Glycolytic Muscle Fibers Research Articles

The Respiratory Compensation Point and the Deoxygenation Break Point Are Not Valid Surrogates for Critical Power and Maximum Lactate Steady State.

The Respiratory Compensation Point and the Deoxygenation Break Point Are Not Valid Surrogates for Critical Power and Maximum Lactate Steady State.

Lipin-1 regulates Bnip3-mediated mitophagy in glycolytic muscle.

Autophagy of mitochondria (mitophagy) is essential for maintaining muscle mass and healthy skeletal muscle. Patients with heritable phosphatidic acid phosphatase lipin-1-null mutations present with severe rhabdomyolysis and muscle atrophy in glycolytic muscle fibers, which are accompanied with mitochondrial aggregates and reduced mitochondrial cytochrome c oxidase activity. However, the underlying mechanisms leading to muscle atrophy as a result of lipin-1 deficiency are still not clear. In this study, we found that lipin-1 deficiency in mice is associated with a marked accumulation of abnormal mitochondria and autophagic vacuoles in glycolytic muscle fibers. Our studies using lipin-1-deficient myoblasts suggest that lipin-1 participates in B-cell leukemia (BCL)-2 adenovirus E1B 19 kDa protein-interacting protein 3 (Bnip3)-regulated mitophagy by interacting with microtubule-associated protein 1A/1B-light chain (LC)3, which is an important step in the recruitment of mitochondria to nascent autophagosomes. The requirement of lipin-1 for Bnip3-mediated mitophagy was further verified in vivo in lipin-1-deficient green fluorescent protein-LC3 transgenic mice (lipin-1-/--GFP-LC3). Finally, we showed that lipin-1 deficiency in mice resulted in defective mitochondrial adaptation to starvation-induced metabolic stress and impaired contractile muscle force in glycolytic muscle fibers. In summary, our study suggests that deregulated mitophagy arising from lipin-1 deficiency is associated with impaired muscle function and may contribute to muscle rhabdomyolysis in humans.-Alshudukhi, A. A., Zhu, J., Huang, D., Jama, A., Smith, J. D., Wang, Q. J., Esser, K. A., Ren, H. Lipin-1 regulates Bnip3-mediated mitophagy in glycolytic muscle.

Lauric Acid Accelerates Glycolytic Muscle Fiber Formation through TLR4 Signaling.

Lauric acid (LA), which is the primary fatty acid in coconut oil, was reported to have many metabolic benefits. TLR4 is a common receptor of lipopolysaccharides and involved mainly in inflammation responses. Here, we focused on the effects of LA on skeletal muscle fiber types and metabolism. We found that 200 μM LA treatment in C2C12 or dietary supplementation of 1% LA increased MHCIIb protein expression and the proportion of type IIb muscle fibers from 0.452 ± 0.0165 to 0.572 ± 0.0153, increasing the mRNA expression of genes involved in glycolysis, such as HK2 and LDH2 (from 1.00 ± 0.110 to 1.35 ± 0.0843 and from 1.00 ± 0.123 to 1.71 ± 0.302 in vivo, respectively), decreasing the catalytic activity of lactate dehydrogenase (LDH), and transforming lactic acid to pyruvic acid. Furthermore, LA activated TLR4 signaling, and TLR4 knockdown reversed the effect of LA on muscle fiber type and glycolysis. Thus, we inferred that LA promoted glycolytic fiber formation through TLR4 signaling.

Ginsenoside Rg1 augments oxidative metabolism and anabolic response of skeletal muscle in mice

BackgroundThe ginsenoside Rg1 has been shown to exert various pharmacological activities with health benefits. Previously, we have reported that Rg1 promoted myogenic differentiation and myotube growth in C2C12 myoblasts. In this study, the in vivo effect of Rg1 on fiber-type composition and oxidative metabolism in skeletal muscle was examined. MethodsTo examine the effect of Rg1 on skeletal muscle, 3-month-old mice were treated with Rg1 for 5 weeks. To assess muscle strength, grip strength tests were performed, and the lower hind limb muscles were harvested, followed by various detailed analysis, such as histological staining, immunoblotting, immunostaining, and real-time quantitative reverse transcription polymerase chain reaction. In addition, to verify the in vivo data, primary myoblasts isolated from mice were treated with Rg1, and the Rg1 effect on myotube growth was examined by immunoblotting and immunostaining analysis. ResultsRg1 treatment increased the expression of myosin heavy chain isoforms characteristic for both oxidative and glycolytic muscle fibers; increased myofiber sizes were accompanied by enhanced muscle strength. Rg1 treatment also enhanced oxidative muscle metabolism with elevated oxidative phosphorylation proteins. Furthermore, Rg1-treated muscles exhibited increased levels of anabolic S6 kinase signaling. ConclusionRg1 improves muscle functionality via enhancing muscle gene expression and oxidative muscle metabolism in mice.

