La contraction musculaire est initiée par des relâchements massifs de calcium intracellulaire après stimulation par le motoneurone. Le couplage entre la stimulation neuronale et la libération de calcium dépend du complexe de relâchement du calcium (CRC), et est réalisé dans un compartiment particulier des cellules musculaires : la triade. Les triades sont formées par une apposition de trois systèmes membranaires, deux citernes terminales du réticulum sarcoplasmique qui encadrent un tubule transverse, qui est une invagination de la membrane plasmique. Toutes les protéines du CRC sont exclusivement localisées à la triade, cependant les mécanismes de formation des triades et d'adressage des protéines du CRC dans ce compartiment spécifique sont encore largement inconnus. Au niveau de la triade, des points de contacts réguliers avec les microtubules ont été observés, et la triadine, une protéine du CRC, a été proposée comme pouvant servir de lien entre les microtubules et les autres protéines du CRC.L'objectif de ce travail est d'étudier les mécanismes à l'origine de l'organisation des membranes de la triade, de la localisation des protéines du CRC, ainsi que l'implication des microtubules dans ces processus. Nous nous sommes intéressés au rôle de deux protéines associées aux microtubules, Climp63 et MAP6. Des travaux de microscopie ont également permis de caractériser le comportement de chimères fluorescentes de triadine exprimées dans des myotubes de souris différenciés en culture.Climp63 en association avec la triadine, forme un lien entre les triades et le réseau microtubulaire. Cependant, la relation fonctionnelle entre le réseau de microtubules et le relâchement de calcium reste complexe à envisager. Si l’étude d’un modèle animal montre clairement que l’absence de la protéine MAP6 affecte la force musculaire, il n’a pas été possible de montrer que ce défaut est sous-tendu par un dysfonctionnement des microtubules. L’étude de la mise en place des triades a révélé que les microtubules participent à cette organisation, en supportant la mobilité des triades en cours de positionnement dans la fibre musculaire. Enfin, nous avons pu montrer que l’adressage de la triadine à la triade se fait par une diffusion de la protéine au sein du RS, et une rétention dans la citerne terminale grâce à un mécanisme complexe, potentiellement indépendant de RYR1, et nécessitant à la fois les domaines lumenal et cytosolique de la protéine. / Muscle contraction is initiated by massive intracellular calcium releases after motoneuron stimulation. The coupling between neuronal stimulation and calcium release depends on the calcium release complex (CRC), and takes place in a very special compartment of muscle cells : the triad. Triads are formed by the apposition of three membrane systems, two terminal cisternae of the sarcoplasmic reticulum, on each side of a transverse tubule, which is an invagination of the plasma membrane. All CRC proteins are exclusively localized at the triads, however the mechanisms leading to triad formation, and CRC protein targeting at this special compartment are still largely unknown. At the triads, regular cross-talks with microtubules were observed, and triadin, one of the CRC protein, was proposed to serve as a link between microtubules and the other CRC proteins.The goal of this work is to study the mechanisms leading to the organization of triad membranes, and to triad CRC proteins targeting, as well as the involvement of microtubules in these processes. We focused our interest on the role of two microtubule-associated proteins, Climp63 and MAP6. Microscopy studies allowed us to characterize the behaviour of fluorescent triadin chimeras expressed in mouse myotubes, differentiated in culture.Climp63 when associated to triadin forms a link between triads and microtubules. However the functional relationship between microtubules and calcium releases remains complex to consider. Even if the study of an animal model shows clearly that the lack of MAP6 protein affects muscle force, we were not able to show that this defect depends on microtubule dysfunction. The study of triad set up revealed that microtubules participate in that organization, by sustaining triads mobility during positioning in the muscle cell. Finally we were able to show that triadin targeting to triads is done by diffusion of the protein in the SR membrane, and retention in the terminal cisternae thanks to a complex mechanism. This mechanism could be independant of RyR1, but needs the lumenal and cytosolic domains of the protein.

