scholarly journals PO-252 Effect of acupuncture intervention on the changes of cytoplasmic and mitochondrial Ca2+ concentration following eccentric contractions in rat skeletal muscle

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Aishan Liu ◽  
Fangming Liu ◽  
Xuelin Zhang ◽  
Yarong Wang ◽  
Mei Kong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Fluorescent Imaging ◽  
Eccentric Contractions ◽  
Rat Skeletal Muscle ◽  
Tetanic Force ◽  
Acupuncture Intervention ◽  
Stimulation Group

  Objective The purpose of this study was to evaluate the effect of acupuncture intervention on the changes of cytoplasmic and mitochondrial Ca2+ concentration following eccentric contractions (ECC) in rat skeletal muscle. Methods 24 healthy male Wistar rats were randomly divided into 4 groups: control group (C, n=6)、electrical stimulation group (E, n=6)、electrical stimulation group with acupuncture intervention (EA, n=6)、electrical stimulation group with acupuncture +TRP channel inhibitor Gd3+ (EAI, n=6). The animal model of eccentric induced skeletal muscle injury was established by electrical stimulation on spinotrapezius muscle of anaesthetised rats in vivo, that is to say, the intact spinotrapezius muscle of adult Wistar rats was exteriorized, and tetanic eccentric contractions (100 Hz, 10 sets of 50 contractions) were elicited by electrical stimulation during synchronized muscle stretch of 10% resting muscle length. Cytoplasmic Ca2+ accumulation were determined by loading the muscle with fura 4-AM using fluorescent imaging in vivo, and mitochondrial Ca2+ concentration were determined by loading the muscle with fura 2-AM using fluorescent imaging in vitro, and recorded changes of muscle maximum tetanic force. Results (1) In vivo, compared with the C , cytoplasmic Ca2+ accumulation increased more rapidly during ECC in the E (P < 0.001). Acupuncture intervention significantly reduced cytosolic Ca2+ accumulation in the EA compared with the E (P < 0.01), and we discovered that muscle deformation generated by acupuncture intervention induced a robust Ca2+ spark response confined in close spatial proximity to the sarcolemmal membrane in intact muscle fibers. Although no significant differences between the EA and EAI, Gd3+ abolished the majority of cytoplasmic Ca2+ accumulation decrease during ECC in the EAI and a robust Ca2+ spark response disappeared compared with the EA. (2) In vitro, compared with the C, mitochondrial Ca2+ concentration did not elevations in MCC in the E. EA cytoplasmic Ca2+ increased rapidly above the C and E (P < 0.01), respectively, but EAI significantly attenuated the increases in  mitochondrial Ca2+ concentration compared with the EA (P < 0.01). (3). Compared with the C , maximum tetanic force was significantly lower in the E after ECC (P < 0.01). EA maximum tetanic force increased rapidly compared with the E after ECC (P < 0.05), but EAL abolished the majority maximum tetanic force increase after ECC (P < 0.05). Conclusions (1)Eccentric contraction caused cytoplasmic Ca2+ accumulation, but  mitochondrial Ca2+ concentration decrease. (2)Acupuncture can effectively reduce cytosolic Ca2+ overload, following by mitochondrial Ca2+ concentration increase , which in turn abnormally high cytoplasmic Ca2+ levels are buffed by the mitochondria, and improved muscle function, and the effect was associated to the TRP channels.  

N tau-methylhistidine release: contributions of rat skeletal muscle, GI tract, and skin

1982 ◽  
Vol 243 (4) ◽  
pp. E293-E297 ◽  
Author(s):  
S. J. Wassner ◽  
J. B. Li
Keyword(s):  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Soft Tissue ◽  
Fractional Catabolic Rate ◽  
Gi Tract ◽  
Rat Skeletal Muscle ◽  
Catabolic Rate ◽  
Total Body

The relative contributions of skeletal muscle, gastrointestinal tract, and skin to urinary N tau-methylhistidine (MH) excretion were estimated during in vitro studies using the rat hemicorpus preparation. After 0.5 h of perfusion, MH release into the perfusate was linear for 3 h and averaged 29.8 nmol . h-1 . 100 g hemicorpus-1. In vivo, 24-h urinary MH excretion averaged 37.3 nmol . h-1 . 100 g body wt-1. The ratio of soft tissue to skin weight is equal (3.2:1) in the whole rat and in the hemicorpus. The gastrointestinal tract released 16.0 nmol . h-1 . 100 g body wt-1 or approximately 41% of the total urinary MH excretion. Preparations perfused with or without skin showed modest differences in the rate of MH release that were not statistically significant. Skeletal muscle contains 89.8% of total body MH content, whereas gastrointestinal tract and skin contain 3.8 and 6.4%, respectively. Gastrointestinal tract actomyosin turns over rapidly with a fractional catabolic rate of 24%/day versus 1.4%/day for skeletal muscle actomyosin.

