Carbon monoxide (CO) binds to soluble guanylate cyclase to lead its activation and elicits smooth muscle relaxation. The vascular tissues have a high capacity to produce CO, since heme oxygenase-2 (HO-2) is constitutively expressed in endothelial and smooth muscle cells, and HO-1 can be greatly up-regulated by oxidative stress. Moreover, the substrate of HO, heme, is readily available for catalysis in vascular tissue. Although the activation of heme oxygenase pathway under various stress conditions may provide a defence mechanism in compromised tissues, the specific role of HO-1-derived CO in the control of aortic contractility still remains to be elucidated. The present study was done to determine the effect of HO-1 induction on the aortic contractility. Thus, the effects of incubation of aortic tissue with S-nitroso-N-acetylpenicillamine (SNAP) for 1 hr on the aortic contractile response to phenylephrine were studied. The preincubation with SNAP resulted in depression of the vasoconstrictor response to phenylephrine. This effect was restored by HO inhibitor or methylene blue but not by NOS inhibitor. The attenuation of vascular reactivity by preincubation with SNAP was also revealed in endothelium-free rings. $AlF4^--evoked$ contraction in control did not differ from that in SNP-treated group. These results suggest that increased production of CO was responsible for the reduction of the contractile response to phenylephrine in aortic ring preincubated with SNAP and this effect of SNAP was independent on endothelium.
Objective: The aim of this study was to determine the peak torques of the knee and ankle joint and local stability of the lower extremity's joints, and muscle activation patterns of the lower extremity's muscles between fallers and non-fallers in the elderly women during walking. Method: Four elderly women (age: $74.5{\pm}5.2yrs.$; height: $152.1{\pm}5.6cm$; mass: $55.3{\pm}5.4kg$; preference walking speed: $1.19{\pm}0.06m/s$) who experienced falls within six months since experiment had been conducted (falls group) and thirty-six subjects ($74.2{\pm}3.09yrs.$; height: $153.6{\pm}4.9cm$; mass: $56.7{\pm}6.4kg$; preference walking speed: $1.24{\pm}0.10m/s$) who had no experience in falls (non-falls group) within this periods participated in this study. They were measured torque peaks of the knee and ankle joint using a Human Norm and while they were walking on a treadmill at their natural pace, kinematic variables and EMG signals were collected with using a 3-D motion capture system and a wireless EMG system, respectively. Lyapunov Exponent (LyE) was determined to observe the dynamic local stability of the lower extremity's joints, and muscles activation and their co-contraction index were also analysed from EMG signals. Hypotheses between falls and non-falls group were tested using paired t-test and Mann-Whitey. Level of significance was set at p<.05. Results: Local dynamic stability in the adduction-abduction movement of the knee joint was significantly lower in falling group than non-falling group (p<.05). Conclusion: In conclusion, muscles which act on the abduction-adduction movement of the knee joint need to be strengthened to prevent from potential falls during walking. However, a small number of samples for fallers make it difficult to generalize the results of this study.
Losartan is a selective angiotensin II (Ang II) type 1 ($AT_1$) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured by Western blot analysis and cell proliferation was measured by MTT assay and flowcytometry. Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the $G_0/G_1$ cell cycle arrest. These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression.
Objectives : This study was conducted to evaluate the anti-atrophic effect of polycan in dexamethasone-induced skeletal muscle atrophy in vitro model. Methods : C2C12 myoblast were differentiated into myotube by 2% horese serum medium for 6 days, and then treated polycan extract at different concentrations for 24h. The effect of dexamethasone on the induction of muscle atrophy and expression of atrophy-related genes in differentiated C2C12 myotubes using a GSH, ROS, real-time PCR, western blots analysis. Results : The results showed that Treatment with polycan (100 and 200 ㎍/㎖) noncytotoxic levels on both myoblast and myotube. Polycan decreased the ROS level overproduced with dexamethasone and improved the depletion of GSH level. Dexamethasone showed a decrease in myotube diameter, which was associated with up-regulation muscle-specific ubiquitin ligases markers, such as atrogin-1, FoxO3, myostatin and muscle RING finger-1 (MuRF1), and down-regulation of myogenin, MEF2, Myogenic regulatory factor 5, 6 and MyoD. The results showed that polycan treatment significantly dose-dependently inhibited it. Furthermore, decreased expressions of PI3K/Akt signal pathway by dexamethasone were reversed by treatment with polycan. Conclusions : Thus, polycan suppresses dexamethasone induced muscle atrophy in C2C12 myotube in vitro model through activation of PI3K/Akt pathway and protective effect of improve skeletal muscle function.
