946 resultados para muscle injuries
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Resumen: INTRODUCCIÓN: Las personas dedicadas a la cosecha del fruto de la palma de aceite durante el desarrollo de sus labores, adoptan diversas posturas y realizan movimientos repetitivos e incluso ejecutan manipulación de cargas, las cuales varían según las características del lugar y la naturaleza del trabajo. Labores de corte del fruto, poda de cada una de las plantas o la recolección y acopio del producto, pueden acarrear desordenes musculares y/o trastornos esqueléticos. En Estados Unidos, el Instituto Nacional para la Seguridad y Salud Ocupacional (NIOSH) precisa que los trastornos musculo-esqueléticos (TME) involucran nervios, tendones, músculos y estructuras de soporte; por tanto es conveniente identificar signos y síntomas y la carga física de esta población trabajadora. Los trastornos musculo-esqueléticos (TME) como menciona la Agencia Europea para la Seguridad y la Salud en el Trabajo, son un problema grave. Para el trabajador causa dolor y pérdida de ingresos, para los empleadores reducen la eficiencia operacional y para el país incrementan los gastos de la seguridad social. En su informe final, Ramírez Vargas destaca la presencia de Colombia como principal productor de aceite de palma con el 38% de la producción de Latinoamérica. Estima que en este oficio hay más de 1950 cosecheros en la región del Meta, departamento de la zona oriental donde se presenta el mayor crecimiento con un área cultivada al año 2011 de 163.447 hectáreas y un promedio de 16 trabajadores por 100 hectáreas. METODOS: Estudio de corte transversal en 204 trabajadores en los cuales se identificaron síntomas y factores de riesgo ergonómico existentes en el puesto de trabajo por medio de una encuesta con base en el modelo de Ergonomía Participativa (ERGOPAR) y la evaluación biomecánica por medio del método Rapid Entire Body Assessment (REBA) en cosecheros de una plantación de palma aceitera en el departamento del Meta 2015. RESULTADOS: El total de cosecheros fueron hombres y su promedio de edad es de 36,4 años cumplidos. El promedio de la permanencia en centro de trabajo es de 19,1 meses y una media de 7 años de experiencia en el oficio en diferentes centros. El 31,9% de los trabajadores encuestados refirieron molestias y el 30,9% dolor en la espalda baja o región lumbar, mientras que en la evaluación biomecánica en aspectos referentes a la carga física de los trabajadores con el método REBA, arrojo niveles de riesgo altos en el 59,1% de la población y riesgo medio en el 43,1%. CONCLUSIONES: La labor de cosechero involucra cargas posturales en todas las zonas evaluadas por la metodología REBA ya sea por posturas o movimientos, la manipulación de carga, la fuerza de mayor o menor magnitud y el agarre; encontrando que los brazos tienen un mayor compromiso en cuanto a la exigencia física, influenciada por la altura de la palma, la cual incide desfavorablemente para la presentación de TME a nivel de tronco en zona lumbar y dorsal La ergonomía participativa puede convertirse en una habilidad empresarial, inducir a los trabajadores para que formen parte de la unión entre el ejercicio ergonómico empresarial y la participación del grupo de implicados, harán que en conjunto se encuentren soluciones específicas enfocadas a la prevención de TME generados por el ambiente laboral, bajo la premisa del empoderamiento de la población para controlar que las medidas acordadas terminen en su verdadera aplicación.
