects against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats. Journal of Clinical Medicine, 9(7). https://doi.org/10.3390/jcm9072292
Seo DY, et al. Exercise Training Protects Against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats. J Clin Med. 2020 Jul 19;9(7) PubMed PMID: 32707695.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exercise Training Protects against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats. AU - Seo,Dae Yun, AU - Heo,Jun-Won, AU - No,Mi-Hyun, AU - Yoo,Su-Zi, AU - Ko,Jeong Rim, AU - Park,Dong-Ho, AU - Kang,Ju-Hee, AU - Kim,Chang-Ju, AU - Jung,Su-Jeen, AU - Han,Jin, AU - Kwak,Hyo-Bum, Y1 - 2020/07/19/ PY - 2020/06/10/received PY - 2020/06/30/revised PY - 2020/07/16/accepted PY - 2020/7/26/entrez PY - 2020/7/28/pubmed PY - 2020/7/28/medline KW - exercise KW - mitochondria KW - myopathy KW - skeletal muscle KW - statin JF - Journal of clinical medicine JO - J Clin Med VL - 9 IS - 7 N2 - Statins are used to prevent and treat atherosclerotic cardiovascular disease, but they also induce myopathy and mitochondrial dysfunction. Here, we investigated whether exercise training prevents glucose intolerance, muscle impairment, and mitochondrial dysfunction in the skeletal muscles of Wistar rats treated with atorvastatin (5 mg kg-1 day-1) for 12 weeks. The rats were assigned to the following three groups: the control (CON), atorvastatin-treated (ATO), and ATO plus aerobic exercise training groups (ATO+EXE). The ATO+EXE group exhibited higher glucose tolerance and forelimb strength and lower creatine kinase levels than the other groups. Mitochondrial respiratory and Ca2+ retention capacity was significantly lower in the ATO group than in the other groups, but exercise training protected against atorvastatin-induced impairment in both the soleus and white gastrocnemius muscles. The mitochondrial H2O2 emission rate was relatively higher in the ATO group and lower in the ATO+EXE group, in both the soleus and white gastrocnemius muscles, than in the CON group. In the soleus muscle, the Bcl-2, SOD1, SOD2, Akt, and AMPK phosphorylation levels were significantly higher in the ATO+EXE group than in the ATO group. In the white gastrocnemius muscle, the SOD2, Akt, and AMPK phosphorylation levels were significantly higher in the ATO+EXE group than in the ATO group. Therefore, exercise training might regulate atorvastatin-induced muscle damage, muscle fatigue, and mitochondrial dysfunction in the skeletal muscles. SN - 2077-0383 UR - https://www.unboundmedicine.com/medline/citation/32707695/Exercise_Training_Protects_against_Atorvastatin_Induced_Skeletal_Muscle_Dysfunction_and_Mitochondrial_Dysfunction_in_the_Skeletal_Muscle_of_Rats_ L2 - https://www.mdpi.com/resolver?pii=jcm9072292 DB - PRIME DP - Unbound Medicine ER -
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