scholarly journals Age Dependent Modification of the Metabolic Profile of the Tibialis Anterior Muscle Fibers in C57BL/6J Mice

2020 ◽  
Vol 21 (11) ◽  
pp. 3923
Author(s):  
Emiliana Giacomello ◽  
Emanuela Crea ◽  
Lucio Torelli ◽  
Alberta Bergamo ◽  
Carlo Reggiani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Tibialis Anterior ◽  
Skeletal Muscles ◽  
Tibialis Anterior Muscle ◽  
Morphological Characteristics ◽  
Oxidative Capacity ◽  
Essential Information ◽  
Metabolic Properties ◽  
Architectural Organization

Skeletal muscle aging is accompanied by mass reduction and functional decline, as a result of multiple factors, such as protein expression, morphology of organelles, metabolic equilibria, and neural communication. Skeletal muscles are formed by multiple fibers that express different Myosin Heavy Chains (MyHCs) and have different metabolic properties and different blood supply, with the purpose to adapt their contraction to the functional need. The fine interplay between the different fibers composing a muscle and its architectural organization determine its functional properties. Immunohistochemical and histochemical analyses of the skeletal muscle tissue, besides evidencing morphological characteristics, allow for the precise determination of protein expression and metabolic properties, providing essential information at the single-fiber level. Aiming to gain further knowledge on the influence of aging on skeletal muscles, we investigated the expression of the MyHCs, the Succinate Dehydrogenase (SDH) activity, and the presence of capillaries and Tubular Aggregates (TAs) in the tibialis anterior muscles of physiologically aging C57BL/6J mice aged 8 (adult), 18 (middle aged), and 24 months (old). We observed an increase of type-IIB fast-contracting fibers, an increase of the oxidative capacity of type-IIX and -IIA fibers, a general decrease of the capillarization, and the onset of TAs in type-IIB fibers. These data suggest that aging entails a selective modification of the muscle fiber profiles.

scholarly journals Hyperbaric Oxygen Exposure Reduces Age-Related Decrease in Oxidative Capacity of the Tibialis Anterior Muscle in Mice

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Takahiro Nishizaka ◽  
Fumiko Nagatomo ◽  
Hidemi Fujino ◽  
Tomoko Nomura ◽  
Tomohiko Sano ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Tibialis Anterior ◽  
Skeletal Muscles ◽  
Tibialis Anterior Muscle ◽  
Oxidative Capacity ◽  
Marker Enzyme ◽  
Histochemical Analysis ◽  
Age Related ◽  
Hyperbaric Oxygen Exposure ◽  
Old Mice

The effects of exposure to hyperbaric oxygen on the oxidative capacity of the skeletal muscles in mice at different ages were investigated. We exposed 5-, 34-, 55-, and 88-week-old mice to 36% oxygen at 950 mmHg for 6 hours per day for 2 weeks. The activities of succinate dehydrogenase (SDH), which is a mitochondrial marker enzyme, of the tibialis anterior muscle in hyperbaric mice were compared with those in age-matched mice under normobaric conditions (21% oxygen at 760 mmHg). Furthermore, the SDH activities of type IIA and type IIB fibers in the muscle were determined using quantitative histochemical analysis. The SDH activity of the muscle in normobaric mice decreased with age. Similar results were observed in both type IIA and type IIB fibers in the muscle. The decrease in the SDH activity of the muscle was reduced in hyperbaric mice at 57 and 90 weeks. The decreased SDH activities of type IIA and type IIB fibers were reduced in hyperbaric mice at 90 weeks and at 57 and 90 weeks, respectively. We conclude that exposure to hyperbaric oxygen used in this study reduces the age-related decrease in the oxidative capacity of skeletal muscles.

scholarly journals PO-169 Effect of Exercise-Induced Skeletal Muscle FSTL1 on Cardiac Structure and Function in Myocardial Infarction Rats

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Meili Hao ◽  
Yue Xi ◽  
Mengxin Cai ◽  
Zhenjun Tian
Keyword(s):  
Myocardial Infarction ◽  
Skeletal Muscle ◽  
Protein Expression ◽  
Resistance Exercise ◽  
Tibialis Anterior ◽  
Heart Function ◽  
Tibialis Anterior Muscle ◽  
Cardiomyocyte Apoptosis ◽  
Cardiomyocyte Proliferation ◽  
Adeno Associated Virus

