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Acta Physiologica Sinica ; (6): 263-274, 2021.
Article in Chinese | WPRIM | ID: wpr-878255


The present study aims to investigate the effects of aerobic exercise and resistance exercise on lipid metabolism of skeletal muscle in high-fat diet (HFD)-induced insulin-resistant (IR) rats and the underlying mechanisms. Male Sprague-Dawley (SD) rats at age of 10 weeks were fed with HFD for 10 weeks to establish IR model. The IR rats were then randomly assigned into 3 groups, including IR control (IR) group, aerobic exercise (AE) group and resistance exercise (RE) group. An additional chow diet sedentary control (CON) group was used as well. Fasting blood glucose (FBG), insulin (FIN), glucagon and lipids, as well as triacylglycerol (TG), free fatty acids (FFA), and the protein expression of fatty acid translocase/cluster of differentiation 36 (FAT/CD36), carnitine palmitoyltransferase-1 (CPT-1), stearoyl-CoA desaturase-1 (SCD-1) and peroxisome proliferators-activated receptors γ (PPARγ) in skeletal muscles were measured after 8-week exercise interventions. The results showed that the contents of FBG, FIN, and LDL-C were increased by IR compared with CON group, and significantly decreased by aerobic exercise and resistance exercise; while aerobic exercise induced an increase in HDL-C as well. Furthermore, IR exhibited no significant effects on TG content of skeletal muscles, but significantly increased FFA level. Both aerobic and resistance exercise led to a decrease in TG content, and FFA level was increased by aerobic exercise but deceased by resistance exercise. In addition, the protein expression of FAT/CD36, SCD-1 and PPARγ was increased and that of CPT-1 was decreased by IR, while both types of exercise resulted in a decrease in the protein expression of FAT/CD36, SCD-1 and PPARγ, and an increase in CPT-1. In conclusion, aerobic and resistance exercise may attenuate IR through decreasing HFD-induced ectopic fat deposition and increasing β-oxidation of fatty acids in skeletal muscle cells, and resistance exercise shows a greater improvement in lipid metabolism of skeletal muscles than aerobic exercise.

Animals , Diet, High-Fat , Insulin/metabolism , Insulin Resistance , Lipid Metabolism , Lipids , Male , Muscle, Skeletal/metabolism , Rats , Rats, Sprague-Dawley
Rev. cuba. invest. bioméd ; 39(3): e645, jul.-set. 2020. tab, graf
Article in Spanish | LILACS, CUMED | ID: biblio-1138943


Introducción: Actualmente existen pocos estudios que relacionen la masa muscular de miembros inferiores y el salto vertical. Objetivo: Describir la asociación entre la masa muscular de miembros inferiores y el salto vertical en sujetos que practican musculación. Método: Estudio correlacional-exploratorio, con enfoque cuantitativo y una muestra a conveniencia de diez hombres (edad de 17,40±2,32 años, talla de 172,10 ± 5,76 cm y un peso corporal de 79,13 ± 19,54 Kg) practicantes de musculación participaron voluntariamente. Para estimar la masa muscular de miembros inferiores se utilizó una ecuación validada y se aplicó el salto con contramovimiento (countermovement jump, CMJ) y sentadilla con salto (squat jump, SJ). El análisis estadístico se efectuó en PSPP para Windows 7 para aplicar la prueba de normalidad de Shapiro-Wilk y el coeficiente correlacional de Pearson. Resultados: Los datos obtenidos presentaron distribución normal (p > 0,05), así mismo la masa muscular de miembros inferiores evidenció una relación negativa y significativa con salto con contramovimiento (countermovement jump, CMJ) (r = -0,73; p = 0,02), e igualmente con sentadilla con salto (squat jump, SJ) (r = -0,73; p = 0,02). Conclusión: La masa muscular de miembros inferiores no es un buen predictor del rendimiento en el salto vertical(AU)

Introduction: Few studies are currently available relating lower limb muscle mass and vertical jump. Objective: Describe the association between lower limb muscle mass and vertical jump in subjects who practice weight training. Method: A quantitative correlational-exploratory study was conducted of a convenience sample of ten men (age 17.40 ± 2.32 years, height 172.10 ± 5.76 cm and body weight 79.13 ± 19.54 kg) who practice weight training. Participation was voluntary. Lower limb muscle mass was estimated with a validated equation, and countermovement jump (CMJ) and squat jump (SJ) were considered. Statistical analysis was based on the software PSPP for Windows 7 to apply the Shapiro-Wilk normality test and Pearson's correlational coefficient. Results: The data obtained displayed a normal distribution (p > 0.05), with lower limb muscle mass exhibiting a negative significant relationship to countermovement jump (CMJ) (r = -0.73; p = 0.02) and squat jump (SJ) (r = -0.73; p = 0.02). Conclusion: Lower limb muscle mass is not a good predictor of vertical jump performance(AU)

Humans , Male , Young Adult , Sports/physiology , Lower Extremity/physiology , Resistance Training , Muscle, Skeletal/metabolism , Evaluation Studies as Topic
Acta Physiologica Sinica ; (6): 804-816, 2020.
Article in Chinese | WPRIM | ID: wpr-878228


