• Title/Summary/Keyword: Muscle Activation Signal

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Activation of Paraspinal, Abdominal, and Hip Muscles During Various Low Back Stabilization Exercises in Males and Females

  • Yoo, Won-Gyu;Lee, Hyun-Ju
    • Physical Therapy Korea
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    • v.11 no.4
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    • pp.19-29
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    • 2004
  • Many muscles of the trunk and hip are capable of contributing to the stabilization and protection of the lumbar spine. To have optimal effectiveness, a training program should include dynamic back/stomach/hip exercises. This study was designed to assess the L5 level paraspinal, external abdominal oblique, and gluteus maximus muscle activities during various low back stabilization exercises. Participants were 26 healthy adults (13 males, 13 Females), aged 21 to 28 years. The surface electromyography (EMG) was recorded from the L5 level paraspinal, external abdominal oblique, and gluteus maximus muscles. The recorded signal was averaged and normalized to the maximal electromyographic amplitude obtained during the maximal voluntary contraction. The measurements were taken during 3 low back stabilization exercises. One-way analysis of variance with repeated measures was used to examine the difference, and a post hoc test was performed with least significant difference. A level of significance was set at p<.05. The significance of difference between men and women, and between the electromyographic recording sites was evaluated by an independent t-test. The EMG activity for the externus oblique and gluteus maximus muscles had significant differences among 3 exercises (p<.05). In males, the EMG activity for the external abdominal oblique muscle had significantly increased differences during exercises 1 and exercise 2 (p<.05). The gluteus maximus muscle had significantly increased differences during exercise 2 and exercise 3 (p<.05). In females, the multifidus muscle had significantly increased difference during exercise 3 (p<.05), the external abdominal oblique muscle had significantly increased difference during exercise 1 (p<.05). and the gluteus maximus muscle had significantly decreased difference during exercise 3 (p<.05). The results were that the external abdominal oblique muscle was apparently activated during the curl-up exercise in females and males, and the multifidus muscle was apparently activated during the bridging exercise in females and during the sling exercise in males and females.1)In comparison of the %MVC between males and females, exercise 2 and exercise 3 apparently activated of the multifidus and gluteus maximus muscles in both males and females (p<.05). The EMG activity of the gluteus maximus muscle of the males significantly increased during exercise 2 and exercise 3 (p<.05). The EMG activity the multifidus muscle of the females was significantly increased during exercise 2 and exercise 3 (p<.05). More research is needed to understand the nature of motor control problems in the deep muscles in patients with low back pain.

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Isolated Activation of the Upper Trapezius in Three Manual Muscle Testing Position : Convergence Study (세 가지 도수근력 검사 자세에서 상부 승모근의 독립적 수축 : 융합적 연구)

  • Ha, Sungmin
    • Journal of the Korea Convergence Society
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    • v.11 no.1
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    • pp.83-88
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    • 2020
  • The purpose of this study was to investigate the optimal position among three manual muscle tested positions for upper trapezius in which to obtain an isolated upper trapezius EMG signal for the normalization of upper trapezius muscle EMG activity. A total of 28 healthy adult men participated in the experiment. The UT (upper trapezius) and LS (levator scapulae) muscle activities were measured using the TeleMyo 2400T and analyzed using MyoResearch software. The muscle activity of the US and LS was measured by performing three manual muscle test positions for the upper trapezius. The UT/LS ratio during the S-MVIC was 80.25 and was significantly higher than that during the T-MVIC (76.50; p = 0.011) and the C-MVIC (60.95; p < 0.001). And, the UT/LS ratio during the T-MVIC and was significantly higher than that during the C-MVIC (p < 0.001). Based on the results of present study, we suggest a switch from T-MVIC to S-MVIC for the independent normalization reliability of upper trapezius EMG activity. The UT muscle strength or normalization test using S-MVIC will be able to measure muscle strength or activity of UT compared to previous measurement methods.

