earticle

영어

Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors), which are cholesterol-lowering drugs widely used in the treatment of cardiovascular disease, cause adverse side effects in skeletal muscle ranging from fatigue to fatal rhabdomyolysis, leading to mitochondrial dysfunction. However, whether statins affect heart mitochondrial function is not clear. In addition, the effects of aerobic exercise training on mitochondrial function in statin-treated heart have not been clearly elucidated. Therefore, the purpose of this study was to determine the effects of in vivo atorvastatin treatment and aerobic exercise training on mitochondrial function (e.g., mitochondrial O2 respiration, H2O2 emission, Ca2+ retention capacity) in the rat heart. Male Wistar rats were randomly assigned to control (CON), 5 mg atorvastatin-treated group (STAT), and 5 mg atorvastatin treatment plus aerobic exercise group (STAT + EX) (N=12 rats/group). Animals were administered via oral gavage with a vehicle, 5 mg/kg/day atorvastatin dissolved in 0.25 % w/v hydroxypropyl methylcellulose for 12 weeks. The left ventricle (LV) was permeabilized by saponin for determination of mitochondrial respiratory capacity, mitochondrial H2O2 emission, and Ca2+ retention capacity. LV mitochondrial O2 respiration and Ca2+ retention capacity were not affected by 12 weeks treatment of atorvastatin. However, aerobic exercise training improved mitochondrial O2 respiration and Ca2+ retention capacity in LV. In contrast, mitochondrial H2O2 emission and Ca2+ retention capacity were reduced by exercise training. These data demonstrated that although LV mitochondrial function was not affected by atorvastatin treatment for 12 weeks, aerobic exercise training improved the mitochondrial function in the rat LV, suggesting that aerobic exercise training plays a pivotal role in improving mitochondrial function in the heart.