Characterization of Mitochondrial Content and Respiratory Capacities of Broiler Chicken Skeletal Muscles with Different Muscle Fiber Compositions.

Mitochondrial content is regarded a useful feature to distinguish muscle-fiber types in terms of energy metabolism in skeletal muscles. Increasing evidence suggests that specific mitochondrial bioenergetic phenotypes exist in metabolically different muscle fibers. A few studies have examined the energetic properties of skeletal muscle in domestic fowls; however, no information on muscle bioenergetics in broiler chickens selectively bred for faster growth is available. In this study, we aimed to characterize the mitochondrial contents and functions of chicken skeletal muscle consisting entirely of type I (oxidative) (M. pubo-ischio-femoralis pars medialis), type IIA (glycolytic/oxidative) (M. pubo-ischio-femoralis pars lateralis), and type IIB (glycolytic) (M. pectoralis) muscle fibers. Citrate synthase (CS) activity was the highest in type IIA muscle tissues and isolated mitochondria, among the muscle tissues tested. Although no difference was registered in mitochondrial CS activity between type IIB and type I muscles, tissue CS activity was significantly higher in the latter. Histochemical staining for NADH tetrazolium reductase and the ratio of muscle-tissue to mitochondrial CS activity indicated that type I, type IIA, and type IIB muscle-fiber types showed decreasing mitochondrial content. Mitochondria from type I muscle exhibited a higher coupled respiration rate induced by pyruvate/malate, palmitoyl-CoA/malate, and palmitoyl-carnitine, as respiratory substrates, than type IIB-muscle mitochondria, while the response of mitochondria from type IIA muscle to those substrates was comparable to that of mitochondria from type I muscle. Type IIA-muscle mitochondria exhibited the highest carnitine palmitoyltransferase-2 level among all tissues tested, which may contribute to the higher fatty acid oxidation in these mitochondria. The results suggest that mitochondrial abundance is one of the features differentiating metabolic characteristics of different chicken skeletal muscle types. Moreover, the study demonstrated that type IIA-muscle mitochondria may have distinct metabolic capacities.

The effects of alpha-lipoic acid on diabetic myopathy.

Increased oxidative stress and impaired antioxidant defense are important mechanisms in the pathogenesis of diabetic myopathy. Since diabetes mellitus type 1 decreases muscle regeneration capacity the present study was designed to determine the influence of alpha-lipoic acid (ALA), a potent biological antioxidant, on the process of regeneration of diabetic rat skeletal muscles. 40 Wistar rats were divided into three groups: control (n=8), untreated diabetic group (n=16) and ALA treated diabetic group (n=16). The regeneration process was provoked in streptozotocin-induced diabetic rats in both slow (m.soleus, SOL) and fast (m.extensor digitorum longus, EDL) skeletal muscles by intramuscular injection of myotoxin bupivacaine. At intervals of 10 days and 4 weeks, muscle histochemical and morphometrical analysis (fiber cross areas and fiber type distribution) was performed. Changes induced by diabetes are evident in redistribution of muscle fibers and in significant level of atrophy. After 4 weeks of diabetes, glycolytic muscle fibers are dominant in both slow and fast muscles. Muscle atrophy is present in all fiber types except in type I of slow skeletal muscle. Treatment with ALA reduce changes in the morphological properties caused by diabetes mellitus type 1 in slow and fast rat skeletal muscles during the process of regeneration. Treatment with lipoic acid during 4 weeks has shown effects on the redistribution of muscle fibers, and can prevent atrophy in slow and fast diabetic muscle.

