• Journal of Acupuncture Research
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• v.28 no.6
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• pp.19-26
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• 2011

Objectives : Although moxibustion is one of the most frequently used methods in oriental medicine, effect of moxibustion in myofiber regeneration and muscle fatigability is hardly studied. This study was researched to observe the effect of moxibustion in myofiber regeneration and muscle fatigability. Methods : We reviewed studies which contained moxibustion and published after 2000s in Pubmed. We also reviewed domestic studies in RISS, KISS and DBPIA, but only three studies were researched. Results : In myofiber regeneration, moxibuston has improved blood flow in muscle tissue and recover tissue injuries fast. Especially, moxibustion trigger an increse of HSP levels, which protect the cell against irreversible damage, apoptosis and death. Thus, that helps to stimulate myofiber regeneration. In many studies, as moxibustion stimulate PMRs and decrease fatigue substances, such as lactate acid and creatinine, so moxibustion is considered to be effective to recover and prevent muscle fatigability. Based on such effects, moxibustion is considered to have an effect on TPs, but have been hardly studied. Conclusions : Although Moxibution is considered to be effective in myofiber regeneration and muscle fatigability, futher study is needed.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.3
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• pp.456-464
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• 2008

Avian and mammalian skeletal muscles exhibit a remarkable ability to adjust to physiological stressors induced by growth, exercise, injury and disease. The process of muscle recovery following injury and myonuclear accretion during growth is attributed to a small population of satellite cells located beneath the basal lamina of the myofiber. Several metabolic factors contribute to the activation of satellite cells in response to stress mediated by illness, injury or aging. This review will describe the regenerative properties of satellite cells, the processes of satellite cell activation and highlight the potential role of satellite cells in skeletal muscle growth, tissue engineering and meat production.

• Korean Journal of Exercise Nutrition
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• v.24 no.2
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• pp.11-21
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• 2020

[Purpose] Doxorubicin (DOX) is a potent anti-cancer drug that appears to have severe myotoxicity due to accumulation. The skeletal muscle has a regeneration capacity through satellite cell activation when exposed to extracellular stimulus or damage. Endurance exercise (EXE) is a therapeutic strategy that improves pathological features and contributes to muscle homeostasis. Thus, this study investigated the effect of EXE training in mitigating chronic DOX-induced myotoxicity. [Methods] Male C57BL/6J mice were housed and allowed to acclimatize with free access to food and water. All the mice were randomly divided into four groups: sedentary control (CON, n=9), exercise training (EXE, n=9), doxorubicin treatment (DOX, n=9), doxorubicin treatment and exercise training (DOX+EXE, n=9) groups. The animals were intraperitoneally injected with 5 mg/kg/week of DOX treatment for 4 weeks, and EXE training was initiated for treadmill adaptation for 1 week and then performed for 4 weeks. Both sides of the soleus (SOL) muscle tissues were dissected and weighed after 24 hours of the last training sessions. [Results] DOX chemotherapy induced an abnormal myofiber's phenotype and transition of myosin heavy chain (MHC) isoforms. The paired box 7 (PAX7) and myoblast determination protein 1 (MYOD) protein levels were triggered by DOX, while no alterations were shown for the myogenin (MYOG). DOX remarkably impaired the a-actinin (ACTN) protein, but the EXE training seems to repair it. DOX-induced myotoxicity stimulated the expression of the forkhead box O3 (FOXO3a) protein, which was accurately controlled and adjusted by the EXE training. However, the FOXO3a-mediated downstream markers were not associated with DOX and EXE. [Conclusion] EXE postconditioning provides protective effects against chronic DOX-induced myotoxicity, and should be recommended to alleviate cancer chemotherapy-induced late-onset myotoxicity.