Objective The aim of this study is to investigate the effect of skeletal muscle-derived FSTL1 on cardioprotection in myocardial infarction rats after resistance exercise or tibialis anterior muscle injection of follistatin-like protein 1 (FSTL1) adeno-associated virus vector and its possible signaling mechanisms. Methods The male Sprague-Dawley rats were randomly divided into five groups (n=10): Sham-operated group(S), sedentary MI group (MI), MI with resistance exercise group (MR), MI with empty adeno-associated virus (AAV) vector group (MV) and MI with FSTL1-AAV group (MF) after the MI model established which was induced by left anterior descending (LAD) coronary artery ligation. S group underwent threading without ligation. 1 week post MI, rats in MR group underwent resistance exercise for 4 weeks, rats in MV and MF group were injected AAV empty vector and FSTL1-AAV in the tibialis anterior muscle of the left limb, respectively. The next day after exercise, rats were anesthetized and heart function was measured. Collagen volume fraction(%) of myocardium were observed and calculated by Masson staining; cardiomyocyte proliferation was measured by immunofluorescence; cardiomyocyte apoptosis was detected by TUNEL staining; The protein expression of skeletal muscle and serum FSTL1 and myocardium FSTL1, DIP2A, pAkt/Akt, p-mTOR/mTOR, CyclinD1, CDK4 and Bcl2/Bax in myocardium were measured by Western blotting. Results The skeletal muscle FSTL1 protein expression was decreased but the serum and myocardium FSTL1 were upregulated in MI group. The myocardium fibrosis, cardiomyocyte proliferation and cardiomyocyte apoptosis were increased and the heart function was declined after MI. After resistance exercise or tibialis anterior muscle injection of FSTL1-AAV, the skeletal muscle, serum and myocardium FSTL1 protein expression were significantly increased, and there was a significant positive correlation between each data. Myocardium fibrosis and cardiomyocyte apoptosis were also decreased, cardiomyocyte proliferation was increased and the heart function was significantly improved after FSTL1-AAV injection. Conclusions Resistance exercise increases skeletal muscle FSTL1 expression. Skeletal muscle-derived FSTL1 can reach the heart through blood circulation, promote cardiomyocyte proliferation, inhibit cardiomyocyte apoptosis, reduce myocardium fibrosis and improve heart function in MI rats. Myocardium FSTL1 binds to its receptor, DIP2A, and activates the Akt-mTOR signaling pathway might be the potential mechanism of this protective effect.

Structure of the cortical cytoskeleton in fibers of postural muscles and cardiomyocytes of mice after 30-day 2-g centrifugation

2015 ◽  
Vol 118 (5) ◽  
pp. 613-623 ◽  
Author(s):  
Irina V. Ogneva ◽  
V. Gnyubkin ◽  
N. Laroche ◽  
M. V. Maximova ◽  
I. M. Larina ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior ◽  
Mechanical Load ◽  
Tibialis Anterior Muscle ◽  
Muscle Fibers ◽  
Control Group ◽  
Negative Effects ◽  
Transverse Stiffness ◽  
G 12 ◽  
Cortical Cytoskeleton

Altered external mechanical loading during spaceflights causes negative effects on muscular and cardiovascular systems. The aim of the study was estimation of the cortical cytoskeleton statement of the skeletal muscle cells and cardiomyocytes. The state of the cortical cytoskeleton in C57BL6J mice soleus, tibialis anterior muscle fibers, and left ventricle cardiomyocytes was investigated after 30-day 2- g centrifugation (“2- g” group) and within 12 h after its completion (“2- g + 12-h” group). We used atomic force microscopy for estimating cell's transverse stiffness, Western blotting for measuring protein content, and RT-PCR for estimating their expression level. The transverse stiffness significantly decreased in cardiomyocytes (by 16%) and increased in skeletal muscles fibers (by 35% for soleus and by 29% for tibialis anterior muscle fibers) in animals of the 2-g group (compared with the control group). For cardiomyocytes, we found that, in the 2- g + 12-h group, α-actinin-1 content decreased in the membranous fraction (by 27%) and increased in cytoplasmic fraction (by 28%) of proteins (compared with the levels in the 2- g group). But for skeletal muscle fibers, similar changes were noted for α-actinin-4, but not for α-actinin-1. In conclusion, we showed that the different isoforms of α-actinins dissociate from cortical cytoskeleton under increased/decreased of mechanical load.

scholarly journals Arrdc2 and Arrdc3 elicit divergent changes in gene expression in skeletal muscle following anabolic and catabolic stimuli