Disturbance of the energy balance, when the energy intake exceeds its expenditure, is a major risk factor for the development of metabolic syndrome (MS). The peroxisome proliferator activated receptor γ (PPARγ) coactivator-1α (PGC-1α) functions as a key regulator of energy metabolism and has become a hotspot in current researches. PGC-1α sensitively responds to the environmental stimuli and nutrient signals, and further selectively binds to different transcription factors to regulate various physiological processes, including glucose metabolism, lipid metabolism, and circadian clock. In this review, we described the gene and protein structure of PGC-1α, and reviewed its tissue-specific function in the regulation of energy homeostasis in various mammalian metabolic organs, including liver, skeletal muscle and heart, etc. At the meanwhile, we summarized the application of potential small molecule compounds targeting PGC-1α in the treatment of metabolic diseases. This review will provide theoretical basis and potential drug targets for the treatment of metabolic diseases.

Animals , Energy Metabolism , Homeostasis , Lipid Metabolism , Liver/metabolism , Muscle, Skeletal/metabolism , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Transcription Factors/metabolism
Acta Physiologica Sinica ; (6): 631-642, 2020.
Article in Chinese | WPRIM | ID: wpr-878208


The aim of the present study was to investigate the effects of exercises with different durations and intensities on mitochondrial autophagy and FUNDC1 in rat skeletal muscles. Sixty male Sprague-Dawley rats were randomly divided into 2- and 4-week control groups (Con), moderate-intensity exercise groups (M-ex groups, treadmill exercise, 16 m/min, 1 h/d, 6 d/week), and high-intensity exercise groups (Hi-ex groups, treadmill exercise, 35 m/min, 20 min/d, 6 d/week). The bilateral soleus muscles were separated after the intervention, and paraffin sections were prepared for transmission electron microscopy. ELISA method was used to detect the content of citrate synthase (CS). The co-localizations of microtubule-associated protein 1 light chain 3 (LC3)/cytochrome c oxidase IV (COX-IV), FUNDC1/COX-IV and LC3/FUNDC1 were observed by immunofluorescent staining in frozen sections. The skeletal muscle mitochondria were extracted, and the expression of autophagy-related proteins, including AMPKα, p-AMPKα, Unc-51 like kinase 1 (ULK1), FUNDC1, LC3 and p62, were detected by Western blot. The results showed that exercise increased mitochondrial function, i.e. peroxisome proliferator-activated receptor γ co-activator-1α (PGC-1α), COX-I protein expression levels and CS content. There was no difference of mitochondrial function parameters between 2-week M-ex and 2-week Hi-ex groups, while mitochondrial function of 4-weeks Hi-ex group was significantly lower than that of 4-week M-ex group. Under the same exercise intensity, mitochondrial autophagy activation in skeletal muscle of 4-week exercise was higher than that in 2-week exercise group; Under the same duration of exercise, mitochondrial autophagy activation of Hi-ex group was higher than that in M-ex group. Both 2- and 4-week exercise intervention increased LC3/COX-IV, COX-IV/FUNDC1, and FUNDC1/LC3 co-localizations. Exercise increased LC3-II/LC3-I ratio, down-regulated p62 protein expression level, up-regulated FUNDC1, ULK1 protein expression levels and AMPKα phosphorylation, and the changes of these proteins in 4-week Hi-ex group were significantly greater than those in 4-week M-ex group. These results suggest exercise induces mitochondrial autophagy in skeletal muscles, and the activity of autophagy is related to the duration and intensity of exercise. The induction mechanism of exercise may involve the mediation of FUNDC1 expression through AMPK-ULK1 pathway.

Animals , Autophagy , Exercise Therapy , Humans , Male , Membrane Proteins/physiology , Mitochondria , Mitochondrial Proteins/physiology , Muscle, Skeletal/metabolism , Rats , Rats, Sprague-Dawley
Braz. j. med. biol. res ; 53(3): e9039, 2020. graf
Article in English | LILACS | ID: biblio-1089345


We previously reported that both the high-carbohydrate diet (HCD) and high-fat diet (HFD) given for two months promote lipid deposition and inflammation in the liver and brain of mice. The results obtained indicate a tissue-specific response to both diets. Herein, we compared the effects of HCD and HFD on fatty acid (FA) composition and inflammation in the gastrocnemius muscle. Male Swiss mice were fed with HCD or HFD for 1 or 2 months. Saturated FA (SFA), monounsaturated FA (MUFA), n-3 polyunsaturated FA (n-3 PUFA), and n-6 PUFA were quantified. The activities of stearoyl-CoA desaturase 1 (SCD-1), Δ-6 desaturase (D6D), elongase 6, and de novo lipogenesis (DNL) were estimated. As for indicators of the inflammatory tissue state, we measured myeloperoxidase (MPO) activity and gene expression of F4/80, tumor necrosis factor-α (TNF-α), interleukin (IL)-4, IL-6, and IL-10. The HCD led to a lower deposition of SFA, MUFA, n-3 PUFA, and n-6 PUFA compared to HFD. However, the HCD increased arachidonic acid levels, SFA/n-3 PUFA ratio, DNL, SCD-1, D6D, and MPO activities, and expression of IL-6, contrasting with the general idea that increased lipid deposition is associated with more intense inflammation. The HCD was more potent to induce skeletal muscle inflammation than the HFD, regardless of the lower lipid accumulation.