Comparative analysis of fat and muscle proteins in fenofibratefed type II diabetic OLETF rats: the fenofibrate-dependent expression of PEBP or C11orf59 protein

  • Hahm, Jong-Ryeal;Ahn, Jin-Sook;Noh, Hae-Sook;Baek, Seon-Mi;Ha, Ji-Hye;Jung, Tae-Sik;An, Yong-Jun;Kim, Duk-Kyu;Kim, Deok-Ryong
    • BMB Reports
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    • v.43 no.5
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    • pp.337-343
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    • 2010
  • Fenofibrate, an agonist of $PPAR{\alpha}$, plays an important role in activating many proteins catalyzing lipid metabolism, and it also has a considerable effect on improvement of insulin sensitivity in the diabetic condition. To investigate fenofibrate-dependent expression of peripheral tissue proteins in diabetes, we analyzed whole muscle or fat proteins of fenofibrate-fed OLETF rats, an animal model of type II diabetes, using 2-dimensional gel electrophoresis. We found that many proteins were specifically expressed in a fenofibrate-dependent manner in these diabetic rats. In particular, a functionally unknown C11orf59 protein was differentially expressed in the muscle tissues (about 5-fold increase) in fenofibrate-fed OLETF rats as compared to control rats. Additionally, the signal proteins phosphatidylethanolamine binding protein and IkB interacting protein were differentially regulated in the fenofibrate-treated adipose tissues. We suggest here that these proteins might be involved in controlling lipid or carbohydrate metabolism in diabetes via $PPAR{\alpha}$ activation.

The Src/PLC/PKC/MEK/ERK Signaling Pathway Is Involved in Aortic Smooth Muscle Cell Proliferation induced by Glycated LDL

  • Cho, Hyun-Mi;Choi, Sung Hee;Hwang, Ki-Chul;Oh, Sue-Young;Kim, Ho-Gyung;Yoon, Deok-Hyo;Choi, Myung-Ae;Lim, So Yeon;Song, Heesang;Jang, Yangsoo;Kim, Tae Woong
    • Molecules and Cells
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    • v.19 no.1
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    • pp.60-66
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    • 2005
  • Low density lipoproteins (LDL) play important roles in the pathogenesis of atherosclerosis. Diabetes is associated with accelerated atherosclerosis leading to cardiovascular disease in diabetic patients. Although LDL stimulates the proliferation of arterial smooth muscle cells (SMC), the mechanisms are not fully understood. We examined the effects of native LDL and glycated LDL on the extracellular signal-regulated kinase (ERK) pathway. Addition of native and glycated LDL to rat aorta SMCs (RASMCs) stimulated ERK phosphorylation. ERK phosphorylation was not affected by exposure to the $Ca^{2+}$ chelator BAPTA-AM but inhibition of protein kinase C (PKC) with GF109203X, inhibition of Src kinase with PP1 ($5{\mu}M$) and inhibition of phospholipase C (PLC) with U73122/U73343 ($5{\mu}M$) all reduced ERK phosphorylation in response to glycated LDL. In addition, pretreatment of the RASMCs with a cell-permeable mitogen-activated protein kinase kinase (MEK) inhibitor (PD98059, $5{\mu}M$) markedly decreased ERK phosphorylation in response to native and glycated LDL. These findings indicate that ERK phosphorylation in response to glycated LDL involves the activation of PKC, PLC, and MEK, but is independent of intracellular $Ca^{2+}$.