2019 ◽  
Vol 51 (6) ◽  
pp. 208-217 ◽  
Author(s):  
Bradley S. Gordon ◽  
Michael L. Rossetti ◽  
Alexey M. Eroshkin
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Tibialis Anterior ◽  
Gene Networks ◽  
Tibialis Anterior Muscle ◽  
The Body ◽  
Molecular Networks ◽  
Expression Of Genes ◽  
Consistent Change ◽  
Mechanical Overload

Skeletal muscle is a highly plastic organ regulating various processes in the body. As such, loss of skeletal muscle underlies the increased morbidity and mortality risk that is associated with numerous conditions. However, no therapies are available to combat the loss of muscle mass during atrophic conditions, which is due in part to the incomplete understanding of the molecular networks altered by anabolic and catabolic stimuli. Thus, the current objective was to identify novel gene networks modulated by such stimuli. For this, total RNA from the tibialis anterior muscle of mice that were fasted overnight or fasted overnight and refed the next morning was subjected to microarray analysis. The refeeding stimulus altered the expression of genes associated with signal transduction. Specifically, expression of alpha arrestin domain containing 2 (Arrdc2) and alpha arrestin domain containing 3 (Arrdc3) was significantly lowered 70–85% by refeeding. Subsequent analysis showed that expression of these genes was also lowered 50–75% by mechanical overload, with the combination of nutrients and mechanical overload acting synergistically to lower Arrdc2 and Arrdc3 expression. On the converse, stimuli that suppress growth such as testosterone depletion or acute aerobic exercise increased Arrdc2 and Arrdc3 expression in skeletal muscle. While Arrdc2 and Arrdc3 exhibited divergent changes in expression following anabolic or catabolic stimuli, no other member of the Arrdc family of genes exhibited the consistent change in expression across the analyzed conditions. Thus, Arrdc2 and Arrdc3 are a novel set of genes that may be implicated in the regulation of skeletal muscle mass.

Inverse alterations of BCKA dehydrogenase activity in cardiac and skeletal muscles of diabetic rats

1999 ◽  
Vol 277 (4) ◽  
pp. E685-E692 ◽  
Author(s):  
Yolanda B. Lombardo ◽  
Cynthia Serdikoff ◽  
Manikkavasagar Thamotharan ◽  
Harbhajan S. Paul ◽  
Siamak A. Adibi
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Protein Expression ◽  
Cardiac Muscle ◽  
Dehydrogenase Activity ◽  
Skeletal Muscles ◽  
Diabetic Rats ◽  
Gene Expressions ◽  
The Difference ◽  
Activity State

Rat cardiac and skeletal muscles, which have been used as model tissues for studies of regulation of branched-chain α-keto acid (BCKA) oxidation, vary greatly in the activity state of their BCKA dehydrogenase. In the present experiment, we have investigated whether they also vary in response of their BCKA dehydrogenase to a metabolic alteration such as diabetes and, if so, to investigate the mechanism that underlies the difference. Diabetes was produced by depriving streptozotocin-treated rats of insulin administration for 96 h. The investigation of BCKA dehydrogenase in the skeletal muscle (gastrocnemius) showed that diabetes 1) increased its activity, 2) increased the protein and gene expressions of all of its subunits (E1α, E1β, E2), 3) increased its activity state, 4) decreased the rate of its inactivation, and 5) decreased the protein expression of its associated kinase (BCKAD kinase) without affecting its gene expression. In sharp contrast, the investigation of BCKA dehydrogenase in the cardiac muscle showed that diabetes 1) decreased its activity, 2) had no effect on either protein or gene expression of any of its subunits, 3) decreased its activity state, 4) increased its rate of inactivation, and 5) increased both the protein and gene expressions of its associated kinase. In conclusion, our data suggest that, in diabetes, the protein expression of BCKAD kinase is downregulated posttranscriptionally in the skeletal muscle, whereas it is upregulated pretranslationally in the cardiac muscle, causing inverse alterations of BCKA dehydrogenase activity in these muscles.

Pretranslational regulation of myoglobin gene expression

1987 ◽  
Vol 252 (4) ◽  
pp. C450-C453 ◽  
Author(s):  
L. E. Underwood ◽  
R. S. Williams
Keyword(s):  
Gene Expression ◽  
Tibialis Anterior ◽  
Skeletal Muscles ◽  
Blot Hybridization ◽  
Oxidative Capacity ◽  
Striated Muscles ◽  
Mrna Content ◽  
Slow Twitch ◽  
Rna Probe ◽  
Fast Twitch