Title: Influence of alcohol on the contractile properties of skeletal muscle Objectives: To identify the impact of alcohol to contractile attribute (Tc - contraction time and Dm - maximal displacement) m. rectus femoris. Method: The diploma thesis corresponds with empirically-theoretical based study. The research has a character of a quasiexperiment. The measured participants were consisted of students (n = 8) of Military Department (VO) and students (n = 3) of civilian (TVS) of attending full-time studies at the Faculty of Physical Education and Sport (FTVS) of Charles University (UK) in Prague. There were used the methods of descriptive statistics to describe it - rate position (arithmetic mean) and a measure of variability (standard deviation). Contractile attributes (Tc, Dm) were measured on the device TGM 100 at an electricity current intensity 80 mA. To analyse the normality of data was used Kolmogorov-Smirkov's test. For further calculations was used parametric method one-way ANOVA for repeated measurements were used statistical significance. For statistical processing was used computer program IBM SPSS Statistics 22 and the individual dose of alcohol relative to body weight was administered in three rounds at 20 minute intervals. Results: The average Tc was 33.23 ± 3.45 ms for the first...

Title: The effect of intensity of voluntary isometric contraction on rheological characteristics of skeletal muscle tissue in vivo, in situ Objectives: The main aim of this study is to determine the effect of intensity of isometric voluntary contraction of skeletal muscle on its viscoelastic characteristics. The work also aims to contribute to the verification of myotonometer as an objective diagnostic instrument and compares it to known methods for evaluation of muscle tone, or its partial characteristics. Methods: We used myotonometer - utility model 29456 for evaluation of changes of stiffness and viscous behavior of skeletal muscle in vivo, in situ in 20 healthy volunteers. The values were compared during 0%, 20%, 35% and 50% of maximal strength of isometric contraction of finger flexors, controlled by hand-held dynamometer. Results: We concluded that both stiffness and viscous behavior of skeletal muscle increases with higher intensity of isometric voluntary contraction. Keywords: myotonometer, skeletal muscle, viscous behavior, stiffness, muscle tone

AN ABSTRACT OF THE DISSERTATION OF Priya Londhe, for the Doctor of Philosophy degree in Biochemistry and Molecular Biology, presented on 30th July, 2013 at Southern Illinois University Carbondale. TITLE: UNRAVELING THE MOLECULAR MECHANISMS OF THE CLASS II TRANSACTIVATOR IN SKELETAL MUSCLE MAJOR PROFESSOR: Dr. Judy Davie The inflammatory cytokine, interferon gamma, IFN-gamma orchestrates a diverse array of fundamental physiological processes and exhibits complex effects on myogenesis. IFN-gamma also induces the class II transactivator, CIITA, which is a critical mediator of IFN-gamma mediated repression and activation. The aims in my dissertation are directed towards understanding the role of IFN-gamma and CIITA in muscle. Stimulation by IFN-gamma in skeletal muscle cells induces CIITA expression as well as MHC class II gene expression. We show that the IFN-gamma induced inhibition of myogenesis is mediated by CIITA, which specifically interacts with myogenin. CIITA acts by both, repressing the expression and inhibiting the activity of myogenin at different stages of myogenesis. The IFN-gamma mediated repression is reversible, with myogenesis proceeding normally upon removal of IFN-gamma. We also show that CIITA is indispensible for the inhibition of myogenesis. To gain a mechanistic insight into the IFN-gamma induced repression of myogenesis, we have discovered that IFN-gamma and CIITA inhibit myogenesis by modifying gene regulation in a muscle cell subject to inflammation. We show that CIITA first interacts with JARID2, a non catalytic subunit of PRC2 complex, which induces a paused RNAPII, phosphorylated at serine 5 and then interacts with the catalytic subunit EZH2, in a JARID2 dependent manner. Our data show that both CIITA and IFN-gamma block myogenesis by the induction and recruitment of the PRC2 complex, which is normally silenced in a differentiating muscle cell. One of my dissertation aims sheds light on the silencing of CIITA in Rhabdomyosarcoma. Silencing of CIITA prevents the expression of MHC Class I and