Animals , Male , Rabbits , Dietary Carbohydrates/administration & dosage , Dietary Fats/administration & dosage , Muscle, Skeletal/metabolism , Inflammation/metabolism , Body Weight , Energy Intake , Dietary Carbohydrates/metabolism , Dietary Fats/metabolism , Gene Expression
Braz. j. med. biol. res ; 53(3): e8969, 2020. tab, graf
Article in English | LILACS | ID: biblio-1089337


This study investigated the repercussions of adjuvant-induced arthritis (AIA) on body composition and the structural organization of the soleus and cardiac muscles, including their vascularization, at different times of disease manifestation. Male rats were submitted to AIA induction by intradermal administration of 100 μL of Mycobacterium tuberculosis (50 mg/mL), in the right hind paw. Animals submitted to AIA were studied 4 (AIA4), 15 (AIA15), and 40 (AIA40) days after AIA induction as well as a control group of animals not submitted to AIA. Unlike the control animals, AIA animals did not gain body mass throughout the evolution of the disease. AIA reduced food consumption, but only on the 40th day after induction. In the soleus muscle, AIA reduced the wet mass in a time-dependent manner but increased the capillary density by the 15th day and the fiber density by both 15 and 40 days after induction. The diameter of the soleus fiber decreased from the 4th day after AIA induction as well as the capillary/fiber ratio, which was most evident on the 40th day. Moreover, AIA induced slight histopathological changes in the cardiac muscle that were more evident on the 15th day after induction. In conclusion, AIA-induced changes in body composition as well as in the soleus muscle fibers and vasculature have early onset but are more evident by the 15th day after induction. Moreover, the heart may be a target organ of AIA, although less sensitive than skeletal muscles.

Animals , Male , Rats , Arthritis, Experimental/pathology , Body Composition , Muscle, Skeletal/pathology , Myocardium/pathology , Arthritis, Experimental/metabolism , Muscle, Skeletal/metabolism , Disease Models, Animal , Myocardium/metabolism
Electron. j. biotechnol ; 40: 30-39, July. 2019. ilus, graf
Article in English | LILACS | ID: biblio-1053221


Background: Myostatin (MSTN) negatively regulates muscle mass and is a potent regulator of energy metabolism. However, MSTN knockout have affect mitochondrial function. This research assessed the mitochondrial energy metabolism of Mstn−/+ KO cells, and wondered whether the mitochondria biogenesis are affected. Results: In this study, we successfully achieved Mstn knockout in skeletal muscle C2C12 cells using a CRISPR/Cas9 system and measured proliferation and differentiation using the Cell-Counting Kit-8 assay and qPCR, respectively. We found that MSTN dysfunction could promote proliferation and differentiation compared with the behaviour of wild-type cells. Moreover, Mstn KO induced an increase in KIF5B expression. The mitochondrial content was significantly increased in Mstn KO C2C12 cells, apparently associated with the increases in PGC-1α, Cox1, Cox2, ND1 and ND2 expression. However, no differences were observed in glucose consumption and lactate production. Interestingly, Mstn KO C2C12 cells showed an increase in IL6 and a decrease in TNF-1α levels. Conclusion: These findings indicate that MSTN regulates mitochondrial biogenesis and metabolism. This gene-editing cells provided favourable evidence for animal breeding and metabolic diseases.

Myostatin/genetics , Mitochondria/genetics , Mitochondria/metabolism , Organelle Biogenesis , Immunoblotting , Cell Differentiation , Muscle, Skeletal/cytology , Muscle, Skeletal/metabolism , Myoblasts/cytology , Myoblasts/metabolism , MicroRNAs , Cell Proliferation , CRISPR-Cas Systems , Flow Cytometry , Gene Editing
Braz. j. biol ; 79(2): 165-168, Apr.-June 2019. tab
Article in English | LILACS | ID: biblio-989437


Abstract Neotropical nectar-feeding bats consume large amounts of sugar and use most of their energy-rich diet directly from the bloodstream, suggesting an adaptation towards lower body energy reserves. Here we tested the hypothesis that bats Glossophaga soricina spare the energy costs of storing energy reserves, even if this would represent a risky susceptibility during fasting. Blood glucose concentrations in 18 h fasted bats showed a 40% decrease. Breast muscle and adipose tissue lipids, as well as carcass fatty acids and liver glycogen, were also decreased following fasting. The inability to keep normoglycemia following a short-term fasting (i.e. 28 h) confirm that nectar bats invest little on storing energy reserves and show a severe fasting susceptibility associated to this pattern. Our study also support the general hypothesis that evolutionary specializations towards nectar diets involve adaptations to allow a decreased body mass, which reduces the energy costs of flight while increases foraging time.