We have used blot hybridization techniques and a specific anti-sense RNA probe to determine whether variation in myoglobin gene expression among mammalian striated muscles is attributable to pretranslational regulatory events. We observed that myoglobin mRNA was expressed to approximately 10- and 5-fold greater levels, respectively, in cardiac and soleus (slow-twitch, oxidative, skeletal) muscles of adult rabbits than in tibialis anterior (fast-twitch, glycolytic, skeletal) muscles. Furthermore, when oxidative capacity of tibialis anterior muscles was increased by 21 days of indirect electrical stimulation, a model of exercise conditioning, myoglobin mRNA content increased approximately 15-fold. We conclude that pretranslational mechanisms are important in regulation of myoglobin gene expression in mammalian muscles.

scholarly journals Effect of Electroacupuncture on the Expression of Agrin and Acetylcholine Receptor Subtypes in Rats with Tibialis Anterior Muscular Atrophy Induced by Sciatic Nerve Injection Injury

2017 ◽  
Vol 35 (4) ◽  
pp. 268-275 ◽  
Author(s):  
Jianqi Yu ◽  
Meng Wang ◽  
Junying Liu ◽  
Xiaoming Zhang ◽  
Shengbo Yang
Keyword(s):  
Sciatic Nerve ◽  
Protein Expression ◽  
Muscle Fibre ◽  
Acetylcholine Receptor ◽  
Muscle Atrophy ◽  
Tibialis Anterior ◽  
Tibialis Anterior Muscle ◽  
Control Group ◽  
Receptor Subtypes ◽  
Injection Injury

Objective To investigate the effects of electroacupuncture (EA) on mRNA and protein expression of agrin, acetylcholine receptor (AChR)-ε and AChR-γ in a rat model of tibialis anterior muscle atrophy induced by sciatic nerve injection injury, and to examine the underlying mechanism of action. Methods Fifty-four adult Sprague-Dawley rats were divided into four groups: healthy control group (CON, n=6); sciatic nerve injury group (SNI, n=24), comprising rats euthanased at 1, 2, 4 and 6 weeks, respectively, after penicillin injection-induced SNI (n=6 each); CON+EA group (n=12), comprising healthy rats euthanased at 4 and 6 weeks (after 2 and 4 weeks, respectively, of EA at GB30 and ST36); and SNI+EA group, comprising rats euthanased at 4 and 6 weeks (after 2 and 4 weeks, respectively, of EA). The sciatic nerve functional index (SFI), tibialis anterior muscle weight, muscle fibre cross-sectional area (CSA), and changes in agrin, AChR-ε, and AChR-γ expression levels were analysed. Results Compared with the control group (CON), SNI rats showed decreased SFI. The weight of the tibialis anterior muscle and muscle fibre CSA decreased initially and recovered slightly over time. mRNA/protein expression of agrin and AChR-ε were downregulated and AChR-γ expression was detectable (vs zero expression in the CON/CON+EA groups). There were no significant differences in CON+EA versus CON groups. However, the SNI+EA group exhibited significant improvements compared with the untreated SNI group (p<0.05). Conclusions EA may alleviate tibialis anterior muscle atrophy induced by sciatic nerve injection injury by upregulating agrin and AChR-ε and downregulating AChR-γ.

scholarly journals Endurance Exercise Training Up-Regulates Lipolytic Proteins and Reduces Triglyceride Content in Skeletal Muscle of Obese Subjects

2013 ◽  
Vol 98 (12) ◽  
pp. 4863-4871 ◽  
Author(s):  
Katie Louche ◽  
Pierre-Marie Badin ◽  
Emilie Montastier ◽  
Claire Laurens ◽  
Virginie Bourlier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Endurance Exercise ◽  
Oxidative Capacity ◽  
Metabolic Effects ◽  
Gene Identification ◽  
Mrna Levels ◽  
Endurance Exercise Training ◽  
Obese Subjects

