scholarly journals On characterizing skeletal muscle contraction properties. Experimental and simulation methodology

1970 ◽  
pp. 63
Author(s):  
M. Sierra ◽  
M.J. Muñoz ◽  
J. Grasa
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior ◽  
Tetanic Contraction ◽  
Simulation Methodology ◽  
Skeletal Muscle Fatigue ◽  
Skeletal Muscle Contraction ◽  
Experimental Parameters ◽  
Male Wistar Rats ◽  
Different Characteristics

The main objective of this work is to characterize the fatigue contractile properties of threedifferent rat muscles (Tibialis Anterior, Extensor Digitorium Longus and Soleus) in order toobtain experimental parameters for numerical simulations.Experiments were conducted “in vivo" on three groups (n = 6) of male Wistar rats (210 +/- 11g)using a protocol developed by authors in previous works. Muscles were subjected to anelectrical stimulus to achieve tetanic contraction during ten seconds. Digital Image Correlationwas used during tests for 3D strain and displacements measurement that allow the correlationwith the finite element simulations.By means of Computed Tomography, a precise reconstruction of both bone and muscle of therat hindlimb geometry was obtained. The methodology proposed allows to obtain and validatecomputational simulations of skeletal muscle fatigue under different characteristics related tofiber types.63

Cachectin/TNF or IL-1 alpha induces cachexia with redistribution of body proteins

1989 ◽  
Vol 256 (3) ◽  
pp. R659-R665 ◽  
Author(s):  
Y. Fong ◽  
L. L. Moldawer ◽  
M. Marano ◽  
H. Wei ◽  
A. Barber ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Muscle Protein ◽  
Interleukin 1 ◽  
Metabolic Effects ◽  
Liver Protein ◽  
Mrna Levels ◽  
Skeletal Muscle Protein ◽  
Male Wistar Rats

Macrophage secretory products are suspected to participate in the severe lean tissue wasting related to chronic illness. The protein metabolic effects of chronic, 7-day cachectin/tumor necrosis factor (cachectin) or interleukin 1 alpha (IL-1 alpha) administration in vivo were studied in male Wistar rats that were 1) freely fed, 2) pair fed, 3) total protein and calorie starved, 4) twice daily lipopolysaccharide (LPS) administered, 5) twice daily cachectin administered, and 6) twice daily IL-1 alpha administered. LPS, cachectin, or IL-1 alpha administration produced anorexia; weight loss in these groups was comparable to respective pair-fed animals. However, LPS, cachectin, or IL-1 alpha accelerated peripheral protein wasting while preserving liver protein content, unlike the pattern in the pair-fed or starved animals in which loss of liver proteins and relative preservation of skeletal muscle protein were observed. The decrease in skeletal muscle protein content in LPS- or cytokine-treated animals was associated with coordinate decreases in muscle mRNA levels for the myofibrillar proteins myosin heavy chain, myosin light chain, actin, and in the 18S and 28S subunits of ribosomal RNA. We conclude that chronic exposure to the cytokines, IL-1 alpha or cachectin, can simulate those body and muscle protein changes seen in experimental LPS administration or chronic disease and markedly differ from the pattern of protein redistribution due to caloric restriction.

scholarly journals Visualization of Mitochondrial Ca2+ Signals in Skeletal Muscle of Zebrafish Embryos with Bioluminescent Indicators

2019 ◽  
Vol 20 (21) ◽  
pp. 5409 ◽  
Author(s):  
Manuel Vicente ◽  
Jussep Salgado-Almario ◽  
Joaquim Soriano ◽  
Miguel Burgos ◽  
Beatriz Domingo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contractions ◽  
Zebrafish Embryos ◽  
Mitochondrial Matrix ◽  
Mitochondrial Calcium Uniporter ◽  
Calcium Uniporter ◽  
Skeletal Muscle Contraction ◽  
Spatio Temporal ◽  
Mitochondrial Uncoupler

