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.
Highlights
Statins are a major group of lipid-lowering drugs that inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase [1,2]
We investigated whether mitochondrial function (e.g., O2 respiration, H2O2 emission, and Ca2+ retention capacity) was affected by in vivo atorvastatin treatment and aerobic exercise training in permeabilized myofibers
We demonstrated that atorvastatin-induced mitochondrial dysfunction was mitigated by exercise training
Summary
Statins are a major group of lipid-lowering drugs that inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase [1,2]. They are used in clinical trials to prevent atherosclerotic cardiovascular disease [3]. There is a growing body of literature that recognizes the importance of statins for patients older than 65 years with cardiovascular disease, who account for approximately 25% of the world’s population [4,5]. This suggests that the number of patients treated with statins will continue to increase; clinical research into the use of statins must be carried out. Despite the well-known positive and negative physiological effects, the exact mechanisms involved in the development of statin-induced myopathy remain unclear
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