Resumo Morcegos nectarívoros que ocorrem na região Neotropical consomem grandes quantidades de carboidratos, e usam a energia obtida da dieta diretamente, a partir da glicose na circulação sanguínea. Esta adaptação sugere que morcegos nectarívoros tenham evoluído no sentido de apresentar adaptações fisiológicas que permitam o baixo armazenamento de reservas energéticas corporais. Nós testamos a hipótese de que morcegos Glossophaga soricina poupam o gasto energético envolvido com a formação de reservas energéticas teciduais, mesmo que isso represente uma arriscada suscetibilidade da espécie frente ao jejum. As concentrações de glicose apresentaram uma diminuição de 40% após 18 h de jejum. As concentrações de lipídios do músculo peitoral e do tecido adiposo, bem como as de ácidos graxos da carcaça e glicogênio hepático também diminuíram após 18 h de jejum. A incapacidade de manter a normoglicemia observada após o jejum de curto-prazo confirma que morcegos nectarívoros desta espécie não investem na formação de reservas energéticas, e apresentam, consequentemente, uma severa susceptibilidade ao jejum. Este estudo suporta a hipótese de que adaptações evolucionárias da espécie envolvem diminuição da massa corporal, reduzindo o custo energético do voo e aumentado o tempo de forrageamento.

Animals , Chiroptera/physiology , Fasting/physiology , Energy Metabolism/physiology , Plant Nectar/metabolism , Blood Glucose/physiology , Adipose Tissue/metabolism , Adipose Tissue/chemistry , Muscle, Skeletal/metabolism , Muscle, Skeletal/chemistry , Feeding Behavior
Braz. j. med. biol. res ; 52(1): e8150, 2019. tab, graf
Article in English | LILACS | ID: biblio-974270


High caloric intake promotes chronic inflammation, insulin resistance, and chronic diseases such as type-2 diabetes, which may be prevented by food restriction (FR). The effect of FR on expression of pro-inflammatory and anti-inflammatory genes in adipose tissue, liver, muscle, and brain was compared. Male Swiss mice were submitted to FR (FR group) or had free access to food (control group) during 56 days. The liver, gastrocnemius muscle, brain, and epididymal white adipose tissue (WAT) were collected for analysis of gene expressions. FR attenuated inflammation in the liver, brain, and gastrocnemius muscle but did not markedly change inflammatory gene expression in epididymal WAT. We concluded that adipose tissue was less responsive to FR in terms of gene expression of pro-inflammatory and anti-inflammatory genes.

Animals , Male , Rabbits , Brain/metabolism , Adipose Tissue/metabolism , Muscle, Skeletal/metabolism , Diet, High-Fat , Liver/metabolism , Triglycerides/blood , Blood Glucose/analysis , Gene Expression , Cholesterol/blood
Einstein (Säo Paulo) ; 17(3): eRB4898, 2019.
Article in English | LILACS | ID: biblio-1019802


ABSTRACT Alongside a proper diet, ergogenic aids with potential direct and/or indirect physical performance enhancing effects are sought after for improved adaptation to physical training. Nutritional ergogenics include diet composition changes and/or dietary supplementation. Branched-chain amino acids valine, leucine and isoleucine are widely popular among products with ergogenic claims. Their major marketing appeal derives from allegations that branched-chain amino acids intake combined with resistance physical exercise stimulates muscle protein synthesis. Evidence supporting the efficacy of branched-chain amino acids alone for muscle hypertrophy in humans is somewhat equivocal. This brief review describes physiological and biochemical mechanisms underpinning the effects of complete protein source and branched-chain amino acid intake on skeletal muscle growth in the postabsorptive and post-exercise state. Evidence in favor of or against potential anabolic effects of isolated branched-chain amino acid intake on muscle protein synthesis in humans is also examined.

RESUMO No treinamento físico, buscam-se, além de uma dieta adequada, recursos ergogênicos que possam maximizar direta e/ou indiretamente o desempenho físico. Entre as categorias de recursos ergogênicos, o nutricional compreende a modulação da composição dietética e/ou uso de suplementação. A comercialização dos suplementos de aminoácidos de cadeia ramificada valina, leucina e isoleucina possui muita popularidade entre aqueles com alegação ergogênica. O principal marketing está na afirmação de que o consumo isolado de aminoácidos de cadeia ramificada associado ao exercício físico resistido estimula a síntese de proteína muscular. As evidências da eficácia da ingestão isolada de aminoácidos de cadeia ramificada para a hipertrofia muscular em humanos parecem equivocadas. Nesta breve revisão, apresentamos a compreensão fisiológica e bioquímica de como a ingestão de uma fonte completa de proteína e de aminoácidos de cadeia ramificada afeta o crescimento do músculo esquelético no estado pós-absortivo e pós-exercício. Mostramos também as evidências que suportam ou não a afirmação dos potenciais efeitos anabólicos na síntese de proteína muscular dos aminoácidos de cadeia ramificada quando consumidos isoladamente em humanos.