Mitochondria are believed to play an important role in shaping the intracellular Ca2+ transients during skeletal muscle contraction. There is discussion about whether mitochondrial matrix Ca2+ dynamics always mirror the cytoplasmic changes and whether this happens in vivo in whole organisms. In this study, we characterized cytosolic and mitochondrial Ca2+ signals during spontaneous skeletal muscle contractions in zebrafish embryos expressing bioluminescent GFP-aequorin (GA, cytoplasm) and mitoGFP-aequorin (mitoGA, trapped in the mitochondrial matrix). The Ca2+ transients measured with GA and mitoGA reflected contractions of the trunk observed by transmitted light. The mitochondrial uncoupler FCCP and the inhibitor of the mitochondrial calcium uniporter (MCU), DS16570511, abolished mitochondrial Ca2+ transients whereas they increased the frequency of cytosolic Ca2+ transients and muscle contractions, confirming the subcellular localization of mitoGA. Mitochondrial Ca2+ dynamics were also determined with mitoGA and were found to follow closely cytoplasmic changes, with a slower decay. Cytoplasmic Ca2+ kinetics and propagation along the trunk and tail were characterized with GA and with the genetically encoded fluorescent Ca2+ indicator, Twitch-4. Although fluorescence provided a better spatio-temporal resolution, GA was able to resolve the same kinetic parameters while allowing continuous measurements for hours.

scholarly journals Muscle-Derived Extracellular Signal-Regulated Kinases 1 and 2 Are Required for the Maintenance of Adult Myofibers and Their Neuromuscular Junctions

2015 ◽  
Vol 35 (7) ◽  
pp. 1238-1253 ◽  
Author(s):  
Bonnie Seaberg ◽  
Gabrielle Henslee ◽  
Shuo Wang ◽  
Ximena Paez-Colasante ◽  
Gary E. Landreth ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior ◽  
Neuromuscular Junctions ◽  
Germ Line ◽  
Fiber Type ◽  
Postnatal Growth ◽  
Mammalian Skeletal Muscle ◽  
Neuromuscular Synapses ◽  
Extracellular Signal

The Ras–extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway appears to be important for the development, maintenance, aging, and pathology of mammalian skeletal muscle. Yet no gene targeting ofErk1/2in muscle fibersin vivohas been reported to date. We combined a germ lineErk1mutation with Cre-loxPErk2inactivation in skeletal muscle to produce, for the first time, mice lacking ERK1/2 selectively in skeletal myofibers. Animals lacking muscle ERK1/2 displayed stunted postnatal growth, muscle weakness, and a shorter life span. Their muscles examined in this study, sternomastoid and tibialis anterior, displayed fragmented neuromuscular synapses and a mixture of modest fiber atrophy and loss but failed to show major changes in fiber type composition or absence of cell surface dystrophin. Whereas the lack of only ERK1 had no effects on the phenotypes studied, the lack of myofiber ERK2 explained synaptic fragmentation in the sternomastoid but not the tibialis anterior and a decrease in the expression of the acetylcholine receptor (AChR) epsilon subunit gene mRNA in both muscles. A reduction in AChR protein was documented in line with the above mRNA results. Evidence of partial denervation was found in the sternomastoid but not the tibialis anterior. Thus, myofiber ERK1/2 are differentially required for the maintenance of myofibers and neuromuscular synapses in adult mice.

scholarly journals Long-chain n-3 DHA reduces the extent of skeletal muscle fatigue in the rat in vivo hindlimb model

2013 ◽  
Vol 111 (6) ◽  
pp. 996-1003 ◽  
Author(s):  
Gregory E. Peoples ◽  
Peter L. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Fish Oil ◽  
Muscle Fatigue ◽  
Muscle Membrane ◽  
Mammalian Skeletal Muscle ◽  
Skeletal Muscle Fatigue ◽  
Arterial Blood ◽  
Oxygen Efficiency ◽  
Long Chain