c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle

  • Lee, Youn-Ri;Lee, Chang-Kwon;Park, Hyo-Jun;Kim, Hyo-Jin;Kim, Jung-Hwan;Kim, Jae-Heung;Lee, Keun-Sang;Lee, Yun-Lyul;Min, Kyung-Ok;Kim, Bo-Kyung
    • Journal of Korean Physical Therapy Science
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    • v.13 no.2
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    • pp.129-135
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    • 2006
  • Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/c-Jun N-terminal kinase (JNK) in vascular smooth muscle contraction has not been defined. We investigated the role of JNK in the contractile response to norepinephrine (NE) in rat aortic smooth muscle. NE evoked contraction in a dose-dependent manner, and this effect was inhibited by the JNK inhibitor SP600125. NE increased the phosphorylation of JNK, which was greater in aortic smooth muscle from hypertensive rats than from normotensive rats. NE-induced JNK phosphorylation was significantly inhibited by SP600125 and the conventional-type PKC (cPKC) inhibitor Go6976, but not by the Rho kinase inhibitor Y27632 or the phosphatidylinositol 3-kinase inhibitor LY294002. Thymeleatoxin, a selective activator of cPKC, increased JNK phosphorylation, which was inhibited by $G{\ddot{o}}6976$. SP600125 attenuated the phosphorylation of caldesmon, an actin-binding protein whose phosphorylation is increased by NE. These results show that JNK contributes to NE-mediated contraction through phosphorylation of caldesmon in rat aortic smooth muscle, and that this effect is regulated by the PKC pathway, especially cPKC.

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Effects of Loading on Biomechanical Analysis of Lower Extremity Muscle and Approximate Entropy during Continuous Stair Walking (지속적인 계단 보행에서 부하가 하지 근육의 생체역학적 변인과 근사 엔트로피에 미치는 영향)

  • Kim, Sung-Min;Kim, Hye-Ree;Ozkaya, Gizem;Shin, Sung-Hoon;Kong, Se-Jin;Kim, Eon-Ho;Lee, Ki-Kwang
    • Korean Journal of Applied Biomechanics
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    • v.25 no.3
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    • pp.323-333
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    • 2015
  • Objective : The purpose of this study was to investigate the changes of gait patterns and muscle activations with increased loads during stair walking. Also, it can be used as descriptive data about continuous stair walking in a real life setting. Method : Twelve sedentary young male adults(Age: $27.0{\pm}1.8yrs$, Weight: $65.8{\pm}9.9kg$) without any lower extremity injuries participated in this study. Participants performed stair walking up 7 floors and their ascending and descending motion on each floor was analyzed. A wireless electromyography(EMG) were attached on the Rectus Femoris(RF), Biceps Femoris(BF), Gastrocnemius(GN), Tibialis Anterior(TA) muscle to calculate integrated EMG(iEMG), median frequency(MDF) and co-contraction index(CI). Chest and left heel accelerometer signal were recorded by wireless accelerometer and those were used to calculate approximate entropy(ApEn) for analyzing gait pattern. All analyses were performed with SPSS 21.0 and for repeated measured ANOVA and Post-hoc was LSD. Results : During ascending stairs, there were a statistically significant difference in Walking time between 1-2nd and other floors(p=.000), GN iEMG between 2-3th and 6-7th(p=.043) floor, TA MDF between 1-2nd and 5-6th(p=.030), 6-7th(p=.015) floor and TA/GN CI between 2-3th and 6-7th(p=.038) floor and ApEn between 1-2nd and 6-7th(x: p=.003, y: p=.005, z: p=.006) floor. During descending stairs, there were a statistically significant difference in TA iEMG between the 6-5th and 3-2nd(p=.026) floor, and for the ApEn between the 1-2nd and 6-7th(x: p=.037, y: p=.000, z: p=.000) floor. Conclusion : Subjects showed more regular pattern and muscle activation response caused by regularity during ascending stairs. Regularity during the first part of stair-descending could be a sign of adaptation; however, complexity during the second part could be a strategy to decrease the impact.