Humans , Amino Acids, Branched-Chain/metabolism , Muscle Proteins/biosynthesis , Exercise/physiology , Muscle, Skeletal/metabolism , Postprandial Period/drug effects , Dietary Supplements , Gastrointestinal Absorption/drug effects , Amino Acids, Branched-Chain/physiology
Braz. j. med. biol. res ; 52(9): e8551, 2019. graf
Article in English | LILACS | ID: biblio-1019565


Fibroblasts are a highly heterogeneous population of cells, being found in a large number of different tissues. These cells produce the extracellular matrix, which is essential to preserve structural integrity of connective tissues. Fibroblasts are frequently engaged in migration and remodeling, exerting traction forces in the extracellular matrix, which is crucial for matrix deposition and wound healing. In addition, previous studies performed on primary myoblasts suggest that the E3 ligase MuRF2 might function as a cytoskeleton adaptor. Here, we hypothesized that MuRF2 also plays a functional role in skeletal muscle fibroblasts. We found that skeletal muscle fibroblasts express MuRF2 and its siRNA knock-down promoted decreased fibroblast migration, cell border accumulation of polymerized actin, and down-regulation of the phospho-Akt expression. Our results indicated that MuRF2 was necessary to maintain the actin cytoskeleton functionality in skeletal muscle fibroblasts via Akt activity and exerted an important role in extracellular matrix remodeling in the skeletal muscle tissue.

Animals , Rats , Cell Differentiation/physiology , Muscle, Skeletal/physiology , Ubiquitin-Protein Ligases/physiology , Cell Proliferation/physiology , Fibroblasts/physiology , Muscle Proteins/physiology , Blotting, Western , Fluorescent Antibody Technique , Muscle, Skeletal/metabolism , Ubiquitin-Protein Ligases/metabolism , Fibroblasts/metabolism , Muscle Proteins/metabolism
Int. j. morphol ; 36(2): 471-477, jun. 2018. graf
Article in English | LILACS | ID: biblio-954139


Duchenne muscular dystrophy (DMD) is a genetic neuromuscular disorder with progressive clinical signs until death, around the second decade of life. Mdx is the most used animal model to pre-clinical studies of DMD. Parameters of exercise on this muscular disease are still unknown. This research aimed to investigate if the low intensity treadmill training would exacerbate the markers of muscle injury, fibrosis, and the composition of the extracellular matrix by type I and III collagens of the mdx model. Dystrophic 11-week-old male mice were separated in exercised (mdxE, n=8) and sedentary (mdxC, n=8) groups. Wild-type mice were used as control (WT, n=8). Exercised group underwent a LIT protocol (9 m/min, 30min, 3days/week, 60 days) on a horizontal treadmill. Gastrocnemius muscle was collected at day 60 and processed to morphological and morphometric analyzes. Sedentary mdx animals presented inflammatory infiltrate and necrotic fibers. Histochemical analysis revealed that the perimysium of the mdxC group is organized into thick and clustered collagen fibers, which generates a larger area of intramuscular collagen fibers for these animals. Histomorphometry attested that fraction area of collagen fibers of mdxC group was higher than mdxE group (p=0.04) and mdxE group values similar to WT group (p=1.00). Centrally located nuclei fibers and the variance coefficient (VC) of minimal Feret's diameter was similar in mdxE and mdxC groups (p=1.00) and both groups presented higher mean values than WT group (p<0.00). Immunohistochemistry revealed the presence of type I collagen mainly in the mdxC group. LIT protocol had not exacerbated muscle injuries resulting from the dystrophindeficiency membrane fragility at the same time that had reduced the intramuscular collagen deposition. LIT had positively influenced these markers of dystrophic muscle injury on gastrocnemius muscle of mdx model.

La distrofia muscular de Duchenne (DMD) es un trastorno neuromuscular genético con signos clínicos progresivos hasta la muerte, alrededor de la segunda década de la vida. Mdx es el modelo animal más utilizado para estudios preclínicos de DMD. Los parámetros del ejercicio en esta enfermedad muscular aún se desconocen. Esta investigación tuvo como objetivo investigar si el entrenamiento de cinta de baja intensidad exacerbaría los marcadores de lesión muscular, fibrosis y la composición de la matriz extracelular por colágenos tipo I y III del modelo mdx. Ratones machos de 11 semanas de edad con distrofia se separaron en grupos ejercitados (mdxE, n = 8) y sedentarios (mdxC, n = 8). Se usaron ratones de tipo salvaje como control (WT, n = 8). El grupo sometido a ejercicio se sometió a un protocolo LIT (9 m / min, 30 min, 3 días / semana, 60 días) en una cinta de trotar horizontal. El músculo gastrocnemio se retiró el día 60 y se procesó para realizar análisis morfológicos y morfométricos. Los animales sedentarios mdx presentaron infiltrado inflamatorio y fibras necróticas. El análisis histoquímico reveló que el perimisio del grupo mdxC está organizado en fibras de colágeno gruesas y agrupadas, lo que genera una mayor área de fibras de colágeno intramusculares para estos animales. La histomorfometría indicó que el área de fracción de las fibras de colágeno del grupo mdxC era más alta que el grupo mdxE (p = 0,04) y los valores del grupo mdxE eran similares al grupo WT (p = 1,00). Las fibras de los núcleos ubicados centralmente y el coeficiente de varianza (VC) del diámetro mínimo de Feret fueron similares en los grupos mdxE y mdxC (p = 1,00) y ambos grupos presentaron valores medios más altos que el grupo WT (p <0,00). La inmunohistoquímica reveló la presencia de colágeno tipo I principalmente en el grupo mdxC. El protocolo LIT no había agravado las lesiones musculares resultantes de la fragilidad de la membrana con deficiencia de distrofina al mismo tiempo que había reducido la deposición intramuscular de colágeno. LIT ha influido positivamente en estos marcadores de lesión muscular distrófica en el músculo gastrocnemio del modelo mdx.