scholarly journals Optogenetic activation of muscle contraction in vivo

2020 ◽  
Author(s):  
Elahe Ganji ◽  
C. Savio Chan ◽  
Christopher W. Ward ◽  
Megan L. Killian
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Fluorescent Imaging ◽  
Triceps Surae ◽  
Light Activation ◽  
Non Invasive ◽  
Optogenetic Stimulation ◽  
Stimulation Of

AbstractOptogenetics is an emerging alternative to traditional electrical stimulation to initiate action potentials in activatable cells both ex vivo and in vivo. Optogenetics has been commonly used in mammalian neurons and more recently, it has been adapted for activation of cardiomyocytes and skeletal muscle. Therefore, the aim of this study was to evaluate the stimulation feasibility and sustain isometric muscle contraction and limit decay for an extended period of time (1s), using non-invasive transdermal light activation of skeletal muscle (triceps surae) in vivo. We used inducible Cre recombination to target expression of Channelrhodopsin-2 (ChR2(H134R)-EYFP) in skeletal muscle (Acta1-Cre) in mice. Fluorescent imaging confirmed that ChR2 expression is localized in skeletal muscle and does not have specific expression in sciatic nerve branch, therefore, allowing for non-nerve mediated optical stimulation of skeletal muscle. We induced muscle contraction using transdermal exposure to blue light and selected 10Hz stimulation after controlled optimization experiments to sustain prolonged muscle contraction. Increasing the stimulation frequency from 10Hz to 40Hz increased the muscle contraction decay during prolonged 1s stimulation, highlighting frequency dependency and importance of membrane repolarization for effective light activation. Finally, we showed that optimized pulsed optogenetic stimulation of 10 Hz resulted in comparable ankle torque and contractile functionality to that of electrical stimulation. Our results demonstrate the feasibility and repeatability of non-invasive optogenetic stimulation of muscle in vivo and highlight optogenetic stimulation as a powerful tool for non-invasive in vivo direct activation of skeletal muscle.

scholarly journals Improved Tetanic Force and Mitochondrial Calcium Homeostasis by Astaxanthin Treatment in Mouse Skeletal Muscle

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 98 ◽  
Author(s):  
Sztretye ◽  
Singlár ◽  
Szabó ◽  
Angyal ◽  
Balogh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Calcium Homeostasis ◽  
Inhibitory Effect ◽  
Calcium Transients ◽  
Muscle Performance ◽  
Control Group ◽  
Mitochondrial Calcium ◽  
Tetanic Force

Background: Astaxanthin (AX) a marine carotenoid is a powerful natural antioxidant which protects against oxidative stress and improves muscle performance. Retinol and its derivatives were described to affect lipid and energy metabolism. Up to date, the effects of AX and retinol on excitation-contraction coupling (ECC) in skeletal muscle are poorly described. Methods: 18 C57Bl6 mice were divided into two groups: Control and AX supplemented in rodent chow for 4 weeks (AstaReal A1010). In vivo and in vitro force and intracellular calcium homeostasis was studied. In some experiments acute treatment with retinol was employed. Results: The voltage activation of calcium transients (V50) were investigated in single flexor digitorum brevis isolated fibers under patch clamp and no significant changes were found following AX supplementation. Retinol shifted V50 towards more positive values and decreased the peak F/F0 of the calcium transients. The amplitude of tetani in the extensor digitorum longus was significantly higher in AX than in control group. Lastly, the mitochondrial calcium uptake was found to be less prominent in AX. Conclusion: AX supplementation increases in vitro tetanic force without affecting ECC and exerts a protecting effect on the mitochondria. Retinol treatment has an inhibitory effect on ECC in skeletal muscle.

Static stretch increases c-Jun NH2-terminal kinase activity and p38 phosphorylation in rat skeletal muscle

2001 ◽  
Vol 280 (2) ◽  
pp. C352-C358 ◽  
Author(s):  
Marni D. Boppart ◽  
Michael F. Hirshman ◽  
Kei Sakamoto ◽  
Roger A. Fielding ◽  
Laurie J. Goodyear
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Protein Kinases ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Eccentric Contractions ◽  
Sprague Dawley ◽  
Static Stretch