Dietary fish oil modifies skeletal muscle membrane fatty acid composition and oxygen efficiency similar to changes in the myocardium. Oxygen efficiency is a key determinant of sustained force in mammalian skeletal muscle. Therefore, in the present study, we tested the effects of a fish-oil diet on skeletal muscle fatigue under the stress of contraction using the rat in vivo autologous perfused hindlimb model. For 8 weeks, male Wistar rats were fed a diet rich in saturated fat (SF), a diet rich in n-6 PUFA or a diet rich in long-chain (LC) n-3 PUFA DHA derived from fish oil. In anaesthetised, mechanically ventilated rats, with their hindlimbs perfused with arterial blood at a constant flow, the gastrocnemius–plantaris–soleus muscle bundle was stimulated via sciatic nerve (2 Hz, 6–12 V, 0·05 ms) to contract repetitively for 30 min. Rats fed the n-3 PUFA diet developed higher maximum twitch tension than those fed the SF and n-6 PUFA diets (P< 0·05) and sustained twitch tension through more repetitions before the tension declined to 50 % of the maximum twitch tension (P< 0·05). The n-3 PUFA group used less oxygen for tension developed and produced higher venous lactate concentrations with no difference in glycogen utilisation compared with the SF and n-6 PUFA groups. These results further support that incorporation of DHA into skeletal muscle membranes increases the efficiency of oxygen use over a range of contractile force and this is expressed as a higher sustained force and prolonged time to fatigue.

scholarly journals Syncoilin is required for generating maximum isometric stress in skeletal muscle but dispensable for muscle cytoarchitecture

2008 ◽  
Vol 294 (5) ◽  
pp. C1175-C1182 ◽  
Author(s):  
Jianlin Zhang ◽  
Marie-Louise Bang ◽  
David S. Gokhin ◽  
Yingchun Lu ◽  
Li Cui ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Striated Muscle ◽  
Neuromuscular Diseases ◽  
Eccentric Contraction ◽  
Lateral Force ◽  
Force Transmission ◽  
Skeletal Muscle Contraction ◽  
Supportive Role

Syncoilin is a striated muscle-specific intermediate filament-like protein, which is part of the dystrophin-associated protein complex (DPC) at the sarcolemma and provides a link between the extracellular matrix and the cytoskeleton through its interaction with α-dystrobrevin and desmin. Its upregulation in various neuromuscular diseases suggests that syncoilin may play a role in human myopathies. To study the functional role of syncoilin in cardiac and skeletal muscle in vivo, we generated syncoilin-deficient ( syncoilin−/−) mice. Our detailed analysis of these mice up to 2 yr of age revealed that syncoilin is entirely dispensable for cardiac and skeletal muscle development and maintenance of cellular structure but is required for efficient lateral force transmission during skeletal muscle contraction. Notably, syncoilin−/− skeletal muscle generates less maximal isometric stress than wild-type (WT) muscle but is as equally susceptible to eccentric contraction-induced injury as WT muscle. This suggests that syncoilin may play a supportive role for desmin in the efficient coupling of mechanical stress between the myofibril and fiber exterior. It is possible that the reduction in isometric stress production may predispose the syncoilin skeletal muscle to a dystrophic condition.

scholarly journals Effect of glucocorticoid excess on skeletal muscle and heart protein synthesis in adult and old rats

1998 ◽  
Vol 79 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Isabelle Savary ◽  
Elisabeth Debras ◽  
Dominique Dardevet ◽  
Claire Sornet ◽  
Pierre Capitan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Food Intake ◽  
Tibialis Anterior ◽  
Muscle Wasting ◽  
Recovery Period ◽  
Disease States ◽  
Old Rats ◽  
Fast Twitch