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A dança é uma actividade de grande exigência atlética, que pode conduzir a um elevado número de lesões, particularmente na região do tornozelo, possivelmente devido à amplitude extrema do movimento articular de flexão plantar do mesmo, que os bailarinos, especialmente do sexo feminino possuem, para realizar a ponta e meia ponta tão características do ballet clássico (Kadel, 2006; Motta-Valencia, 2006; Russel, Kruse, Koutedakis, McEwan, Wyon, 2010). Estas posições de flexão plantar extrema produzem força excessiva na região posterior do tornozelo, o que muitas vezes pode resultar em conflito, dor e incapacidade, representando na maioria das vezes um desafio de diagnóstico. O síndrome do conflito posterior do tornozelo refere-se a um grupo de entidades patológicas que resultam da flexão plantar forçada do tornozelo, de forma repetitiva ou traumática, causando um conflito das estruturas ósseas e/ou de tecidos moles (Hamilton, Geppert, Thompson, 1996; Hamilton, 2008) . Os objectivos deste projecto são compreender os quais os factores de risco, mecânicos e funcionais que contribuem para a mecânica patológica da lesão descritos na literatura, e proceder a uma avaliação biomecânica do movimento de flexão plantar do tornozelo. Método. Realizar uma revisão sistemática de literatura dirigida á mecânica patológica do síndrome do conflito posterior do tornozelo em bailarinas e conduzir um estudo caso-controlo, cujo objectivo é avaliar, comparar e descrever o movimento da flexão plantar do tornozelo realizado ao efectuar os movimentos de ponta e meia-ponta, em bailarinas pré-profissionais com e sem lesão recorrente resultante do conflito posterior do tornozelo. Resultados. Não foram encontrados estudos relacionados especificamente com a mecânica patológica do tornozelo, no entanto vários estudos foram encontrados considerando as características clínicas e anatómicas assim como os procedimentos de tratamento, indicando que os principais factores de risco relacionados com a lesão se dividem em factores mecânicos e funcionais que quando combinados entre si e associados ao sobre-uso podem resultar no conflito posterior do tornozelo. Na avaliação do movimento foram observadas diferenças na actividade muscular entre os sujeitos com lesão e controlos, tendo sido possível a observação de um padrão na sequência de activação para um dos movimentos testados. Na oscilação postural e na rigidez do tornozelo foram também observadas diferenças entre os sujeitos bem como entre as posições realizadas. Conclusão. Concluiu-se que não sendo possível alterar a anatomia do bailarino, por vezes é possível intervir a nível funcional melhorando a capacidade técnica de forma obter um melhor desempenho e a actuar preventivamente em relação às lesões, uma vez que estas podem apresentar padrões cinéticos próprios, relacionados com a função muscular, a estabilidade postural e a rigidez articular.
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Physical rehabilitation of brain injuries and strokes is a time consuming and costly process. Over the past decade several studies have emerged looking at the use of highly sophisticated technologies, such as robotics and virtual reality to tap into the needs of clinicians and patients. While such technologies can be a valuable tool to facilitate intensive movement practice in a motivating and engaging environment, success of therapy also depends on self-administered therapy beyond hospital stay. With the emergence of low-cost gaming consoles such as the Nintendo Wii, new opportunities arise for home-therapy paradigms centred on social interactions and values, which could reduce the sense of isolation and other depression related complications. In this paper we examine the potential, user acceptance and usability of an unmodified Nintendo Wii gaming console as a low-cost treatment alternative to complement current rehabilitation programmes.
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Commercially supplied chicken breast muscle was subjected to simultaneous heat and pressure treatments. Treatment conditions ranged from ambient temperature to 70 °C and from 0.1 to 800 MPa, respectively, in various combinations. Texture profile analysis (TPA) of the treated samples was performed to determine changes in muscle hardness. At treatment temperatures up to and including 50 °C, heat and pressure acted synergistically to increase muscle hardness. However, at 60 and 70 °C, hardness decreased following treatments in excess of 200 MPa. TPA was performed on extracted myofibrillar protein gels that after treatment under similar conditions revealed similar effects of heat and pressure. Differential scanning calorimetry analysis of whole muscle samples revealed that at ambient pressure the unfolding of myosin was completed at 60 °C, unlike actin, which completely denatured only above 70 °C. With simultaneous pressure treatment at >200 MPa, myosin and actin unfolded at 20 °C. Unfolding of myosin and actin could be induced in extracted myofibrillar protein with simultaneous treatment at 200 MPa and 40 °C. Electrophoretic analysis indicated high pressure/temperature regimens induced disulfide bonding between myosin chains.