A Proteomic Approach to Identify Alterations in the Small Ubiquitin-like Modifier (SUMO) Network during Controlled Mechanical Ventilation in Rat Diaphragm Muscle

The small ubiquitin-like modifier (SUMO) is as a regulator of many cellular functions by reversible conjugation to a broad number of substrates. Under endogenous or exogenous perturbations, the SUMO network becomes a fine sensor of stress conditions by alterations in the expression level of SUMO enzymes and consequently changing the status of SUMOylated proteins. The diaphragm is the major inspiratory muscle, which is continuously active under physiological conditions, but its structure and function is severely affected when passively displaced for long extents during mechanical ventilation (MV). An iatrogenic condition called Ventilator-Induced Diaphragm Dysfunction (VIDD) is a major cause of failure to wean patients from ventilator support but the molecular mechanisms underlying this dysfunction are not fully understood. Using a unique experimental Intensive Care Unit (ICU) rat model allowing long-term MV, diaphragm muscles were collected in rats control and exposed to controlled MV (CMV) for durations varying between 1 and 10 days. Endogenous SUMOylated diaphragm proteins were identified by mass spectrometry and validated with in vitro SUMOylation systems. Contractile, calcium regulator and mitochondrial proteins were of specific interest due to their putative involvement in VIDD. Differences were observed in the abundance of SUMOylated proteins between glycolytic and oxidative muscle fibers in control animals and high levels of SUMOylated proteins were present in all fibers during CMV. Finally, previously reported VIDD biomarkers and therapeutic targets were also identified in our datasets which may play an important role in response to muscle weakness seen in ICU patients. Data are available via ProteomeXchange with identifier PXD006085. Username: reviewer26663@ebi.ac.uk, Password: rwcP5W0o.

Modulation of oxidative and glycolytic skeletal muscle fibers Na+/H+ exchanger1 (NHE1) and Na+/HCO3- co-transporter1 (NBC1) genes and proteins expression in type 2 diabetic rat (Streptozotocin + high fat diet) following long term endurance training.

Diabetes is known to alter both oxidative and glycolytic pathways in a fiber type-dependent manner. The aim of present study was to investigate the effects of endurance training on muscle NHE1 and NBC1 genes and proteins expression in type 2 diabetic rats. Male wistar rats (n=30), 4 weeks old and 95.7±10.8g, were randomly selected and divided into control, diabetic without training and diabetic with training groups. Diabetes was induced by injection of low dose of streptotozin and feeding with high-fat diet. The Endurance training was performed for 7 weeks that started with relatively low speed and duration of 20 m min-1 for 20 min in the first week and gradually reached to 30 m min-1 for 35min in the last week. NHE1 and NBC1 genes and proteins expression were determined by Real time-PCR and western blotting techniques, respectively, in Soleus as an oxidative and EDL (Extensor digitorum longus) as a glycolytic muscle preparation. NHE1 mRNA and protein expression reduced significantly in EDL and Soleus in the diabetic without training group compared with the control group. However, reduction in the expression of NBC1 gene and protein in the diabetic without training group compared to controls did not significant. Endurance training increased NHE1 and NBC1 genes and proteins expression in both EDL and Soleus in the diabetic training group compared to control groups. In conclusion, endurance training may improve the capacity of pHi regulation in muscles by lactate-independent pathway.

Measures of Growth Processes and Myogenesis in Glycolytic and Oxidative Muscle Fibers in Rats after Indirect Electrical Stimulation

We report here a comparative study of activity in signal pathways and gene expression in the red (RGM) and white (WGM) parts of the gastrocnemius muscle in rats after series of short (1 sec) tetanic contractions evoked by stimulation of the motor nerve at a frequency of 100 Hz and an amplitude sufficient to activate all the motor units of the muscle. At 2 h after stimulation, WGM showed more marked increases in the level of ERK1/2 phosphorylation than RGM, though increases in AMPK phosphorylation were no different. Furthermore, the increases in MyoD and myogenin mRNA in WGM were significantly greater than those in RGM, while the effects of stimulation on expression of the IGF-1, MaFbx, and MuRF genes were weak and similar in WGM and RGM. There was also an increase in the content of myostatin mRNA in RGM. Thus, glycolytic muscle fibers in WGM display more marked regulatory hypertrophic-type shifts than the oxidative muscle fibers making up RGM.