This study was carried out to analyse glucocorticoid-induced muscle wasting and subsequent recovery in adult (6-8 months) and old (18-24 months) rats because the increased incidence of various disease states results in hypersecretion of glucocorticoids in ageing. Adult and old rats received dexamethasone in their drinking water for 5 or 6 d and were then allowed to recover for 3 or 7 d. As dexamethasone decreased food intake, all groups were pair-fed to dexamethasonetreated old rats (i.e. the group that had the lowest food intake). At the end of the treatment, adult and old rats showed significant increases in blood glucose and plasma insulin concentrations. This increase disappeared during the recovery period. Protein synthesis of different muscles was assessed in vivo by a flooding dose of [13C]valine injected subcutaneously 50 min before slaughter. Dexamethasone induced a significant decrease in protein synthesis in fast-twitch glycolytic and oxidative glycolytic muscles (gastrocnemius, tibialis anterior, extensor digitorum longus). The treatment affected mostly ribosomal efficiency. Adult dexamethasone-treated rats showed an increase in protein synthesis compared with their pair-fed controls during the recovery period whereas old rats did not. Dexamethasone also significantly decreased protein synthesis in the predominantly oxidative soleus muscle but only in old rats, and increased protein synthesis in the heart of adult but not of old rats. Thus, in skeletal muscle, the catabolic effect of dexamethasone is maintained or amplified during ageing whereas the anabolic effect in heart is depressed. These results are consistent with muscle atrophy occurring with ageing.

scholarly journals Skeletal muscle metabolism in sea-acclimatized king penguins. I. Thermogenic mechanisms

2020 ◽  
Vol 223 (21) ◽  
pp. jeb233668
Author(s):  
Damien Roussel ◽  
Marion Le Coadic ◽  
Jean-Louis Rouanet ◽  
Claude Duchamp
Keyword(s):  
Skeletal Muscle ◽  
Muscle Metabolism ◽  
Exact Nature ◽  
Skeletal Muscle Metabolism ◽  
Energy Demands ◽  
Skeletal Muscle Contraction ◽  
Drastic Increase ◽  
Shivering Thermogenesis

ABSTRACTAt fledging, king penguin juveniles undergo a major energetic challenge to overcome the intense and prolonged energy demands for thermoregulation and locomotion imposed by life in cold seas. Among other responses, sea acclimatization triggers fuel selection in skeletal muscle metabolism towards lipid oxidation in vitro, which is reflected by a drastic increase in lipid-induced thermogenesis in vivo. However, the exact nature of skeletal muscle thermogenic mechanisms (shivering and/or non-shivering thermogenesis) remains undefined. The aim of the present study was to determine in vivo whether the capacity for non-shivering thermogenesis was enhanced by sea acclimatization. We measured body temperature, metabolic rate, heart rate and shivering activity in fully immersed king penguins (Aptenodytes patagonicus) exposed to water temperatures ranging from 12 to 29°C. Results from terrestrial pre-fledging juveniles were compared with those from sea-acclimatized immature penguins (hereafter ‘immatures’). The capacity for thermogenesis in water was as effective in juveniles as in immatures, while the capacity for non-shivering thermogenesis was not reinforced by sea acclimatization. This result suggests that king penguins mainly rely on skeletal muscle contraction (shivering or locomotor activity) to maintain endothermy at sea. Sea-acclimatized immature penguins also exhibited higher shivering efficiency and oxygen pulse (amount of oxygen consumed or energy expended per heartbeat) than pre-fledging juvenile birds. Such increase in shivering and cardiovascular efficiency may favor a more efficient activity–thermoregulatory heat substitution providing penguins with the aptitude to survive the tremendous energetic challenge imposed by marine life in cold circumpolar oceans.

scholarly journals REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

2014 ◽  
Vol 307 (11) ◽  
pp. E983-E993 ◽  
Author(s):  
Florian A. Britto ◽  
Gwenaelle Begue ◽  
Bernadette Rossano ◽  
Aurélie Docquier ◽  
Barbara Vernus ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Tibialis Anterior ◽  
Skeletal Muscle Mass ◽  
Gastrocnemius Muscle ◽  
Mtorc1 Signaling ◽  
Inhibition Of Protein Synthesis ◽  
Stress Dependent