Kim, Kyung-Hwan;Park, Rae-Jun;Jang, Jun-Hyeok;Lee, Woo-Hyung;Ki, Kyong-Il
Journal of the Korean Society of Physical Medicine
/
v.5
no.3
/
pp.405-412
/
2010
Purpose : The purpose of this study was to assess the effects of the trunk muscle activity on bridging exercise according to the knee joint angle. Methods : Twenty-five healthy adults volunteered to participate in this study. Subjects were required to complete following four bridging exercises; knee joint flexion $120^{\circ}$, $90^{\circ}$, $60^{\circ}$, $45^{\circ}$. Surface electromyography from selected trunk muscles was normalized to maximum voluntary isometric contraction. Muscle activity was measured by QEMG-4 system(LXM 3204, Laxtha Korea). A repeated measures of one-way ANOVA with post-hoc Bonferroni's correction was used to determine the influence of bridging exercise on muscle activity for each muscle and descriptive statistics was used to determine local/global muscle ratio. Results : The internal oblique of bridging exercises $120^{\circ}$, $90^{\circ}$ showed significantly(p<.05). The erctor spinae of all bridging exercises showed significant excepted between $60^{\circ}$ and $45^{\circ}$(p<.05). Median of internal oblique/rectus abdominis ratio of $120^{\circ}$ was 4.41, $90^{\circ}$ was 3.94, $60^{\circ}$ was 3.58, $45^{\circ}$ was 3.39. Median of internal oblique/external oblique ratio of $120^{\circ}$ was 2.66, $90^{\circ}$ was 2.43, $60^{\circ}$ was 2.87, $45^{\circ}$ was 2.64. Conclusion : Angular motion decreasing with knee joint flexion made erector spinae activation increase. on the other hand, as decreasing abdomen muscle activation, the more performing motor learning is required for abdomen muscle strength and co-contraction for the trunk stabilization.
Transactions on Control, Automation and Systems Engineering
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v.4
no.1
/
pp.43-48
/
2002
We show that humans execute the postural control ingeniously by regulating the impedance properties of the musculo-skeletal system as the motor command against the alteration of the environment. Adjusting muscle activity can control the impedance properties of the musculo-skeletal system. To quantify the changes in human arm viscoelasticity on the vertical plane during interaction with the environment, we asked our subject to hold an object. By utilizing surface electromyographic(EMG) studies, we determined a relationship between the perturbation and a time-varying muscle co-activation. Our study showed when the subject lifts the object by himself the muscle stiffness increases while the torque remains the same just before the lift-off. These results suggest that the central nervous system(CNS) simultaneously controls not only the equilibrium point(EP) and the torque, but also the muscle stiffness as themotor command in posture control during the contact task.
Purpose: This study identified the co-activation of quadriceps and hamstring muscles during hamstring strengthening exercises in healthy adults. Methods: Twenty-one participants were required for the present study design to achieve 80% power, 0.8 effect size (η2), and an alpha level of 0.05. Thus, this study recruited 21 healthy adults. All participants performed Nordic exercises, bridge exercises, and one-leg deadlifts randomly. The activity of the rectus femoris, vastus medialis (VM), vastus lateralis (VL), biceps femoris (BF), and semitendinosus (SM) were measured. In addition, the ratios of VM/VL and hamstring/quadriceps (HQ) were measured during the three hamstring strengthening exercises using electromyography. One-way ANOVA was used to compare the co-activation of quadriceps and hamstring muscles in the three exercises. Results: The activity of VM and VL during the performance of one-leg deadlifts was significantly higher than the other two exercises. The BF had significantly higher activity during the Nordic exercises compared to the other two exercises. In addition, the SM activation was significantly greater during Nordic exercises than one-leg deadlifts. Additionally, there was significant difference in HQ ratio among hamstring strengthening exercises. In specific, the one-leg deadlifts yielded a significantly lower HQ ratio. Conclusion: This study revealed that one-leg deadlifts are effective in rehabilitation for anterior cruciate ligament injury. In addition, Nordic exercises can be recommended to facilitate hamstring muscle activation.
