http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Effects of acute exercise on mitochondrial dynamics and mitophagy in the rat skeletal muscles
Su-Zi Yoo,Jun-Won Heo,Mi-Hyun No,Dong-Ho Park,Ju-Hee Kang,Hyo-Bum Kwak 한국운동재활학회 2018 한국운동재활학회 학술대회 Vol.2018 No.10
The current study aims to investigate how mitochondrial dynamics and mitophagy are changed by a single bout aerobic exercise. Four month Fischer 344 rats were divided into 2 groups: sedentary group (SED, n=6) and acute exercise group (AEX, n=6). Rats were performed in a single bout treadmill exercise for 60 minutes. Mitochondrial fusion (e.g., Mfn1, Mfn2, Opa1), mitochondrial fission (e.g., Drp1, Fis1), and mitophagy (e.g., Parkin, Pink1, BNIP3, LC3) were measured in the permeabilized skeletal muscles (e.g., soleus, white gastrocnemius). Mitochondrial fusion-related protein (Opa1) was decreased in soleus of AEX compared with SED. Also, mitochondrial fission-related protein (Drp1) was reduced in soleus of AEX compared with SED. Similarly, in soleus muscle of AEX, mitochondrial autophagy-related protein (LC3) was decreased compared with SED. However, other proteins of mitochondrial dynamics and mitophagy didn’t show significant difference in soleus and white gastrocnemius. A single bout aerobic exercise showed tissue-specific results in mitochondrial dynamics and mitophagy. It demonstrates that acute aerobic exercise may improve mitochondrial function predominantly in soleus muscle (type I fiber). However, further research is needed to understand the cellular and molecular mechanism by which acute aerobic exercise affects mitochondrial dynamics and mitophagy in different types of muscle fibers.
Su-Zi Yoo,Mi-Hyun No,Jun-won Heo,Dae-Yun Seo,Su-Jeen Jung,Hyo-Bum Kwak 한국운동재활학회 2019 한국운동재활학회 학술대회 Vol.2019 No.05
The purpose of this study was to determine the effects of in vivo atorvastatin, L-carnosine, and resistance exercise training on mitochondria-mediated apoptotic signaling in the rat skeletal muscle. Male Wistar rats were randomly assigned to control (CON), 5 mg atorvastatin treated group (STAT), 5 mg atorvastatin plus resistance (ladder climbing) exercise training group (STAT + EX), 5 mg atorvastatin plus L-carnosine treatment group (STAT + CAR), and 5 mg atorvastatin treatment plus resistance exercise training plus L-carnosine treatment group (STAT + EX + CAR) (n=12 rats/group). Animals were administered via oral gavage with a vehicle, 5 mg/kg/day atorvastatin, and 250 mg/kg/day L-carnosine dissolved in 0.25 % w/v hydroxypropyl methylcellulose for 12 weeks. Also, animals were trained for 12 weeks on a ladder with a gradient of about 80 degrees. Mitochondria-mediated apoptotic signaling (e.g., Bax, Bcl-2, mPTP opening, cytochrome c, cleaved caspase-3) were measured in skeletal muscles (e.g., soleus, white gastocnemius). Bax , pro-apoptotic protein, was increased in STAT in both soleus and white gastrocnemius and decreased in STAT + EX, STAT + CAR, and STAT + EX + CAR in both soleus and white gastrocnemius. In contrast, Bcl-2, anti-apoptotic protein, was elevated in STAT + EX, STAT + CAR, and STAT + EX + CAR in both soleus and white gastrocnemius and reduced in STAT in both soleus and white gastrocnemius. Also, mPTP opening, cytochrome c, and cleaved caspase-3 showed the same patterns like Bax in both soleus and white gastrocnemius. These data demonstrated that skeletal muscle mitochondria-mediated apoptotic signaling was impaired by atorvastatin treatment for 12 weeks. However, L-carnosine and resistance exercise training protected against statin-induced mitochondria-mediated apoptotic signaling in the rat skeletal muscle, suggesting that both L-carnosine and resistance exercise training play a pivotal role in ameliorating apoptosis in statin-induced myopathy.
