• Title/Summary/Keyword: 근위축

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The Effect of Atrophy of the Inpraspinatus on Strength and ROM in Shoulder Joint of Male Volleyball Players (배구선수들의 극하근 근위축이 어깨 관절 회전근력과 운동범위에 미치는 영향)

  • Lee, Byoung-Kwon
    • Korean Journal of Applied Biomechanics
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    • v.19 no.3
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    • pp.549-555
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    • 2009
  • The purpose of this study was to quantify the isokinetic peak torque and range of motion at the shoulder in 8 national male volleyball players who played during the 2008 professional leagues. In this study the strength and range of motion data in the internal rotation(IR) and external rotation(ER) of shoulder joint were measured with isokinetic measurement system(Biodex Inc) and motion analysis system (Simi motion system Inc.) from 3 volleyball players with atrophy of the infrasupinatus and 5 volleyball players without atrophy of the infraspinatus. Peak torques were determined using isokinetic measurement on the shoulder joint rotator at the point of angular velocities of $60^{\circ}$/s. Significant difference was found in the peak torque, IR / ER ratio and the range of motion through assessment of the dominant shoulder between two groups. we recommended functional exercises that improve both external rotators strength and stretching exercise for internal rotation in the dominant side during the prevention programs in volleyball players.

Does Sarcopenic Obesity Affect Physical Function and Physical Fitness of Korean Older Women? (근위축비만이 국내 여성고령자의 신체기능과 체력에 미치는 영향)

  • Hong, Seung-youn
    • 한국노년학
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    • v.30 no.3
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    • pp.831-842
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    • 2010
  • BACKGROUND: Sarcopenic obesity(SO), a condition of the reduction in muscle mass paired with an increased fat mass has been paid attention because of its association with disability in later life. A few evidence, however, has reported the association with these factors. PURPOSE: To explore the association among SO, physical function and fitness in older women. METHOD: 257 older women(age of 74) were recruited from Y city and 7 physical functions and 4 fitness tests were measured. Participants were classified into one of four groups based on their body fat and muscle mass: Normal group (GR-A), high fat(GR-B), sarcopenia(GR-C), and sarcopenic obese(GR-D). GLMand LSD-test were conducted with SPSS 12.0. RESULTS: Chair stand, arm-curl, back-scratch, 2-min steps of GR-A was higher than GR-C and GR-D(p<.05). One-leg stand of GR-A was higher than GR-D(p<.01) and of GR-C was higher than GR-D(p<.01).8ft-TUG of GR-D was lower than GR-A(p<.01). Grip strength, knee extension of GR-A was higher than that of GR-C and GR-D(p<.01) and knee flexion of GR-A was also higher than that of GR-C and GR-D(p<.01). CONCLUSION: Based on our findings, we conclude that SO is significantly associated with lower physical function and fitness in older Korean women, which alarm the risk of frailty induced by SO.

Induction of Muscle Atrophy by Dexamethasone and Hydrogen Peroxide in Differentiated C2C12 Myotubes (C2C12 근관세포에서 dexamethasone 및 hydrogen peroxide에 의한 근위축 유도)

  • Park, Cheol;Jeong, Jin-Woo;Choi, Yung Hyun
    • Journal of Life Science
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    • v.27 no.12
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    • pp.1479-1485
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    • 2017
  • Muscle atrophy due to aging, starvation, and various chronic diseases leads to a decrease in muscle fiber area and density due to reduced muscle protein synthesis and increased protein breakdown. This study investigated the effect of dexamethasone and hydrogen peroxide on the induction of muscle atrophy and expression of atrophy-related genes in differentiated C2C12 myotubes. C2C12 myoblasts were differentiated into myotubes in differentiation medium. During myoblast differentiation, muscle-specific transcription factors, such as myogenin, and MyoD expression increased. Differentiated C2C12 myotubes exposed to noncytotoxic levels of dexamethasone and hydrogen peroxide showed a decrease in myotube diameter, which was associated with up-regulation of muscle-specific ubiquitin ligases, such as muscle atrophy F-box (MAFbx)/atrogin-1 and muscle RING finger-1 (MuRF1), and down-regulation of myogenin and MyoD. These results demonstrated that dexamethasone and hydrogen peroxide induced atrophy through regulation of muscle-specific ubiquitin ligases and muscle-specific transcription factors in C2C12 myotubes. In this study, we confirmed the process of differentiation of C2C12 myoblasts into myotubes in in vitro experiments in the presence of atrophy. This muscle atrophy model of C2C12 cells induced by dexamethasone or hydrogen peroxide seems suited to studies of the mechanism of muscle atrophy suppression and to exploit the experiment for excavating new muscle atrophy.