Diverse Mechanisms of Relaxin's Action in the Regulation of Smooth Muscles and Extracellular Matrix of Vasculature and Fibrosis (혈관과 섬유증의 평활근 및 세포외기질 조절에 대한 릴랙신의 다양한 작용기전)

  • Min, Gyesik
    • Journal of Life Science
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    • v.32 no.2
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    • pp.175-188
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    • 2022
  • Relaxin has been demonstrated to have regulatory functions on both the smooth muscle and extracellular matrix (ECM) of blood vessels and fibrotic organs. The diverse mechanisms by which relaxin acts on small resistance arteries and fibrotic organs, including the bladder, are reviewed here. Relaxin induces vasodilation by inhibiting the contractility of vascular smooth muscles and by increasing the passive compliance of vessel walls through the reduction of ECM components, such as collagen. The primary cellular mechanism whereby relaxin induces arterial vasodilation is mediated by the endothelium-dependent production of nitric oxide (NO) through the activation of RXFP1/PI3K, Akt phosphorylation, and eNOS. In addition, relaxin triggers different alternative pathways to enhance the vasodilation of renal and mesenteric arteries. In small renal arteries, relaxin stimulates the activation of the endothelial MMPs and EtB receptors and the production of VEGF and PlGF to inhibit myogenic contractility and collagen deposition, thereby bringing about vasodilation. Conversely, in small mesenteric arteries, relaxin augments bradykinin (BK)-evoked relaxation in a time-dependent manner. Whereas the rapid enhancement of the BK-mediated relaxation is dependent on IKCa channels and subsequent EDH induction, the sustained relaxation due to BK depends on COX activation and PGI2. The anti-fibrotic effects of relaxin are mediated by inhibiting the invasion of inflammatory immune cells, the endothelial-to-mesenchymal transition (EndMT), and the differentiation and activation of myofibroblasts. Relaxin also activates the NOS/NO/cGMP/PKG-1 pathways in myofibroblasts to suppress the TGF-β1-induced activation of ERK1/2 and Smad2/3 signaling and deposition of ECM collagen.

The Activity of Hypertension-related Protein Kinase C and the Relationship of Physical Therapy (고혈압-연관 단백질 부활효소 C의 활성과 물리치료의 상관성)

  • Kim, Jung-Hwan
    • The Journal of Korean Physical Therapy
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    • v.20 no.3
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    • pp.61-68
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    • 2008
  • Purpose: Protein kinase C (PKC) is a member of a family of serine/threonine kinases that are activated by diacylglycerol (DG) and PKC stimulants. PKC play a key role in signal transduction, including muscle contraction, cell migration, apoptosis, cell proliferation and differentiation. However, the mechanism relating mitogen-activated protein kinases (MAPKs) and PKC, especially in the volume-dependent hypertensive state, remains unclear. Methods: In the present study, I investigated the relationship between PKC and MAPKs for isometric contraction, PKC translocation, and enzymatic activity from normotensive sham-operated rats (NSR) and aldosterone-analogue deoxycorticosterone acetate (DOCA) hypertensive rats (ADHR). Results: Systolic blood pressure was significantly increased in ADHR than in NSR. Physiological salt solution (PSS)-induced resting tension and the intracellular $Ca^{2+}$ concentration ([$Ca^{2+}{_i}$]) were different in the ADHR and NSR. The expression of PKC$\alpha$, PKC$\beta$II, PKC$\delta$, PKC$\varepsilon$ and PKC$\xi$ were different between the cytoplasmic and membranous fractions. However, expression of the PKC isoforms did not differ for the ADHR and NSR. The use of 12-deoxyphorbol 13-isobutyrate (DPB, a PKC stimulant) induced isometric contraction in $Ca^{2+}$-free medium, which was diminished in muscle strips from ADHR as compared to NSR. Increased vasoconstriction and phosphorylation induced by the use of 1 ${\mu}$M DPB were inhibited by treatment with 10 ${\mu}$M PD098059 and 10 ${\mu}$M SB203580, inhibitors of extracellular-regulated protein kinase 1/2 (ERK1/2) and p38 MAPK from ADHR, respectively. Conclusion: These results suggest that the development of aldosterone analogue-induced hypertension is associated with an altered blood pressure, resting tension, [$Ca^{2+}{_i}$], and that the $Ca^{2+}$-independent contraction evoked by PKC stimulants is due to the activation of ERK1/2 and p38 MAPK in volume-dependent hypertension. Therefore, it is suggested that PKC activity affects volume-dependent hypertension and the need to develop cardiovascular disease-specialized physical therapy.