II genes. We have found that IFN-gamma signaling is intact in these cells, but pSTAT1 and IRF1 do not bind to the CIITA PIV promoter. The CIITA promoter is not hypermethylated in RD (ERMS) cells, but shows a modestly enhanced methylation status in SJRH30 (ARMS) cells. We have also observed that histone acetylation, which normally increases on the CIITA PIV promoter following IFN-gamma treatment, is blocked in both types of RMS cells. Further, our studies also impart a novel role for IFN-gamma and CIITA in inhibiting the IGF induced activation of muscle specific genes. Our data show that IFN-gamma does not block the signaling cascade of IGF. However, blocking exogenous IFN-gamma restores IGF activation of muscle specific genes. My dissertation also reveals an important role for the FACT complex in the early steps of gene activation through its histone chaperone activities that serve to open chromatin structure and facilitate transcription promoting muscle differentiation. We show that myogenin interacts with the FACT complex and the recruitment of FACT complex to muscle specific genes is dependent on myogenin. The final aim in my dissertation highlights the distinct binding profiles of the MRFs and E proteins during proliferation and differentiation. Our sequential ChIP assays show that MYOD, MYOG, and MYF5 co-occupy promoters. Taken together, my dissertation provides a comprehensive understanding of the molecular mechanisms during myogenesis and reveals the deleterious effects of chronic inflammation in skeletal muscle.

Le muscle strié squelettique subit de graves lésions d’ischémie-reperfusion (IR) au cours de la progression de l’artériopathie oblitérante des membres inférieurs et lors d’interventions chirurgicales qui nécessitent l’interruption transitoire du flux sanguin dans les artères des membres. Dans ce contexte, nos objectifs étaient de mettre à profit deux modèles expérimentaux d’IR des membres inférieurs par clampage aortique et garrotage unilatéral pour : ° tester l’efficacité d’une alternative médicamenteuse au postconditionnement ischémique par l’utilisation de la cyclosporine A (CsA). En se liant à la cyclophiline D, la CsA empêche l’ouverture du pore de transition mitochondrial (mPTP) à un niveau très distal de la cascade d’évènements qui conduit à la nécrose après IR. ° déterminer de quelle façon deux comorbidités fréquemment retrouvées chez des patients souffrant d’atteinte artérielle (le diabète et l’âge) influencent l’effet de la cyclosporine. Avec les protocoles de conditionnement et aux doses que nous avons utilisées, la cyclosporine a des effets différents sur les conséquences musculaires de l’ischémie-reperfusion des membres inférieurs, dépendant de la pathologie sous-jacente des animaux étudiés. Il semble intéressant d’étudier l’effet dose-réponse de la cyclosporine A pour déterminer l’intervalle thérapeutique optimal, celui-ci pouvant être différent chez l’animal sain et pathologique. D’autre part, étant donné l’importance considérable du stress oxydant chez les animaux diabétiques et sénescents, la co-administration de cyclosporine et d’un antioxydant au moment de la reperfusion pourrait rétablir une protection. / Peripheral arterial disease and many surgical procedures (requiring vascular clamping or tourniquet application) induce severe skeletal muscle ischemia-reperfusion (IR) injuries. As a result, using experimental hind limb ischemia-reperfusion models, our goals were: ° To test a pharmacologic substitute to ischemic postconditioning by using cyclosporine A, that acts on a very downstream step of IR injury cascade by binding to cyclophilin D and inhibiting mitochondrial transition pore opening. We wondered if cyclosporine could alleviate mitochondrial dysfunction and reduce ROS production in skeletal muscles submitted to IR. ° To determine how diabetes and senescence would influence cyclosporine A protective effects. In conclusion, the protective effects of pharmacologic postconditioning with cyclosporine A seem to critically depend on the model under study. A variable and narrow dose-effect relationship is likely and makes it necessary to perform a dose finding study in every pathologic model. Considering the narrow relationships between mitochondrial protection and oxidative stress, combing cyclosporine A postconditioning with antioxidant therapy may restore a more robust protective effect but this hypothesis has to be validated.