RNA-seq and metabolomic analyses of Akt1-mediated muscle growth reveals regulation of regenerative pathways and changes in the muscle secretome

BackgroundSkeletal muscle is a major regulator of systemic metabolism as it serves as the major site for glucose disposal and the main reservoir for amino acids. With aging, cachexia, starvation, and myositis, there is a preferential loss of fast glycolytic muscle fibers. We previously reported a mouse model in which a constitutively-active Akt transgene is induced to express in a subset of muscle groups leading to the hypertrophy of type IIb myofibers with an accompanying increase in strength. This muscle growth protects mice in various cardio-metabolic disease models, but little is known about the underlying cellular and molecular mechanisms by which fast-twitch muscle impacts disease processes and regulates distant tissues. In the present study, poly (A) + tail mRNA-seq and non-targeted metabolomics were performed to characterize the transcriptome and metabolome of the hypertrophic gastrocnemius muscle from Akt1-transgenic mice.ResultsCombined metabolomics and transcriptomic analyses revealed that Akt1-induced muscle growth mediated a metabolic shift involving reductions in glycolysis and oxidative phosphorylation, but enhanced pentose phosphate pathway activation and increased branch chain amino acid accumulation. Pathway analysis for the 4,027 differentially expressed genes in muscle identified enriched signaling pathways involving growth, cell cycle regulation, and inflammation. Consistent with a regenerative transcriptional signature, the transgenic muscle tissue was found to be comprised of fibers with centralized nuclei that are positive for embryonic myosin heavy chain. Immunohistochemical analysis also revealed the presence of inflammatory cells associated with the regenerating fibers. Signal peptide prediction analysis revealed 240 differentially expressed in muscle transcripts that potentially encode secreted proteins. A number of these secreted factors have signaling properties that are consistent with the myogenic, metabolic and cardiovascular-protective properties that have previously been associated with type IIb muscle growth.ConclusionsThis study provides the first extensive transcriptomic sequencing/metabolomics analysis for a model of fast-twitch myofiber growth. These data reveal that enhanced Akt signaling promotes the activation of pathways that are important for the production of proteins and nucleic acids. Numerous transcripts potentially encoding muscle secreted proteins were identified, indicating the importance of fast-twitch muscle in inter-tissue communication.

Muscle atrophy is associated with cervical spinal motoneuron loss in BACHD mouse model for Huntington's disease.

Involuntary choreiform movements are clinical hallmark of Huntington's disease, an autosomal dominant neurodegenerative disorder caused by an increased number of CAG trinucleotide repeats in the huntingtin gene. Involuntary movements start with an impairment of facial muscles and then affect trunk and limbs muscles. Huntington's disease symptoms are caused by changes in cortex and striatum neurons induced by mutated huntingtin protein. However, little is known about the impact of this abnormal protein in spinal cord motoneurons that control movement. Therefore, in this study we evaluated abnormalities in the motor unit (spinal cervical motoneurons, motor axons, neuromuscular junctions and muscle) in a mouse model for Huntington's disease (BACHD). Using light, fluorescence, confocal, and electron microscopy, we showed significant changes such as muscle fibers atrophy, fragmentation of neuromuscular junctions, axonal alterations, and motoneurons death in BACHD mice. Noteworthy, the surviving motoneurons from BACHD spinal cords were smaller than WT. We suggest that this loss of larger putative motoneurons is accompanied by a decrease in the expression of fast glycolytic muscle fibers in this model for Huntington's disease. These observations show spinal cord motoneurons loss in BACHD that might help to understand neuromuscular changes in Huntington's disease.

Inhibition of Intracellular Triglyceride Lipolysis Suppresses Cold-Induced Brown Adipose Tissue Metabolism and Increases Shivering in Humans

Indirect evidence from human studies suggests that brown adipose tissue (BAT) thermogenesis is fueled predominantly by fatty acids hydrolyzed from intracellular triglycerides (TGs). However, no direct experimental evidence to support this assumption currently exists in humans. The aim of this study was to determine the role of intracellular TG in BAT thermogenesis, in cold-exposed men. Using positron emission tomography with 11C-acetate and 18F-fluorodeoxyglucose, we showed that oral nicotinic acid (NiAc) administration, an inhibitor of intracellular TG lipolysis, suppressed the cold-induced increase in BAT oxidative metabolism and glucose uptake, despite no difference in BAT blood flow. There was a commensurate increase in shivering intensity and shift toward a greater reliance on glycolytic muscle fibers without modifying total heat production. Together, these findings show that intracellular TG lipolysis is critical for BAT thermogenesis and provides experimental evidence for a reciprocal role of BAT thermogenesis and shivering in cold-induced thermogenesis in humans.