Animals , Male , Mice , Exercise/physiology , Muscle, Skeletal/pathology , Muscular Dystrophy, Duchenne/pathology , Immunohistochemistry , Adaptation, Physiological , Collagen/analysis , Muscle, Skeletal/metabolism , Muscular Dystrophy, Duchenne/metabolism , Mice, Inbred C57BL
Actual. osteol ; 13(1): 58-66, Ene - Abr. 2017. ilus
Article in English | LILACS | ID: biblio-1118913


Connexins (Cxs) are a family of transmembrane proteins that form gap junctions and hemi-channels, which mediate cell-cell communication between neighboring cells and the respective extracellular milieu in different tissues. Most tissues and cell types throughout the body express one or more Cx proteins, highlighting its importance in regulating cell growth, differentiation, adhesion, migration, cell death and others. Moreover, Cx can propagate intracellular signals through its C-terminus domain, and thus function beyond a mere channel. Cx43 is the most highly expressed and most well studied Cx in bone and musculoskeletal tissues, although Cx40, Cx45, Cx46 and more recently, the Cx37 have been described in bone tissue, along with Cx26, Cx32 and Cx39 in other musculoskeletal tissues. Here, we discuss the basic structure of gap junctions and the role of the Cxs in musculoskeletal tissue, with special focus on Cx37. (AU)

Las conexinas (Cxs) son una familia de proteínas transmembrana que forman uniones en hendidura y hemicanales encargados de mediar la comunicación entre células vecinas y el respectivo medio extracelular en diferentes tejidos. La mayoría de los tejidos y células expresan una o más proteínas conexina, jugando un papel importante en la regulación de la proliferación celular, diferenciación, adhesión, migración y muerte celular, entre otras funciones. Además de actuar como un canal, las conexinas pueden propagar señales intracelulares a través del dominio C-terminal. La Cx43 es la conexina mas expresada y mejor estudiada en el tejido óseo y el músculo, aunque las Cx40, Cx45, Cx46, y mas recientemente Cx37, son también detectadas en el hueso. A su vez la expresión de la Cx26, Cx32 y Cx39 ha sido observada en otros tejidos músculoesqueléticos. En este manuscrito describimos la estructura básica de las uniones tipo gap y el papel que las Cxs, y en especial la Cx37, tienen en tejidos músculo-esqueléticos. (AU)

Humans , Bone and Bones/metabolism , Bone Resorption/prevention & control , Connexins/physiology , Osteoblasts/metabolism , Osteocytes/metabolism , Tendons/metabolism , Signal Transduction/physiology , Cartilage/metabolism , Cell Communication/physiology , Cell Physiological Phenomena , Gap Junctions/drug effects , Gap Junctions/physiology , Connexin 43/physiology , Muscle, Skeletal/metabolism , Bone Density Conservation Agents/therapeutic use , Ligaments/metabolism , Anti-Arrhythmia Agents/adverse effects
Rev. Assoc. Med. Bras. (1992) ; 63(2): 148-155, Feb. 2017. graf
Article in English | LILACS | ID: biblio-842539


Summary The skeletal muscle tissue has a remarkable ability to alter its plastic structural and functional properties after a harmful stimulus, regulating the expression of proteins in complex events such as muscle regeneration. In this context, considering that potential therapeutic agents have been widely studied, nutritional strategies have been investigated in order to improve the regenerative capacity of skeletal muscle. There is evidence of the modulatory action of fatty acids, such that oleic and linoleic acids, that are abundant in Western diets, on muscle function and trophism. Thus, fatty acids appear to be potential candidates to promote or impair the recovery of muscle mass and function during regeneration, since they modulate intracellular pathways that regulate myogenesis. This study is the first to describe and discuss the effect of fatty acids on muscle plasticity and trophism, with emphasis on skeletal muscle regeneration and in vitro differentiation of muscle cells.