Desde seu desenvolvimento na década de 60, a fototerapia têm sido utilizada no tratamento de diversas condições patológicas, havendo um considerável corpo de evidências acerca de sua ação regenerativa, analgésica e anti-inflamatória. Tais efeitos terapêuticos podem ser explicados pela capacidade que a energia luminosa possui de ser absorvida pelos tecidos e estimular ou inibir processos intracelulares. Estudos recentes têm apresentado resultados promissores desta terapia também sobre a redução da fadiga e do dano muscular induzido pelo exercício. A fadiga muscular é um fenômeno multifacetado caracterizado por uma progressiva redução da capacidade de produção de força do músculo. O dano muscular, causado principalmente pelas ações excêntricas do exercício, é caracterizado pela desorganização da estrutura microscópica do músculo e redução da capacidade contrátil deste tecido. Assim, o objetivo do presente trabalho foi verificar o efeito da fototerapia aplicada imediatamente antes do exercício sobre: (1) a fadiga muscular de extensores de joelho submetidos a exercício isocinético concêntrico; (2) o dano muscular de extensores de joelho submetidos a exercício isocinético excêntrico. No primeiro estudo, 17 homens saudáveis e fisicamente ativos participaram de um desenho experimental cruzado no qual foram submetidos a 30 repetições concêntricas máximas de flexo-extensão do joelho, precedidas de tratamento com fototerapia ou placebo. A fototerapia foi aplicada através de um equipamento de light emitting diodes therapy (LEDT) composto por 35 diodos infravermelhos de 850 nm e 34 diodos vermelhos de 660 nm. O tratamento foi realizado em três pontos do quadríceps com aplicação de uma dose total de 125,1 J. Mensurações da função muscular dos extensores de joelho foram realizadas antes e imediatamente após o exercício através de contrações voluntárias máximas (CVM) de extensores de joelho a 60º de flexão da articulação. Como resultado, observou-se que os voluntários apresentaram um decréscimo de torque significativamente menor quando tratados com fototerapia em comparação ao tratamento placebo. No segundo estudo, 36 homens saudáveis e fisicamente ativos foram randomizados em grupo fototerapia (n=18) e grupo placebo (n=18), e submetidos a cinco séries de 15 contrações excêntricas máximas de extensores de joelho. Avaliações de dor muscular e níveis séricos das enzimas lactato desidrogenase (LDH) e creatina kinase (CK) foram mensuradas pré-exercício, 24 e 48 horas pós-exercício. Avaliações da função muscular (CVM de extensores de joelho) foram realizadas pré-exercício, imediatamente após, 24 e 48 horas após o exercício. Um equipamento de low level laser therapy (LLLT) composto por cinco diodos infravermelhos de 810 nm foi utilizado para aplicar o tratamento em seis pontos do quadríceps e transmitir uma dose total de 180 J. Como resultado, observou-se que o grupo fototerapia apresentou: (1) menores incrementos de LDH 48 horas após o exercício; (2) menores incrementos de CK 24 e 48 horas após o exercício; e (3) menor decréscimo do torque de extensores de joelho imediatamente após, 24 e 48 horas após o exercício, em comparação ao grupo placebo. Os achados destes estudos permitem concluir que o tratamento com fototerapia foi capaz de atenuar os efeitos da fadiga e do dano muscular induzidos por exercício em dinamômetro isocinético. / Since its development in the 60’s, phototherapy has been used in the treatment of several pathological conditions, with a considerable body of evidence with respect to its regenerative, analgesic and anti-inflammatory action. These therapeutic effects may be explained by the capacity that the light energy has of being absorbed by soft tissues and stimulate or inhibit intracellular processes. Recent studies have also shown promising results regarding the reduction of muscle fatigue and exercise induced muscle damage. Muscle fatigue is a multifaceted phenomenon characterized by a progressive reduction in muscle force production capacity. Muscle damage, mainly caused by eccentric exercise, is characterized