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Background: Intravenous infusions of glucose and amino acids increase both nitrogen balance and muscle accretion. We hypothesised that co-infusion of glucose ( to stimulate insulin) and essential amino acids (EAA) would act additively to improve nitrogen balance by decreasing muscle protein degradation in association with alterations in muscle expression of components of the ubiquitin-proteasome proteolytic pathway. Methods: We examined the effect of a 5 day intravenous infusions of saline, glucose, EAA and glucose + EAA, on urinary nitrogen excretion and muscle protein degradation. We carried out the study in 6 restrained calves since ruminants offer the advantage that muscle protein degradation can be assessed by excretion of 3 methyl-histidine and multiple muscle biopsies can be taken from the same animal. On the final day of infusion blood samples were taken for hormone and metabolite measurement and muscle biopsies for expression of ubiquitin, the 14-kDa E2 ubiquitin conjugating enzyme, and proteasome sub-units C2 and C8. Results: On day 5 of glucose infusion, plasma glucose, insulin and IGF-1 concentrations were increased while urea nitrogen excretion and myofibrillar protein degradation was decreased. Co-infusion of glucose + EAA prevented the loss of urinary nitrogen observed with EAA infusions alone and enhanced the increase in plasma IGF-1 concentration but there was no synergistic effect of glucose + EAA on the decrease in myofibrillar protein degradation. Muscle mRNA expression of the ubiquitin conjugating enzyme, 14-kDa E2 and proteasome sub-unit C2 were significantly decreased, after glucose but not amino acid infusions, and there was no further response to the combined infusions of glucose + EAA. Conclusion: Prolonged glucose infusion decreases myofibrillar protein degradation, prevents the excretion of infused EAA, and acts additively with EAA to increase plasma IGF-1 and improve net nitrogen balance. There was no evidence of synergistic effects between glucose + EAA infusion on muscle protein degradation or expression of components of the ubiquitin-proteasome proteolytic pathway.
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The increase in fractional rate of protein synthesis (K-s) in the skeletal muscle of growing rats during the transition from fasted to fed state has been explained by the synergistic action of a rise in plasma insulin and branched-chain amino acids (BCAA). Since growing lambs Also exhibit an increase in K-s with level of feed intake, the objective of the present study was to determine if this synergistic relationship between insulin and BCAA also occurs in ruminant animals. Six 30 kg fasted (72 h) lambs (8 months of age) received each of four treatments, which were based on continuous infusion into the jugular vein for 6 h of: (1) saline (155 mmol NaCl/l); (2) a mixture of BCAA (0.778 mumol leucine, 0.640 mumol isoleucine and 0.693 mumol valine/min.kg); (3) 18.7 mumol glucose/min.kg (to induce endogenous insulin secretion): (4) co-infusion of BCAA and glucose. Within each period all animals received the same isotope of phenylalanine, (Phe) as follows: (1) L-[1-C-13]Phe; (2) L-phenyl-[ring H-2(5)]-alanine; (3) L-[N-15]Phe; (4) L-[ring 2,6-H-3]Phe. Blood was sampled serially during infusions to measure plasma concentrations of insulin, glucose and amino acids, and plasma free Phe isotopic activity; biopsies were taken 6 h after the beginning of infusions to determine K-s in in. longissimus dorsi and vastus muscle. Compared with control (saline-infused) lambs, K-s was increased by an average of 40% at the end of glucose infusion, but this effect was not statistically significant in either of the muscles sampled. BCAA infusion, alone or in combination with glucose, also had no significant effect on K-s compared with control sheep. K-s was approximately 60% greater for vastus muscle than for m. longissimus dorsi (P<0.01), regardless of treatment. It is concluded that there are signals other than insulin and BCAA that are responsible for the feed-induced increase in K-s in muscle of growing ruminant animals.
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Myostatin, a member of the TGF-beta family, has been identified as a powerful inhibitor of muscle growth. Absence or blockade of myostatin induces massive skeletal muscle hypertrophy that is widely attributed to proliferation of the population of muscle fiber-associated satellite cells that have been identified as the principle source of new muscle tissue during growth and regeneration. Postnatal blockade of myostatin has been proposed as a basis for therapeutic strategies to combat muscle loss in genetic and acquired myopathies. But this approach, according to the accepted mechanism, would raise the threat of premature exhaustion of the pool of satellite cells and eventual failure of muscle regeneration. Here, we show that hypertrophy in the absence of myostatin involves little or no input from satellite cells. Hypertrophic fibers contain no more myonuclei or satellite cells and myostatin had no significant effect on satellite cell proliferation in vitro, while expression of myostatin receptors dropped to the limits of detectability in postnatal satellite cells. Moreover, hypertrophy of dystrophic muscle arising from myostatin blockade was achieved without any apparent enhancement of contribution of myonuclei from satellite cells. These findings contradict the accepted model of myostatin-based control of size of postnatal muscle and reorient fundamental investigations away from the mechanisms that control satellite cell proliferation and toward those that increase myonuclear domain, by modulating synthesis and turnover of structural muscle fiber proteins. It predicts too that any benefits of myostatin blockade in chronic myopathies are unlikely to impose any extra stress on the satellite cells.