Transfer of \u03b2-hydroxy-\u03b2-methylbutyrate from sows to their offspring and its impact on muscle fiber type transformation and performance in pigs

BackgroundPrevious studies suggested that supplementation of lactating sows with β-hydroxy-β-methylbutyrate (HMB) could improve the performance of weaning pigs, but there were little information in the muscle fiber type transformation of the offspring and the subsequent performance in pigs from weaning through finishing in response to maternal HMB consumption. The purpose of this study was to determine the effect of supplementing lactating sows with HMB on skeletal muscle fiber type transformation and growth of the offspring during d 28 and 180 after birth. A total of 20 sows according to their body weight were divided into the control (CON, n = 10) or HMB groups (HMB, n = 10). Sows in the HMB group were supplemented with β-hydroxy-β-methylbutyrate calcium (HMB-Ca) 2 g /kg feed during d 1 to 27 of lactation. After weaning, 48 mixed sex piglets were blocked by sow treatment and fed standard diets for post-weaning, growing, finishing periods. Growth performance was recorded during d 28 to 180 after birth. Pigs were slaughtered on d 28 (n = 6/treatment) and 180 (n = 6/treatment) postnatal, and the longissimus dorsi (LD) was collected, respectively.ResultsThe HMB-fed sows during lactation showed increased HMB concentration (P < 0.05) in milk and LD of weaning piglets (P < 0.05). In addition, offsprings in HMB group had a higher finishing BW and lean percentage than did pigs in CON group (P < 0.05), meanwhile, compared with pigs from sows fed the CON diet, pigs from sows fed HMB diet showed higher type II muscle fiber cross-sectional area (CSA), elevated myosin heavy chain (MyHC) IIb and Sox6 mRNA, and fast-MyHC protein levels in LD (P < 0.05).ConclusionsHMB supplemented to sow diets throughout lactation increases the levels of HMB in maternal milk and skeletal muscle of pigs during d 28 after birth and promotes subsequent performance of pigs between d 28 and 180 of age by enhancing glycolytic muscle fiber transformation.

Resistance Training Alters the Proportion of Skeletal Muscle Fibers but Not Brain Neurotrophic Factors in Young Adult Rats.

Antonio-Santos, J, Ferreira, DJS, Gomes Costa, GL, Matos, RJB, Toscano, AE, Manhães-de-Castro, R, and Leandro, CG. Resistance training alters the proportion of skeletal muscle fibers but not brain neurotrophic factors in young adult rats. J Strength Cond Res 30(12): 3531–3538, 2016—Resistance training (RT) is related to improved muscular strength and power output. Different programs of RT for rats have been developed, but peripheral and central response has not been evaluated directly in the same animal. To test the hypothesis that RT induces central and peripheral adaptations, this study evaluated the effects of a RT on the performance of a weekly maximum overload test, fiber-type typology, and brain neurotrophic factors in young adult rats. Thirty-one male Wistar rats (65 ± 5 days) were divided in 2 groups: nontrained (NT, n = 13) and trained (T, n = 18). Trained group was submitted to a program of RT ladder climbing, gradually added mass, 5 days per week during 8 weeks at 80% of individual maximum overload. This test was weekly performed to adjust the individual load throughout the weeks for both groups. After 48 hours from the last session of exercise, soleus and extensor digital longus (EDL) muscles were removed for myofibrillar ATPase staining analysis. Spinal cord, motor cortex, and cerebellum were removed for RT-PCR analysis of BDNF and insulin-like growth factor-1 (IGF-1) gene expression. In EDL muscle, T animals showed an increase in the proportion of type IIb fibers and a reduction of type IIa fibers. Insulin-like growth factor-1 gene expression was reduced in the cerebellum of T animals (NT: 1.025 ± 0.12; T: 0.57 ± 0.11). Our data showed that 8 weeks of RT were enough to increase maximum overload capacity and the proportion of glycolytic muscle fibers, but there were no associations with the expression of growth neurotrophic factors.