by the microscopic disorganization of muscle structure and reduction of the contractile capacity of this tissue. Thus, the purpose of this study was to verify the effect of phototherapy applied immediately before exercise on: (1) knee extensors muscle fatigue after isokinetic concentric exercise; (2) knee extensor muscle damage after isokinetic eccentric exercise. In the first study 17 healthy and physically active male subjects participated of a cross-over design trial. Subjects were subjected to 30 maximal concentric repetitions of knee flexion-extension, preceded by placebo or phototherapy treatment. Phototherapy was applied with a light emitting diodes therapy (LEDT) equipment composed by 35 infrared diodes of 850 nm wavelength and 34 red diodes of 660 nm. Treatment was applied in three different points of the quadriceps muscle with a total dose of 125.1 J. Measurements of knee extensor muscle function were obtained before and immediately after exercise by maximal voluntary contractions (MVC) at a knee angle of 60º of joint flexion. Subjects showed a significant smaller decrease in torque when treated with phototherapy compared to placebo treatment. On the second study, 36 healthy and physically active male subjects were randomized into a phototherapy (n=18) and a placebo (n=18) group, and subjected to five series of 15 maximal knee extensor eccentric contractions. Measurements of pain and serum levels of lactate dehydrogenase (LDH) and creatine kinase (CK) enzymes were obtained pre-exercise, 24 and 48 hours postexercise. Evaluations of muscle function (knee extensor MVC) were obtained preexercise, immediately after, and 24 and 48 hours after exercise. A low level laser therapy (LLLT) equipment composed by five infrared diodes of 810 nm wavelength was used to apply the treatment on six different points of the quadriceps muscle with a total dose of 180 J. The phototherapy group showed: (1) smaller increments of LDH 48 hours after exercise; (2) smaller increments of CK 24 and 48 hours after exercise; and (3) smaller decrease on knee extensor torque immediately after, 24 and 48 hours after exercise compared to the placebo group. These findings allow us to conclude that the phototherapy treatment was able to attenuate the effects of fatigue and muscle damage induced by isokinetic exercise.

Made available in DSpace on 2014-06-11T19:25:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-02-26Bitstream added on 2014-06-13T20:33:22Z : No. of bitstreams: 1 damatto_rl_me_botfm.pdf: 863048 bytes, checksum: 20cdd00e6c2f8499693cd4baea8e854d (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / A insuficiência cardíaca (IC) caracteriza-se por redução da tolerância aos exercícios com a ocorrência precoce de fadiga e dispnéia. Além de disfunção cardíaca e pulmonar, anormalidades intrínsicas da musculatura esquelética têm sido responsabilizadas pela intolerância aos esforços físicos. Em músculos periféricos e respiratórios, frequentemente são observadas atrofia e modificação nas isoformas das cadeias pesadas de miosina (MyHC) na IC. Os mecanismos e vias intracelulares de sinalização responsáveis por essas alterações ainda não estão completamente definidos. Em modelos experimentais de IC induzida por estenose aórtica ou infarto do miocárdio, verificamos que alterações na expressão dos fatores de regulação miogênica e da via miostatina/folistatina podem modular o trofismo muscular e a composição das MyHCs. Um dos modelos experimentais muito utilizados para o estudo da IC é o rato espontaneamente hipertenso (SHR). Estes animais apresentam, precocemente, hipertensão arterial e hipertrofia ventricular esquerda e, em idade avançada, desenvolvem IC. Não identificamos estudos que avaliaram o comprometimento da musculatura esquelética de SHR com IC. O objetivo deste estudo foi caracterizar as alterações da musculatura esquelética de SHR com IC por meio de avaliação da morfologia, das isoformas das cadeias pesadas de miosina e da expressão gênica e protéica dos fatores de regulação miogênica e da via miostatina/folistatina. A partir