Ethanol Extract of Mori Folium Inhibits AICAR-induced Muscle Atrophy Through Inactivation of AMPK in C2C12 Myotubes (C2C12 근관세포에서 상엽에 의한 AMPK의 불활성화와 AICAR로 유도된 근위축 억제의 연관성에 관한 연구)

  • Lee, Yu Sung;Kim, Hong Jae;Jeong, Jin-Woo;Han, Min-Ho;Hong, Su Hyun;Choi, Yung Hyun;Park, Cheol
    • Journal of Life Science
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    • v.28 no.4
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    • pp.435-443
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    • 2018
  • AMP-activated protein kinase (AMPK) functions as a metabolic master through regulating and restoring cellular energy balance. In skeletal muscle, AMPK increases myofibril protein degradation through the expression of muscle-specific ubiquitin ligases. Mori Folium, the leaf of Morus alba, is a traditional medicinal herb with various pharmacological functions; however, the effects associated with muscle atrophy have not been fully identified. In this study, we confirmed the effects of AMPK activation by examining the effects of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an activator of AMPK, on the induction of atrophy and expression of atrophy-related genes in C2C12 myotubes. We also investigated the effects of the ethanol extract of Mori Folium (EEMF) on the recovery of AICAR-induced muscle atrophy in C2C12 myotubes. It was found that exposure to AICAR resulted in the stimulation of Forkhead box O3a (FOXO3a); an up-regulation of muscle-specific ubiquitin ligases such as Muscle Atrophy F-box (MAFbx)/atrogin-1 and muscle RING finger-1 (MuRF1), and a down-regulation of muscle-specific transcription factors, such as MyoD and myogenin; with the activation of AMPK. In addition, AICAR without cytotoxicity indicated a decrease in diameter of C2C12 myotubes. However, treatment with EEMF significantly suppressed AICAR-induced muscle atrophy of C2C12 myotubes in a dose-dependent manner as confirmed by a decrease in myotube diameter, which is associated with a reversed stimulation of FOXO3a by the inhibition of AMPK activation. These results indicate that the activation of AMPK by AICAR induces muscle atrophy, and EEMF has preeminent effects on the inhibition of AICAR-induced muscle atrophy through the AMPK signaling pathway.

Effects of polygalacin D extracted from Platycodon grandiflorum on myoblast differentiation and muscle atrophy (길경에서 추출한 polygalacin D가 근원세포 분화 및 근위축에 미치는 영향)

  • Eun-Ju Song;Ji-Won Heo;Jee Hee Jang;Eonmi Kim;Yun Hee Jeong;Min Jung Kim;Sung-Eun Kim
    • Journal of Nutrition and Health
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    • v.56 no.6
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    • pp.602-614
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    • 2023
  • Purpose: The balance between synthesis and degradation of proteins plays a critical role in the maintenance of skeletal muscle mass. Mitochondrial dysfunction has been closely associated with skeletal muscle atrophy caused by aging, cancer, and chemotherapy. Polygalacin D is a saponin derivative isolated from Platycodon grandiflorum (Jacq.) A. DC. This study aimed to investigate the effects of polygalacin D on myoblast differentiation and muscle atrophy in association with mitochondrial function in in vitro and in zebrafish models in vivo. Methods: C2C12 myoblasts were cultured in differentiation media containing different concentrations of polygalacin D, followed by the immunostaining of the myotubes with myosin heavy chain (MHC). The mRNA expression of markers related to myogenesis, muscle atrophy, and mitochondrial function was determined by real-time quantitative reverse transcription polymerase chain reaction. Wild type AB* zebrafish (Danio rerio) embryos were treated with 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) with or without polygalacin D, and immunostained to detect slow and fast types of muscle fibers. The Tg(Xla.Eef1a1:mitoEGFP) zebrafish expressing mitochondria-targeted green fluorescent protein was used to monitor mitochondrial morphology. Results: The exposure of C2C12 myotubes to 0.1 ng/mL of polygalacin D increased the formation of MHC-positive multinucleated myotubes (≥ 8 nuclei) compared with the control. Polygalacin D significantly increased the expression of MHC isoforms (Myh1, Myh2, Myh4, and Myh7) involved in myoblast differentiation while it decreased the expression of atrophic markers including muscle RING-finger protein-1 (MuRF1), mothers against decapentaplegic homolog (Smad)2, and Smad3. In addition, polygalacin D promoted peroxisome proliferator-activated receptor-gamma coactivator (Pgc1α) expression and reduced the level of mitochondrial fission regulators such as dynamin-1-like protein (Drp1) and mitochondrial fission 1 (Fis1). In a zebrafish model of FOLFIRI-induced muscle atrophy, polygalacin D improved not only mitochondrial dysfunction but also slow and fast muscle fiber atrophy. Conclusion: These results demonstrated that polygalacin D promotes myogenesis and alleviates chemotherapy-induced muscle atrophy by improving mitochondrial function. Thus, polygalacin D could be useful as nutrition support to prevent and ameliorate muscle wasting and weakness.