Resumo O tecido muscular esquelético possui a notável capacidade plástica de alterar suas propriedades estruturais e funcionais após um estímulo lesivo, regulando a expressão de proteínas durante eventos complexos como a regeneração muscular. Nesse contexto, considerando que possíveis agentes terapêuticos vêm sendo amplamente estudados, estratégias nutricionais têm sido investigadas na perspectiva de melhorar a capacidade regenerativa do músculo esquelético. Há evidências da ação modulatória dos ácidos graxos, como os ácidos oleico e linoleico, que são abundantes nas dietas ocidentais, sobre a função muscular e o trofismo. Nesse sentido, os ácidos graxos parecem ser potenciais candidatos para promover ou prejudicar a recuperação da massa e a função muscular durante a regeneração, uma vez que modulam vias intracelulares reguladoras da miogênese. Este trabalho é o primeiro a descrever e discutir o efeito dos ácidos graxos sobre a plasticidade e o trofismo muscular, com ênfase na regeneração do músculo esquelético e na diferenciação de células musculares in vitro.

Humans , Regeneration/physiology , Muscle, Skeletal/physiology , Fatty Acids/metabolism , Cell Differentiation/drug effects , Muscle, Skeletal/cytology , Muscle, Skeletal/metabolism , Muscle Fibers, Skeletal/cytology , Muscle Fibers, Skeletal/metabolism , Myoblasts, Skeletal/cytology
Braz. j. med. biol. res ; 50(12): 6327, 2017. tab, graf
Article in English | SES-SP, LILACS, SES-SP, SESSP-IDPCPROD, SES-SP | ID: biblio-888973


Heart failure is characterized by the inability of the cardiovascular system to maintain oxygen (O2) delivery (i.e., muscle blood flow in non-hypoxemic patients) to meet O2 demands. The resulting increase in fractional O2 extraction can be non-invasively tracked by deoxygenated hemoglobin concentration (deoxi-Hb) as measured by near-infrared spectroscopy (NIRS). We aimed to establish a simplified approach to extract deoxi-Hb-based indices of impaired muscle O2 delivery during rapidly-incrementing exercise in heart failure. We continuously probed the right vastus lateralis muscle with continuous-wave NIRS during a ramp-incremental cardiopulmonary exercise test in 10 patients (left ventricular ejection fraction <35%) and 10 age-matched healthy males. Deoxi-Hb is reported as % of total response (onset to peak exercise) in relation to work rate. Patients showed lower maximum exercise capacity and O2 uptake-work rate than controls (P<0.05). The deoxi-Hb response profile as a function of work rate was S-shaped in all subjects, i.e., it presented three distinct phases. Increased muscle deoxygenation in patients compared to controls was demonstrated by: i) a steeper mid-exercise deoxi-Hb-work rate slope (2.2±1.3 vs 1.0±0.3% peak/W, respectively; P<0.05), and ii) late-exercise increase in deoxi-Hb, which contrasted with stable or decreasing deoxi-Hb in all controls. Steeper deoxi-Hb-work rate slope was associated with lower peak work rate in patients (r=-0.73; P=0.01). This simplified approach to deoxi-Hb interpretation might prove useful in clinical settings to quantify impairments in O2 delivery by NIRS during ramp-incremental exercise in individual heart failure patients.

Humans , Male , Middle Aged , Oxygen Consumption/physiology , Hemoglobins/analysis , Muscle, Skeletal/metabolism , Heart Failure/physiopathology , Leg/blood supply , Case-Control Studies , Prospective Studies , Muscle, Skeletal/physiopathology , Spectroscopy, Near-Infrared , Exercise Test , Heart Failure/metabolism , Leg/physiopathology
Motriz (Online) ; 23(spe): e101609, 2017. ilus
Article in English | LILACS | ID: biblio-841856


Abstract Glucose uptake is an important phenomenon for cell homeostasis and for organism health. Under resting conditions, skeletal muscle is dependent on insulin to promote glucose uptake.Insulin, after binding to its membrane receptor, triggers a cascade of intracellular reactions culminating in activation of the glucose transporter 4, GLUT4, among other outcomes.This transporter migrates to the plasma membrane and assists in glucose internalization.However, under special conditions such as physical exercise, alterations in the levels of intracellular molecules such as ATP and calcium actto regulate GLUT4 translocation and glucose uptake in skeletal muscle, regardless of insulinlevels.Regular physical exercise, due to stimulating pathways related to glucose uptake, is an important non-pharmacological intervention for improving glycemic control in obese and diabetic patients. In this mini-review the main mechanisms involved in glucose uptake in skeletal muscle in response to muscle contraction will be investigated.(AU)

Humans , Male , Female , Energy Metabolism/physiology , Exercise/physiology , Glucose/metabolism , Muscle, Skeletal/metabolism
Braz. j. med. biol. res ; 50(6): e6141, 2017. graf
Article in English | LILACS | ID: biblio-839302


Cannabinoid type 1 receptor (CB1R) inhibition tends to be one of the promising strategies for the treatment of obesity and other related metabolic disorders. Although CB1R inhibition may cause adverse psychiatric effects including depression and anxiety, the investigation of the role of peripheral CB1R on weight loss and related metabolic parameters are urgently needed. We first explored the effect of rimonabant, a selective CB1R antagonist/inverse agonist, on some metabolic parameters in high fat-diet (HFD)-induced obesity in mice. Then, real-time PCR and electrophysiology were used to explore the contribution of high voltage-activated Ca2+ channels (HVACCs), especially Cav1.1, on rimonabant's effect in skeletal muscle (SM) in HFD-induced obesity. Five-week HFD feeding caused body weight gain, and decreased glucose/insulin tolerance in mice compared to those in the regular diet group (P<0.05), which was restored by rimonabant treatment compared to the HFD group (P<0.05). Interestingly, HVACCs and Cav1.1 were decreased in soleus muscle cells in the HFD group compared to the control group. Daily treatment with rimonabant for 5 weeks was shown to counter such decrease (P<0.05). Collectively, our findings provided a novel understanding for peripheral CB1R's role in the modulation of body weight and glucose homeostasis and highlight peripheral CB1R as well as Cav1.1 in the SM as potential targets for obesity treatment.