Context: Skeletal muscle lipase and intramyocellular triglyceride (IMTG) play a role in obesity-related metabolic disorders. Objectives: The aim of the present study was to investigate the impact of 8 weeks of endurance exercise training on IMTG content and lipolytic proteins in obese male subjects. Design and Volunteers: Ten obese subjects completed an 8-week supervised endurance exercise training intervention in which vastus lateralis muscle biopsy samples were collected before and after training. Main Outcome Measures: Clinical characteristics and ex vivo substrate oxidation rates were measured pre- and posttraining. Skeletal muscle lipid content and lipolytic protein expression were also investigated. Results: Our data show that exercise training reduced IMTG content by 42% (P &lt; .01) and increased skeletal muscle oxidative capacity, whereas no change in total diacylglycerol content and glucose oxidation was found. Exercise training up-regulated adipose triglyceride lipase, perilipin (PLIN) 3 protein, and PLIN5 protein contents in skeletal muscle despite no change in mRNA levels. Training also increased hormone sensitive–lipase Ser660 phosphorylation. No significant changes in comparative gene identification 58, G0/G1 switch gene 2, and PLIN2 protein and mRNA levels were observed in response to training. Interestingly, we noted a strong relationship between skeletal muscle comparative gene identification 58 and mitochondrial respiratory chain complex I protein contents at baseline (r = 0.87, P &lt; .0001). Conclusions: Endurance exercise training coordinately up-regulates fat oxidative capacity and lipolytic protein expression in skeletal muscle of obese subjects. This physiological adaptation probably favors fat oxidation and may alleviate the lipotoxic lipid pressure in skeletal muscle. Enhancement of IMTG turnover may be required for the beneficial metabolic effects of exercise in obesity.

scholarly journals Compressed air massage: repeated treatment causes less muscle oedema than a single treatment

2007 ◽  
Vol 63 (2) ◽  
Author(s):  
M. A. Gregory ◽  
M. Mars
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior ◽  
Tibialis Anterior Muscle ◽  
Fibre Diameter ◽  
Compressed Air ◽  
Repeated Treatment ◽  
Vervet Monkeys ◽  
Single Muscle ◽  
Single Treatment ◽  
Similar Treatment

Compressed air massage is a new treatment modality that has been shown to cause skeletal muscle capillary dilation for up to 24 hours after a single treatment and significantly hastens healing of diabetic ulcers. This study compares the effect of one treatment of a single muscle group, with repeated treatments of several muscle groups. Methods: Four vervet monkeys underwent one, 15 min, treatment of compressed air massage at 1 Bar, to the tibialis anterior muscle and four animals received similar treatment to the whole lower leg on three consecutive days. The tibialis anterior of the treated and untreated limbs was biopsied immediately after the final treatment. Muscle fibre diameters were measured from 1µm thick toluidine blue stained resin embedded sections using light microscopy and computerized image analysis software. Results: For treatment of the whole lower limb, the mean fibre diameter increased by 6.0% from 47.31±13.4µm(95%CI:46.47-48.16) in control biopsies to 50.14±13.93µm (95%CI:49.26-51.02) in treated muscle (p<0.001).Treatment of a single muscle showed an increase in diameter of 11.3%, from 48.21±12.68µm (95%CI:47.31-49.11) to53.63+14.29µm (95%CI:52.61-54.66 (p<0.001). Treatment of a single muscle caused significantly more oedema thantreatment of the whole limb (p<0.001). Conclusions: Repeated treatment causes skeletal muscle oedema, and this appears to be dose related. Skeletal muscleoedema after three treatments is less than after a single treatment. Further studies on the use of compressed air massage on injured muscle are warranted.

scholarly journals Fatigue and neuromuscular block in mammalian skeletal muscle

1949 ◽  
Vol 136 (883) ◽  
pp. 182-195 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior ◽  
Neuromuscular Block ◽  
Tibialis Anterior Muscle ◽  
Muscle Fibres ◽  
Mammalian Skeletal Muscle ◽  
Direct Electrical Stimulation ◽  
Average Response ◽  
Response Frequency ◽  
Tension Time

Records have been taken of the tetanic tensions of the decerebrate cat’s soleus and tibialis anterior muscle, while these were excited maximally by direct electrical stimulation, or through the nerve at frequencies up to 250/sec. and for some 20 sec. The tension-time curves with both methods of stimulation were almost identical for any given frequency. Assessment of the neuromuscular block as fatigue progresses was made from observation of the tension changes which followed a sudden switch from direct to indirect excitation or vice versa. At frequencies above 40/sec., block can be demonstrated before there is any fall in tension. The block which develops is not absolute; fibres to which transmission is failing respond to some, but not to all nerve impulses. This enables block to be measured in terms of the average response frequency of the fibres. The response frequency of the muscle fibres during a tetanus depends only on the total number of stimuli which the nerve has received. The relation is of the form response frequency = a /(total stimuli) b where a and b are constants independent of frequency and duration of nerve stimulation. These constants are such that the average response frequency of the muscle fibres has fallen to 25/sec. after the nerve has received about 1000 stimuli at a frequency of 100/sec. Fibres which are rested by block can, when they do respond, develop up to three times the tension-time of unfatigued fibres. The development of neuromuscular block is not responsible for the fall of tension which occurs as the system fatigues.

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