REDD1 (regulated in development and DNA damage response 1) has been proposed to inhibit the mechanistic target of rapamycin complex 1 (mTORC1) during in vitro hypoxia. REDD1 expression is low under basal conditions but is highly increased in response to several catabolic stresses, like hypoxia and glucocorticoids. However, REDD1 function seems to be tissue and stress dependent, and its role in skeletal muscle in vivo has been poorly characterized. Here, we investigated the effect of REDD1 deletion on skeletal muscle mass, protein synthesis, proteolysis, and mTORC1 signaling pathway under basal conditions and after glucocorticoid administration. Whereas skeletal muscle mass and typology were unchanged between wild-type (WT) and REDD1-null mice, oral gavage with dexamethasone (DEX) for 7 days reduced tibialis anterior and gastrocnemius muscle weights as well as tibialis anterior fiber size only in WT. Similarly, REDD1 deletion prevented the inhibition of protein synthesis and mTORC1 activity (assessed by S6, 4E-BP1, and ULK1 phosphorylation) observed in gastrocnemius muscle of WT mice following single DEX administration for 5 h. However, our results suggest that REDD1-mediated inhibition of mTORC1 in skeletal muscle is not related to the modulation of the binding between TSC2 and 14-3-3. In contrast, our data highlight a new mechanism involved in mTORC1 inhibition linking REDD1, Akt, and PRAS40. Altogether, these results demonstrated in vivo that REDD1 is required for glucocorticoid-induced inhibition of protein synthesis via mTORC1 downregulation. Inhibition of REDD1 may thus be a strategy to limit muscle loss in glucocorticoid-mediated atrophy.

scholarly journals Anesthesia with Disuse Leads to Autophagy Up-regulation in the Skeletal Muscle

2015 ◽  
Vol 122 (5) ◽  
pp. 1075-1083 ◽  
Author(s):  
Aki Kashiwagi ◽  
Sachiko Hosokawa ◽  
Yoshihiro Maeyama ◽  
Ryusuke Ueki ◽  
Masao Kaneki ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
General Anesthesia ◽  
Tibialis Anterior ◽  
Fluorescent Protein ◽  
Short Term ◽  
Western Blots ◽  
Pentobarbital Anesthesia ◽  
Prolonged Sedation ◽  
Green Fluorescent

Abstract Background: It has been known that skeletal muscles show atrophic changes after prolonged sedation or general anesthesia. Whether these effects are due to anesthesia itself or disuse during anesthesia has not been fully clarified. Autophagy dysregulation has been implicated in muscle-wasting conditions. This study tested the hypothesis that the magnitude of skeletal muscle autophagy is affected by both anesthesia and immobility. Methods: The extent of autophagy was analyzed chronologically during general anesthesia. In vivo microscopy was performed using green fluorescent protein–tagged LC3 for the detection of autophagy using sternomastoid muscles of live mice during pentobarbital anesthesia (n = 6 and 7). Western blotting and histological analyses were also conducted on tibialis anterior muscles (n = 3 to 5). To distinguish the effect of anesthesia from that due to disuse, autophagy was compared between animals anesthetized with pentobarbital and those immobilized by short-term denervation without continuation of anesthesia. Conversely, tibialis anterior and sternomastoid muscles were electrically stimulated during anesthesia. Results: Western blots and microscopy showed time-dependent autophagy up-regulation during pentobarbital anesthesia, peaking at 3 h (728.6 ± 93.5% of basal level, mean ± SE). Disuse by denervation without sustaining anesthesia did not lead to equivalent autophagy, suggesting that anesthesia is essential to cause autophagy. In contrast, contractile stimulation of the tibialis anterior and sternomastoid muscles significantly reduced the autophagy up-regulation during anesthesia (85% at 300 min). Ketamine, ketamine plus xylazine, isoflurane, and propofol also up-regulated autophagy. Conclusions: Short-term disuse without anesthesia does not lead to autophagy, but anesthesia with disuse leads to marked up-regulation of autophagy.

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