Animals , Male , Blood Glucose/drug effects , Calcium Channels/drug effects , Cannabinoid Receptor Antagonists/pharmacology , Muscle, Skeletal/drug effects , Piperidines/pharmacology , Pyrazoles/pharmacology , Receptor, Cannabinoid, CB1/antagonists & inhibitors , Body Weight/drug effects , Calcium Channels, L-Type/drug effects , Calcium Channels, L-Type/metabolism , Calcium Channels/metabolism , Diet, High-Fat/adverse effects , Glucose Intolerance/etiology , Insulin Resistance , Mice, Inbred C57BL , Models, Animal , Muscle, Skeletal/metabolism , Obesity/etiology , Receptor, Cannabinoid, CB1/physiology
Braz. j. med. biol. res ; 49(11): e5226, 2016. tab, graf
Article in English | LILACS | ID: lil-797885


The aim of this research was to investigate the effects of endurance training on reduction of plasma glucose during high intensity constant and incremental speed tests in Wistar rats. We hypothesized that plasma glucose might be decreased in the exercised group during heavy (more intense) exercise. Twenty-four 10-week-old male Wistar rats were randomly assigned to sedentary and exercised groups. The prescription of endurance exercise training intensity was determined as 60% of the maximum intensity reached at the incremental speed test. The animals were trained by running on a motorized treadmill, five days/week for a total period of 67 weeks. Plasma glucose during the constant speed test in the exercised group at 20 m/min was reduced at the 14th, 21st and 28th min compared to the sedentary group, as well at 25 m/min at the 21st and 28th min. Plasma glucose during the incremental speed test was decreased in the exercised group at the moment of exhaustion (48th min) compared to the sedentary group (27th min). Endurance training positively modulates the mitochondrial activity and capacity of substrate oxidation in muscle and liver. Thus, in contrast to other studies on high load of exercise, the effects of endurance training on the decrease of plasma glucose during constant and incremental speed tests was significantly higher in exercised than in sedentary rats and associated with improved muscle and hepatic oxidative capacity, constituting an important non-pharmacological intervention tool for the prevention of insulin resistance, including type 2 diabetes mellitus.

Animals , Male , Rats , Blood Glucose/metabolism , Liver/metabolism , Muscle, Skeletal/metabolism , Physical Conditioning, Animal , Physical Endurance/physiology , Acetyl-CoA Carboxylase/metabolism , Cytochromes c/metabolism , Exercise Test , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Protein Kinases/metabolism , Rats, Wistar
Braz. j. med. biol. res ; 49(11): e5512, 2016. tab, graf
Article in English | LILACS | ID: lil-797888


Chronic exposure to cigarette smoke seems to be related to an increase of pro-inflammatory cytokines, oxidative stress and changes in muscular and physical performances of healthy smokers. However, these parameters have not yet been evaluated simultaneously in previous studies. The participants of this study were healthy males divided into two groups: smokers (n=20) and non-smokers (n=20). Inflammation was evaluated by measuring plasma levels of the cytokines IL-10, IL-6 e TNF-α, and of the soluble receptors sTNFR1 and sTNFR2. Oxidative stress was evaluated by determination of thiobarbituric acid reactive substances (TBARS) plasma levels, total antioxidant capacity of plasma and erythrocytes activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase. Muscular performance was evaluated by measuring the peak torque of knee flexors and extensors, and by determining the total work of the knee extensors. Physical performance was assessed by measuring the peak oxygen uptake (VO2 peak), the maximum heart rate (HRmax) and the walking distance in the shuttle walking test. Smokers showed an increase in the levels of the sTNFR1 and TBARS and a decrease in the total antioxidant capacity of plasma, in the catalase activity and in the total work (P<0.05). IL-6, IL-10, sTNFR2, SOD, peak torque, VO2 peak, HRmax and walking distance were similar between groups. Smokers presented increased oxidative stress and skeletal muscle dysfunction, demonstrating that the changes in molecular and muscular parameters occur simultaneously in healthy smokers.

Humans , Male , Adult , Middle Aged , Muscle, Skeletal/physiopathology , Oxidative Stress/physiology , Smoking/physiopathology , Case-Control Studies , Inflammation/blood , Muscle, Skeletal/metabolism , Receptors, Tumor Necrosis Factor, Type II/blood , Receptors, Tumor Necrosis Factor, Type I/blood , Thiobarbituric Acid Reactive Substances/metabolism , Tumor Necrosis Factor-alpha/blood