Physical exercise and contraction increase c-Jun NH2-terminal kinase (JNK) activity in rat and human skeletal muscle, and eccentric contractions activate JNK to a greater extent than concentric contractions in human skeletal muscle. Because eccentric contractions include a lengthening or stretch component, we compared the effects of isometric contraction and static stretch on JNK and p38, the stress-activated protein kinases. Soleus and extensor digitorum longus (EDL) muscles dissected from 50- to 90-g male Sprague-Dawley rats were subjected to 10 min of electrical stimulation that produced contractions and/or to 10 min of stretch (0.24 N tension, 20–25% increase in length) in vitro. In the soleus muscle, contraction resulted in a small, but significant, increase in JNK activity (1.8-fold above basal) and p38 phosphorylation (4-fold). Static stretch had a much more profound effect on the stress-activated protein kinases, increasing JNK activity 19-fold and p38 phosphorylation 21-fold. Increases in JNK activation and p38 phosphorylation in response to static stretch were fiber-type dependent, with greater increases occurring in the soleus than in the EDL. Immunohistochemistry performed with a phosphospecific antibody revealed that activation of JNK occurred within the muscle fibers. These studies suggest that the stretch component of a muscle contraction may be a major contributor to the increases in JNK activity and p38 phosphorylation observed after exercise in vivo.

Lack of functional effects of neuromuscular electrical stimulation on skeletal muscle oxidative metabolism in healthy humans

2012 ◽  
Vol 113 (7) ◽  
pp. 1101-1109 ◽  
Author(s):  
Simone Porcelli ◽  
Mauro Marzorati ◽  
Lorenzo Pugliese ◽  
Saverio Adamo ◽  
Julien Gondin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Oxidative Metabolism ◽  
Near Infrared ◽  
Neuromuscular Electrical Stimulation ◽  
Work Rate ◽  
Functional Evaluation ◽  
Rate Relationship

A recent study has demonstrated that neuromuscular electrical stimulation (NMES) determines, in vitro, a fast-to-slow shift in the metabolic profile of muscle fibers. The aim of the present study was to evaluate if, in the same subjects, these changes would translate, in vivo, into an enhanced skeletal muscle oxidative metabolism. Seven young men were tested (cycle ergometer) during incremental exercises up to voluntary exhaustion and moderate and heavy constant-load exercises (CLE). Measurements were carried out before and after an 8-wk training program by isometric bilateral NMES (quadriceps muscles), which induced an ∼25% increase in maximal isometric force. Breath-by-breath pulmonary O2 uptake (V̇o2) and vastus lateralis oxygenation indexes (by near-infrared spectroscopy) were determined. Skeletal muscle fractional O2 extraction was estimated by near-infrared spectroscopy on the basis of changes in concentration of deoxygenated hemoglobin + myoglobin. Values obtained at exhaustion were considered “peak” values. The following functional evaluation variables were unaffected by NMES: peak V̇o2; gas exchange threshold; the V̇o2 vs. work rate relationship (O2 cost of cycling); changes in concentration of deoxygenated hemoglobin + myoglobin vs. work rate relationship (related to the matching between O2 delivery and V̇o2); peak fractional O2 extraction; V̇o2 kinetics (during moderate and heavy CLE) and the amplitude of its slow component (during heavy CLE). Thus NMES did not affect several variables of functional evaluation of skeletal muscle oxidative metabolism. Muscle hypertrophy induced by NMES could impair peripheral O2 diffusion, possibly counterbalancing, in vivo, the fast-to-slow phenotypic changes that were observed in vitro, in a previous work, in the same subjects of the present study.

Nonradioisotope Assay of Glucose Uptake Activity in Rat Skeletal Muscle Using Enzymatic Measurement of 2-Deoxyglucose 6-Phosphate in vitro and in vivo

Neurosignals ◽  
2000 ◽  
Vol 9 (5) ◽  
pp. 267-274 ◽  
Author(s):  
Atsunori Ueyama ◽  
Takashi Sato ◽  
Hidehiro Yoshida ◽  
Kiyohiko Magata ◽  
Nobuyuki Koga
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Rat Skeletal Muscle ◽  
Uptake Activity

scholarly journals Effect of ANG II on endothelial cell apoptosis and survival and its impact on skeletal muscle angiogenesis after electrical stimulation

2008 ◽  
Vol 294 (6) ◽  
pp. H2814-H2821 ◽  
Author(s):  
Micheline M. de Resende ◽  
Andrew S. Greene
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Endothelial Cell ◽  
High Salt ◽  
Ang Ii ◽  
High Salt Diet ◽  
Salt Diet ◽  
Angiogenic Response