Muscle fiber-type conversion in the transgenic pigs with overexpression of PGC1α gene in muscle

The peroxisome proliferator-activated receptor gamma, co-activator 1 alpha(PGC1α) effectively induced the biosynthesis of the mitochondria and the energy metabolism, and also regulated the muscle fiber-type shift. Overexpression of PGC1α gene in mice led to higher oxidative muscle fiber composition in muscle. However, no researches about the significant differences of muscle fiber phenotype in pigs after PGC1α overexpression had been reported. The composition of muscle fiber-types which were distinguished by four myosin heavy chain(MYHC) isoforms, can significantly affect the muscle functions. In our study, we generated the transgenic pigs to investigate the effect of overexpression of PGC1α gene on muscle fiber-type conversion. The results showed that the number of oxidative muscle fiber(type1 muscle fiber) was increased and the number of glycolytic muscle fiber(type2b muscle fiber) was decreased in the transgenic pigs. Furthermore, we found that PGC1α overexpression up-regulated the expression of MYHC1 and MYHC2a and down-regulated the expression of MYHC2b.The analysis of genes expression demonstrated the main differentially expressed genes were MSTN, Myog and FOXO1. In conclusion, the overexpression of PGC1α gene can promote the glycolytic muscle fiber transform to the oxidative muscle fiber in pigs.

The impact of gender and age on the nutritional parameters of alpaca (Vicugna pacos) meat, colour stability and fat traits

Meat quality parameters for 50 huacaya alpacas, representing three age groups (18, 24 and 36months) and two genders (females and castrated males) were studied. Prior to chilling, samples of m. longissimus thoracis et lumborum (LL) were taken to determine isocitrate dehydrogenase activity and glycogen concentration, and further meat quality samples were taken after 24h. Alpaca meat has low levels (<1%) of intramuscular fat in the LL, m. semimembranosus and m. biceps femoris, but the level in the LL increases with animal age, with levels of desirable polyunsaturated fatty acids (PUFA) ranging from 96.3 to 136.4mg/100g. Lipid oxidisation post retail display ranged from 1.27 to 1.96MDA/kg meat. Colour stability testing indicated alpaca meat was relatively stable during retail display with day of display having no significant effect on lightness (L*), or the 630nm/580nm ratio. These results may relate to the high proportion (76%) of glycolytic and type IIX muscle fibres in LL.

Abstract B08: Altering cellular differentiation and energy metabolism by the mTORC1 inhibitor NPRL2

Abstract Nitrogen permease regulator-like 2 (NPRL2) is a component of an evolutionarily conserved complex that inhibits mTORC1 (mechanistic Target Of Rapamycin Complex 1) in response to amino acid insufficiency. The NPRL2 complex functions as a GTPase activating protein against the RAG proteins, which are located on the lysosomal surface and stimulate mTORC1 activity when bound to GTP. Since the loss of NPRL2 expression is frequently associated with different types of cancers, including renal and lung, our aim is to investigate the biological function of NPRL2 in vivo and determine how this pathway can contribute to cancer growth. Previous data from our lab show that NPRL2 is required for mouse viability and that its absence significantly compromises fetal liver hematopoiesis in embryos with defective lysosomal processing of vitamin B12 and methionine/SAM homeostasis contributing to the phenotype. Here we show that loss of NPRL2 in muscle alters the differentiation of fiber-types, leading to increased size and number of glycolytic muscle fibers in the mice. Consistent with this phenotype, the NPRL2 muscle specific knockout mice show a sprinting phenotype and increased glucose utilization. These findings demonstrate that NPRL2 is able to regulate cellular differentiation patterns potentially by altering cellular methylation and represents a genetic link between amino acid metabolism and carbohydrate utilization, two hallmarks that are frequently altered in cancer. Citation Format: Paul A. Dutchak, SandiJo Terpack, Benjamin P. Tu. Altering cellular differentiation and energy metabolism by the mTORC1 inhibitor NPRL2. [abstract]. In: Proceedings of the AACR Special Conference: Developmental Biology and Cancer; Nov 30-Dec 3, 2015; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(4_Suppl):Abstract nr B08.