Yoo, Su-Zi,No, Mi-Hyun,Heo, Jun-Won,Park, Dong-Ho,Kang, Ju-Hee,Kim, Joon-Hee,Seo, Dae-Yun,Han, Jin,Jung, Su-Jeen,Kwak, Hyo-Bum Korean Continence Society 2019 International Neurourology Journal Vol.23 No.S1
<P><B>Purpose</B></P><P>This study aimed to investigate the effects of single-bout exercise on mitochondrial function, dynamics (fusion, fission), and mitophagy in cardiac and skeletal muscles.</P><P><B>Methods</B></P><P>Fischer 344 rats (4 months old) were randomly divided into the control (CON) or acute exercise (EX) group (n=10 each). The rats performed a single bout of treadmill exercise for 60 minutes. Mitochondrial function (e.g., O<SUB>2</SUB> respiration, H<SUB>2</SUB>O<SUB>2</SUB> emission, Ca<SUP>2+</SUP> retention capacity), mitochondrial fusion (e.g., Mfn1, Mfn2, Opa1), mitochondrial fission (e.g., Drp1, Fis1), and mitophagy (e.g., Parkin, Pink1, LC3II, Bnip3) were measured in permeabilized cardiac (e.g., left ventricle) and skeletal (e.g., soleus, white gastrocnemius) muscles.</P><P><B>Results</B></P><P>Mitochondrial O<SUB>2</SUB> respiration and Ca<SUP>2+</SUP> retention capacity were significantly increased in all tissues of the EX group compared with the CON group. Mitochondrial H<SUB>2</SUB>O<SUB>2</SUB> emissions showed tissue-specific results; the emissions showed no significant differences in the left ventricle or soleus (type I fibers) but was significantly increased in the white gastrocnemius (type II fibers) after acute exercise. Mitochondrial fusion and fission were not altered in any tissues of the EX group. Mitophagy showed tissue-specific differences: It was not changed in the left ventricle or white gastrocnemius, whereas Parkin and LC3II were significantly elevated in the soleus muscle.</P><P><B>Conclusions</B></P><P>A single bout of aerobic exercise may improve mitochondrial function (e.g., O<SUB>2</SUB> respiration and Ca<SUP>2+</SUP> retention capacity) in the heart and skeletal muscles without changes in mitochondrial dynamics or mitophagy.</P>
Effects of aerobic exercise training on hypertrophy signaling in old rat heart
Mi-Hyun No,Su-Zi Yoo,Jun-Won Heo,Hyo-Bum Kwak 한국운동재활학회 2019 한국운동재활학회 학술대회 Vol.2019 No.05
Aging is a significant risk factor for cardiovascular diseases and plays a critical role in the pathologic mechanisms of cardiac failure or diseases. A characteristic of the typical physiological change of cardiac muscle by aging is the reduction of heart function due to reactive hypertrophy. The purpose of this study was to determine whether aerobic exercise training attenuates aging-induced hypertrophy signaling in the rat heart. Fischer 344 rats were divided into young sedentary (YS; n=10, 4 months) group, young exercise (YE; n=10, 4months) group, old sedentary (OS; n=10, 20 months) group, and old exercise (OE; n=10, 20 months) group. Exercise training groups ran on a treadmill at 15 m/min (young) or 10 m/min (old), 45 min/day, 5 days/week for 8 weeks. Left ventricle was extracted to determine the protein levels of Akt/mTOR signaling pathway (Akt, mTOR, p70s6k, and 4E-BP1) through Western immunoblot analysis. The protein levels of Akt/mTOR signaling were not significantly increased in the OS compared with YS. However, Akt/mTOR signaling levels were significantly increased by exercise training. The data demonstrated that aerobic exercise training activated the Akt/mTOR signaling pathway of rat heart, suggesting that aerobic exercise training may induce muscle growth in left ventricle, leading to cardiac muscle hypertrophy in rats.
Effects of exercise training on mitochondrial function in atorvastatin-treated rat heart
Jun-Won Heo,Mi-Hyun No,Su-Zi Yoo,Dong-Ho Park,Ju-Hee Kang,Su-Jeen Jung,Hyo-Bum Kwak 한국운동재활학회 2018 한국운동재활학회 학술대회 Vol.2018 No.10
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.