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CSRP3 or muscle LIM protein (MLP) is a nucleocytoplasmic shuttling protein and a mechanosensor in cardiac myocytes. MLP regulation and function was studied in cultured neonatal rat myocytes treated with pharmacological or mechanical stimuli. Either verapamil or BDM decreased nuclear MLP while phenylephrine and cyclic strain increased it. These results suggest that myocyte contractility regulates MLP subcellular localization. When RNA polymerase II was inhibited with alpha-amanitin, nuclear MLP was reduced by 30%. However, when both RNA polymerase I and II were inhibited with actinomycin D, there was a 90% decrease in nuclear MLP suggesting that its nuclear translocation is regulated by both nuclear and nucleolar transcriptional activity. Using cell permeable synthetic peptides containing the putative nuclear localization signal (NLS) of MLP, nuclear import of the protein in cultured rat neonatal myocytes was inhibited. The NLS of MLP also localizes to the nucleolus. Inhibition of nuclear translocation prevented the increased protein accumulation in response to phenylephrine. Furthermore, cyclic strain of myocytes after prior NLS treatment to remove nuclear MLP resulted in disarrayed sarcomeres. Increased protein synthesis and brain natriuretic peptide expression were also prevented suggesting that MLP is required for remodeling of the myo filaments and gene expression. These findings suggest that nucleocytoplasmic shuttling MLP plays an important role in the regulation of the myocyte remodeling and hypertrophy and is required for adaptation to hypertrophic stimuli. (C) 2009 Elsevier Inc. All rights reserved.
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Inhibition of myostatin signalling or its biological activity has recently emerged as a potential remedial approach against muscle wasting and degenerative diseases such as muscular dystrophies. In the present study we systemically administered a recombinant AAV8 vector expressing a mutated myostatin propeptide (AAV8ProMyo) to healthy mice in order to assess its impact on the histological, cellular and physiological properties of the skeletal muscle, exploiting the fact that myostatin is naturally inhibited by its own propeptide. We report that a single intravenous administration of AAV8ProMyo leads to increases in muscle mass of tibialis anterior, extensor digitorum longus and gastrocnemius muscles 8 weeks post-injection and tibialis anterior, gastrocnemius and rectus femoris muscles 17 weeks post-injection. Moreover, treatment resulted in muscle fibre hypertrophy but not hyperplasia, with IIB myofibres responding to the greatest extent following propeptide-induced myostatin inhibition. Additionally, myofibre nuclear: cytoplasmic ratio was decreased in the AAV8ProMyo treated animals. Importantly, the hypertrophic EDL muscle 8 weeks after AAV8ProMyo treatment did not show the dramatic decrease in specific force displayed by the germline myostatin null mice. (C) 2009 Elsevier B.V. All rights reserved.
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Skeletal muscle constitutes a highly adaptable and malleable tissue that responds to environmental and physiological challenges by changing its phenotype in terms of size and composition, outcomes that are brought about by changes in gene expression, biochemical and metabolic properties. Both the short- and long-term effects of nutritional alterations on skeletal muscle homeostasis have been defined as the object of intensive research over the last thirty years. This review focuses predominantly on assimilating our understanding of the changes in muscle fibre phenotype and functional properties induced by either food restriction or alternatively existing on a high fat diet. Firstly, food restriction has been shown in a number of studies to decrease the myofibre cross sectional area and consistently, it has been found that glycolytic type IIB fibres are more prone to atrophy than oxidative fibres. Secondly, in rodents, a high fat diet has been shown to induce an oxidative profile in skeletal muscle, although obese humans usually show higher numbers of glycolytic type IIB fibres. Moreover, attention is paid to the effect of prenatal maternal food restriction on muscle development of the offspring in various species. A key point related to these experiments is the timing of food restriction for the mother. Furthermore, we explore extensively the seemingly species-specific response to maternal malnutrition. Finally, key signalling molecules that play a pivotal role in energy metabolism, fibre type transitions and muscle hypertrophy are discussed in detail.