Jeon, Sang Kyu;Kim, Ok Hyeon;Park, Su Mi;Lee, Ju-Hee;Park, Sun-Dong
Herbal Formula Science
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v.28
no.1
/
pp.29-39
/
2020
Objectives : Glucoraphanin is one of the well-known natural glucosinolates found in cruciferous plants. In the present study, we investigated the effects and molecular mechanism of glucoraphanin in dexamethasone-induced skeletal muscle atrophy in vitro model. Methods : The cytotoxic effects of glucoraphanin on C2C12 myoblasts or myotubes were evaluated by MTT assay. The glucoraphanin was evaluated effects in dexamethasone-induced skeletal muscle atrophy in C2C12 myotubes using a real-time PCR, western blots analysis, and immunofluorescence staining of myosin heavy chain. Result : Glucoraphanin had no cytotoxicity on both C2C12 myoblasts or myotubes. Dexamethasone markedly induced muscle atrophy by up-regulating muscle-specific ubiquitin E3 ligase markers, atrogin-1 and MuRF1, and down-regulating MyoD, a myogenic regulatory factor whereas co-treatment of glucoraphanin and dexamethasone dose-dependently inhibited it. Furthermore, decreased expressions of p-Akt, p-FOXO1, and p-FOXO3a induced by dexamethasone were reversed by co-treatment with glucoraphanin and dexamethasone. In addition, dexamethasone obviously reduced myotube diameters, while co-treatment of glucoraphanin and dexamethasone increased those to a similar level as control. Conclusions : These results show that glucoraphanin suppresses dexamethasone-induced muscle atrophy in C2C12 myotubes through activation of Akt/FOXO signaling pathway.
Objective: To investigate the effect of short-term vibration frequencies on muscle force generation capabilities. Method: Six healthy participants were recruited for this study and only their dominant leg was tested. The subjects were tested under five conditions of vibration frequencies with constant amplitude: 0 Hz (no vibration), 30 Hz, 60 Hz, and 90 Hz, and the vibration amplitude was 10 mm for all frequency conditions. The vibration was applied to the rectus femoris (RF). The subjects were then instructed to maintain a steady-state isometric knee joint torque (100 Nm) for the first 6 s. After the steady-state torque production, the subjects were required to produce isometric knee joint torque by leg extension as hard as possible with a start signal within the next 3 s. The vibration was applied for ~4 s starting from 1 s before initiation of the change in the steady-state knee joint torque. Results: The results showed that the maximum voluntary torque (MVT) of the knee joint increased with the vibration frequencies. On average, the MVTs were 756.47 Nm for 0 Hz (no vibration) and 809.61 Nm for 90 Hz. There was a significant positive correlation (r = 0.71) between the MVTs and integrated electromyograms (iEMGs). Further, the co-contraction indices (CCIs) were computed, which represent the ratio of the iEMGs of the antagonist muscle to the iEMGs of all involved muscles. There was a significant negative correlation (r = 0.62) between the CCIs and MVTs, which was accompanied by a significant positive correlation (r = 0.69) between the iEMGs of the vibrated muscle (RF). There was no significant correlation between the MVTs and iEMGs of the antagonist muscle. Conclusion: The results of this study suggest that the short-term vibration on the muscle increases the level of muscle activation possibly owing to the increased Ia afferent activities, which enhances the muscle force generation capability.
The peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) is a nuclear transcription factor that plays a central role in lipid metabolism and obesity. Exercise also is a powerful modifier of the manifestations of the lipid metabolism and obesity in animal models and humans with obesity and metabolic syndrome. However, effects of exercise on lipid metabolism and obesity in normal-weight younger female subjects, having functional ovaries and not metabolic disease, remain unexplained. To explore the effects of exercise on the development of obesity and its molecular mechanism in high fat diet-fed female C57BL/6J mice, we experimented the effects of swim training on body weight, adipose tissue mass, serum lipid levels, morphological changes of adipocytes and the expression of PPAR$\alpha$ target genes involved in fat oxidation in skeletal muscle tissue of female C57BL/6J mice. Swim-trained mice had significantly decreased body weight, adipose tissue mass, serum triglycerides compared with female control mice. Histological studies showed that swim training significantly decreased the average size of adipoctyes in parametrial adipose tissue. Swim training did not affect the expression of PPAR$\alpha$ mRNA in skeletal muscle. Concomitantly, swim training did not increase mRNA levels of PPAR$\alpha$ target genes responsible for fatty acid $\beta$-oxidation, such as carnitine palmitoyltransferase 1, medium chain acyl-CoA dehydrogenase, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase, and thiolase in skeletal muscle. In conclusion, these results indicate that swim training regulates lipid metabolism and obesity in high fat diet fed-female mice although swim training did not increase mRNA levels of PPAR$\alpha$ target genes involved in fatty acid $\beta$-oxidation in skeletal muscle, suggesting that swim training may prevent obesity and improve fitness through other mechanisms in female with ovaries, not through the activation of skeletal muscle PPAR$\alpha$.
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