Image Analysis of Oxidative and Glycolytic Muscle Fibers During Reperfusion Injury by Segmentation Based on Regions

Different situations cause ischemia and reperfusion injury, affecting tissues under the level of compression. In this research, abnormal characteristics in distribution of muscle fibers types in soleus and extensor carpi radialis longus, during short periods of ischemia and short and long periods of reperfusion, were determined. Fibers were classified by enzyme histochemistry techniques NADH-TR and myosin-ATPase. Measurements of areas were carried out through semiautomatic image processing by using segmentation based on regions, which evidenced significant changes in distribution during reperfusion followed to one and three hours of ischemia, as well as in comparisons of areas for all periods of reperfusion. This study strengthens the evidence about using practical procedures of image analysis in the diagnosis of tisular abnormalities.

Short-term ursolic acid promotes skeletal muscle rejuvenation through enhancing of SIRT1 expression and satellite cells proliferation.

Ursolic acid (UA) is a triterpenoid compound, which exerts its influences on the skeletal muscles. However, the mechanisms underlying these effects are still unclear. In this study, muscle satellite cells were isolated and purified by high-throughput pre-plating method (∼>60%) from 10 days old mice skeletal muscles. Evaluation of paired-box 7 (Pax7) expressions then confirmed the purification. Treatment of the cells with UA showed that UA up-regulated SIRT1 (∼35 folds) and overexpressed PGC-1α (∼175 folds) gene significantly. Moreover, the number of muscle satellite cells, which accompanied by initiation of neomyogenesis in the animal skeletal muscles, was increased (∼3.4 times). We also evaluated UA-mediated changes in the cellular energy status in the skeletal muscles. The results revealed that in the UA-treated mice, ATP and ADP contents in the various skeletal muscle tissue types, including: Gastrocnemius (Gas), Tibialis Anterior (Tib) and Gluteus Maximus (Glu) have been significantly decreased (P≤0.001); 2.2, 3.2, 2 times for ATP, and 9.6, 35.7, 11.6 times for ADP, respectively; however to compensate this process mitochondrial biogenesis occurred (12.33%±1.5 times). Furthermore, a rise in ATP/ADP ratio was observed 2.5, 4.5, 2.05 times for Gas, Tib and Glu muscles, respectively (P≤0.001). Alternatively, UA enhanced the expression of myoglobin (∼2 folds) in concert with remodeling of glycolytic muscle fibers to mainly fast IIA (∼30%) and slow-twitch (∼4%) types as well. Finally, our study indicated that UA indirectly mimicked beneficial effects of short-term calorie restriction and exercise (fast-oxidative) by directing the skeletal muscle composition toward oxidative metabolism.

Comparisons of different myosin heavy chain types, AMPK, and PGC-1α gene expression in the longissimus dorsi muscles in Bama Xiang and Landrace pigs

Bama Xiang and Landrace pigs are the local fatty and lean breeds, respectively, in China. We compared differences in carcass traits, meat quality traits, and myosin heavy chain (MyHC) types in the longissimus dorsi muscles between Bama Xiang and Landrace pigs. This was done in pigs of the same age, using real-time PCR, to investigate the relationship between MyHC fiber types and carcass characteristics, meat quality traits, and the key factors regulating muscle fiber type. Bama Xiang pigs exhibited smaller size and slower growth than Landrace pigs (P < 0.01). We found that the superior meat quality, especially the high intramuscular fat (IMF) content in Bama Xiang pig, was related to elevated type I oxidative muscle fiber content (P < 0.01). In contrast, Landrace pig muscle had a higher glycolytic type IIb muscle fiber content (P < 0.01). MyHC I gene expression was significantly positively correlated with backfat thickness and IMF content (P < 0.01). MyHC IIb was significantly negatively correlated with IMF content (P < 0.05), and positively correlated with carcass yield (P < 0.05). AMP-activated protein kinase and peroxisome proliferator-activated receptor-g coactivator-1a are suggested to be the two key factors regulating muscle fiber type in pigs. Our results indicate that muscle fiber composition is one of the key differences leading to the differences of meat quality between Bama Xiang and Landrace pigs. These results may provide a theoretical basis for further studies of the molecular mechanism underlying the excellent meat quality of the Bama Xiang pig.