Ethanol Extract of Schisandra chinensis (Turcz.) Baill. Reduces AICAR-induced Muscle Atrophy in C2C12 Myotubes (마우스 C2C12 근관세포에서 AICAR로 유도된 근위축에 미치는 오미자 추출물의 영향)

  • Kang, Young-Soon;Park, Cheol;Han, Min-Ho;Hong, Su-Hyun;Hwang, Hye-Jin;Kim, Byung Woo;Kim, Cheol Min;Choi, Yung Hyun
    • Journal of Life Science
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    • v.25 no.3
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    • pp.293-298
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    • 2015
  • Muscle atrophy, known as a sarcopenia, is defined as a loss of muscle mass resulting from a reduction in the muscle fiber area or density due to a decrease in muscle protein synthesis and an increase in protein breakdown. Schisandrae fructus (SF) extract of the fruits of Schisandra chinensis (Turcz) Baillon has been used as a tonic in traditional medicine for thousands of years. Although a great deal of work has been carried out on the therapeutic potential of SF, its pharmacological mechanisms of action in muscle diseases actions remain unclear. In the present study, we investigated the inhibitory effects of SF ethanol extracts on the production of muscle atrophy factors in C2C12 myotubes stimulated with 5-aminoimidazole-4-carboxamide-ribonucleotide (AICAR), an AMP-activated kinase (AMPK) activator, and sought to determine the underlying mechanisms of action. AICAR upregulated atrophy-related ubiquitin ligase muscle RING finger-1 (MuRF-1) and stimulated the levels of the forkhead box O3a (FoxO3a) transcription factor in the C2C12 myotubes. SF supplementation effectively and concentration- dependently counteracted AICAR-induced muscle cell atrophy and reversed the increased expression of MuRF-1 and FoxO3a. Our study demonstrates that SF can reverse the muscle cell atrophy caused by AICAR through regulation of the AMPK and FoxO3a signaling pathways, followed by inhibition of MuRF-1.

A Study of Pre-application of Neuromuscular Electrical Stimulation on Atrophic Muscle Function (신경근 전기자극의 사전적용이 위축근 기능에 미치는 영향)

  • Kang, Jong-Ho;Kim, Yong-Nam
    • The Journal of the Korea Contents Association
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    • v.9 no.12
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    • pp.691-698
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    • 2009
  • The purpose of this study was to examine the effect of neuromuscular electrical stimulation(LFES) during hindlimb suspension on weight and function of rat hindlimb muscles. Sprague-Dawley rats(body weight 300-350g) were randomly assigned to five groups: a HLS(n=5) that were hindlimb suspended for 14 days, a WB(n=5) that kept as control, a ES14 that were hind limb suspended for 14days with pre-application of LFES for 14 days, ES11 that were hindlimb suspended for 14 days with pre-application of LFES for 11 days, a LFES 7 that were hindlimb suspended for 14 days with pre-application of LFES for 7 days. Gastrocnemius muscle weight, stride length were significantly decreased and toe out angle were significantly increased in HLS and ES7 groups, whereas muscle weight, stride length, toe out angle were maintained in ES14, ES11. this indicated that LFES for 14 days, LFES for 11 days could prevent muscle atrophy and retain function.

Germinated Rhynchosia nulubilis Hydrolysate Ameliorates Dexamethasone-induced Muscle Atrophy by Downregulating MAFbx Expression in C2C12 Cells and C57BL/6 Mice (발아 서목태 가수분해물의 근위축 억제 효과)

  • Won Keong Lee;Eun Ji Kim;Sang Gon Kim;Young Min Goo;Young Sook Kil;Seung Mi Sin;Min Ju Ahn;Min Cheol Kang;Young-Sool Hah
    • Journal of Life Science
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    • v.33 no.3
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    • pp.277-286
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    • 2023
  • Sarcopenia is the age-related loss of muscle mass and function. It is a natural part of aging and can lead to decreased mobility and increased frailty. The ubiquitin-proteasome pathway, which is involved in muscle protein degradation, is closely linked to sarcopenia. Germinated Rhynchosia nulubilis hydrolysate (GRH) has been reported to have anti-inflammatory and antioxidant properties, but there have been no reports on its inhibitory effect on muscle reduction. However, no study has yet explored the relationship between GRH and muscle loss inhibition. In this study, we evaluated the effects of GRH on muscle atrophy inhibitory activity in dexamethasone (Dexa)-induced muscle atrophy C2C12 myotubes and mouse models. Moreover, we identified a molecular pathway underlying the effects of GRH on skeletal muscle. May Grunwald-Giemsa staining showed that the length and area of myotubes increased in the groups treated with GRH. In addition, the GRH-treated group significantly reduced the expression of muscle ring finger protein 1 and muscular atrophy F-box (MAFbx) in the Dexa-induced muscular atrophy C2C12 model. GRH also improved muscle strength in C57BL/6 mice with Dexa-induced muscle atrophy, resulting in prolonged running exhaustive time and increased grip strength. We found that muscle strengthening by GRH was correlated with a decreased expression of the MAFbx gene in mouse muscle tissue. In conclusion, GRH can attenuate Dexa-induced muscle atrophy by inhibiting the ubiquitin-proteasome pathway via downregulation of the MAFbx gene expression.