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The Bioinformatics and Molecular Biology Approaches for Vascular Cell Signaling by Advanced Glycation Endproducts Receptor and Small Ubiquitin-Related Modifier

  • Kim, June Hyun
    • Interdisciplinary Bio Central
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    • v.4 no.4
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    • pp.12.1-12.6
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    • 2012
  • The advanced glycation endproducts receptor (AGE-R) is a signal transduction receptor for multiligand such as S100b and AGEs. S100b has been demonstrated to activate various cells with important links to atherosclerosis initiation and progression including endothelial cells, and smooth muscle cells via AGE-R, triggering activation of multiple signaling cascades through its cytoplasmic domain. Many studies have suggested AGE-R might even participate in the cardiovascular complications involved in the pathogenesis of type I diabetes. Recently, Small Ubiquitin-Related Modifier 1 (SURM-1 also known as SUMO-1) has been recognized as a protein that plays an important role in cellular post-translational modifications in a variety of cellular processes, such as transport, transcriptional, apoptosis and stability. Computer Database search with SUMOplot Analysis program identified the five potential SURMylation sites in human AGE-R: K43, K44, K123, and K273 reside within the extracellular domain of AGE-R, and lastly K374 resides with the cytosolic domain of AGE-R. The presence of the consensus yKXE motif in the AGE-R strongly suggests that AGE-R may be regulated by SURMylation process. To test this, we decided to determine if AGE-R is SURMylated in living vascular cell system. S100b-stimulated murine aortic vascular smooth muscle cells were used for western blot analysis with relevant antibodies. Taken together, bioinformatics database search and molecular biological approaches suggested AGE-R is SURMylated in living cardiovascular cell system. Whilst SURMylation and AGE-R undoubtedly plays an important role in the cardiovascular biology, it remains unclear as to the exact nature of this contribution under both physiological and pathological conditions.

Silencing MR-1 attenuates atherosclerosis in ApoE-/- mice induced by angiotensin II through FAK-Akt -mTOR-NF-kappaB signaling pathway

  • Chen, Yixi;Cao, Jianping;Zhao, Qihui;Luo, Haiyong;Wang, Yiguang;Dai, Wenjian
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.2
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    • pp.127-134
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    • 2018
  • Myofibrillogenesis regulator-1 (MR-1) is a novel protein involved in cellular proliferation, migration, inflammatory reaction and signal transduction. However, little information is available on the relationship between MR-1 expression and the progression of atherosclerosis. Here we report atheroprotective effects of silencing MR-1 in a model of Ang II-accelerated atherosclerosis, characterized by suppression focal adhesion kinase (FAK) and nuclear factor kappaB ($NF-{\kappa}B$) signaling pathway, and atherosclerotic lesion macrophage content. In this model, administration of the siRNA-MR-1 substantially attenuated Ang II-accelerated atherosclerosis with stabilization of atherosclerotic plaques and inhibited FAK, Akt, mammalian target of rapamycin (mTOR) and NF-kB activation, which was associated with suppression of inflammatory factor and atherogenic gene expression in the artery. In vitro studies demonstrated similar changes in Ang II-treated vascular smooth muscle cells (VSMCs) and macrophages: siRNA-MR-1 inhibited the expression levels of proinflammatory factor. These studies uncover crucial proinflammatory mechanisms of Ang II and highlight actions of silencing MR-1 to inhibit Ang II signaling, which is atheroprotective.