We have previously shown that skeletal muscle angiogenesis induced by electrical stimulation is significantly attenuated when SS-13BN/Mcwi rats are fed a high-salt diet. This effect was associated with a large increase in endothelial cell (EC) apoptosis. We hypothesized that the low levels of ANG II during high-salt diet would increase EC apoptosis and consequently diminish the angiogenic response. To test this hypothesis, a series of in vitro and in vivo studies was performed. EC apoptosis and viability were evaluated after incubation with ANG II under serum-free conditions. After 24 h of incubation, ANG II increased EC viability and Bcl-2-to-Bax ratio along with a dose-dependent decrease in EC apoptosis. This effect was blocked by the ANG II type 1 receptor antagonist losartan. To confirm our in vitro results, ANG II (3 ng·kg−1·min−1) was chronically infused in rats fed a high-salt diet (4% NaCl). ANG II decreased EC apoptosis and produced a significant increase (40%) in skeletal muscle angiogenesis after electrical stimulation. These in vivo results were in agreement with our in vitro results and demonstrate that the attenuation of ANG II levels during a high-salt diet may induce EC apoptosis and consequently block the angiogenic response induced by electrical stimulation. Furthermore, under normal conditions, ANG II increases EC viability and protects EC from apoptosis possibly by inactivation of the mitochondrial apoptotic pathway.

scholarly journals Activation of the multicatalytic proteinase from rat skeletal muscle by fatty acids or sodium dodecyl sulphate

1985 ◽  
Vol 228 (1) ◽  
pp. 171-177 ◽  
Author(s):  
B Dahlmann ◽  
M Rutschmann ◽  
L Kuehn ◽  
H Reinauer
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Conformational Changes ◽  
Sodium Dodecyl Sulphate ◽  
Muscle Protein ◽  
Sodium Dodecyl ◽  
Rat Skeletal Muscle ◽  
Multicatalytic Proteinase

A multicatalytic proteinase from rat skeletal muscle contains active site(s) catalysing the degradation of benzoyl-Val-Gly-Arg 4-methyl-7-coumarylamide, succinyl-Ala-Ala-Phe 4-methylcoumarylamide and [14C]methylcasein as well as benzyloxy-carbonyl-Leu-Leu-Glu 2-naphthylamide. These activities are 7-14-fold activated by 1 mM-sodium dodecyl sulphate. The activation leads to a higher susceptibility to the proteinase inhibitor chymostatin and to a lower ability to be inhibited and precipitated by antibodies raised against the non-activated enzyme. Since no changes in Mr or subunit composition were observed in the SDS-activated form, some conformational changes seem to occur during the activation step. More pronounced activation was observed in the presence of physiological concentrations of fatty acids; oleic acid at 100 microM concentrations stimulated the proteinase about 50-fold. In contrast with the non-activated proteinase, the activated enzyme considerably degrades muscle cytoplasmic proteins in vitro. Thus it is not unlikely that, in vivo, potential activators such as fatty acids can induce the multicatalytic proteinase to participate in muscle protein breakdown.

In vitro simulation of calorie restriction-induced decline in glucose and insulin leads to increased insulin-stimulated glucose transport in rat skeletal muscle

2007 ◽  
Vol 293 (6) ◽  
pp. E1782-E1788 ◽  
Author(s):  
Edward B. Arias ◽  
Gregory D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Insulin Receptor ◽  
Glucose Transport ◽  
Calorie Restriction ◽  
Serine Phosphorylation ◽  
Rat Skeletal Muscle ◽  
Extracellular Glucose ◽  
In Vitro Simulation

In vivo calorie restriction [CR; consuming 60% of ad libitum (AL) intake] induces elevated insulin-stimulated glucose transport (GT) in skeletal muscle. The mechanisms triggering this adaptation are unknown. The aim of this study was to determine whether physiological reductions in extracellular glucose and/or insulin, similar to those found with in vivo CR, were sufficient to elevate GT in isolated muscles. Epitrochlearis muscles dissected from rats were incubated for 24 h in media with glucose (8 mM) and insulin (80 μU/ml) at levels similar to plasma values of AL-fed rats and compared with muscles incubated with glucose (5.5 mM) and/or insulin (20 μU/ml) at levels similar to plasma values of CR rats. Muscles incubated with CR levels of glucose and insulin for 24 h had a subsequently greater ( P < 0.005) GT with 80 μU/ml insulin and 8 mM [3H]-3- O-methylglucose but unchanged GT without insulin. Reducing only glucose or insulin for 24 h or both glucose and insulin for 6 h did not induce altered GT. Increased GT after 24-h incubation with CR levels of glucose and insulin was not attributable to increased insulin receptor tyrosine phosphorylation, Akt serine phosphorylation, or Akt substrate of 160 kDa phosphorylation. Nor did 24-h incubation with CR levels of glucose and insulin alter the abundance of insulin receptor, insulin receptor substrate-1, GLUT1, or GLUT4 proteins. These results provide the proof of principle that reductions in extracellular glucose and insulin, similar to in vivo CR, are sufficient to induce an increase in insulin-stimulated glucose transport comparable to the increase found with in vivo CR.

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