de 18 meses de idade, ratos espontaneamente hipertensos foram avaliados duas vezes por semana à procura de evidências clínicas de IC como taquipnéia, perda de peso e apatia. Após a detecção de IC, os animais foram submetidos a ecocardiograma transtorácico para a confirmação de disfunção ventricular e eutanasiados. No momento da eutanásia, foram... / Heart failure (HF) is characterized by limited exercise tolerance due to increased muscle fatigue and impaired endurance. Besides cardiac and pulmonary dysfunction, intrinsic skeletal muscle abnormalities have been shown to be involved on reduced exercise tolerance. muscle mass loss and a shift in myosin heavy chain (MyHC) isoforms have been frequently observed in peripheral and respiratory skeletal muscles during HF. The pathophysiological mechanisms and intracellular pathways responsible for muscle changes are not completely defined. We observed that myogenic regulatory factors expression and myostation/follistatin pathway modulate muscle trophism and MyHC isoforms in experimental aortic stenosis- and myocardial infarction-induced HF. The spontaneously hypertensive rat (SHR) is often used in HF studies. These rats develop systemic arterial hypertension and left ventricular hypertrophy early and HF at 18-22 month-age approximately. To the best of our knowledgement, there is not study on skeletal muscle evaluation in SHR with HF. The aim of this study was to characterize skeletal myopathy of SHR with HF by evaluating soleus muscle morphology, MyHC isoforms, and gene and protein expression of myogenic regulatory factors, myostatin, and follistatin. Eighteen month-old spontaneously hypertensive rats were evaluated twice a week to identify HF clinical features such as taquipnea, weight loss, and apathy. After detecting HF, rats were subjected to transthoracic echocardiogram. During euthanasia, we evaluated pathological evidences of HF such as pleuropericardial effusion, ascites, left atrial thrombi, right ventricular hypertrophy, and lung congestion. Agematched Wistar-Kyoto rats used as controls. Soleus morphology was analyzed in haematoxyin and eosin and picro-sirius red stained sections, and MyHC isoforms were evaluated by protein... (Complete abstract click electronic access below)

Assessments of skeletal muscle functional capacity or bilateral muscular asymmetry often necessitate maximal contractile effort, which exacerbates muscle fatigue or injury. Tensiomyography (TMG) has been investigated in laboratory settings, as a means to assess muscle contractile function following fatigue; however observations have not been contextualised by concurrent physiological measures. TMG has more sparingly been applied in the field, with elite athletes. The aim of this thesis was to examine acute alterations and underlying variations in muscle contractile mechanics, through the application of TMG, contextualised with established physiological measures; and to apply TMG within high performance sports programmes. TMG successfully detected fatigue, evident from reduced strength, by displaying impaired muscle displacement, accompanied by elevated resting muscle tension. Greater asymmetry was detected in individuals with asymmetric strength; however, symmetry was masked during more complex tasks. Increased day-to-day variability was detected among highly trained athletes compared to recreationally active individuals. Acute training adaptations were detected, in contractile mechanics, in individual muscles. TMG could be useful in establishing fatigue status of skeletal muscle without exacerbating the functional decrements of the muscle, whilst also providing useful screening information for detecting asymmetry which may not be apparent during functional actions.

Master of Science / Department of Kinesiology / Brad J. Behnke / Prostate cancer is the most common type of non-skin cancer found in men and preliminary evidence suggests prostate cancer has atrophic effects on cardiac and left ventricle (LV) mass which are associated with reduced endurance exercise capacity in rats. Using a pre-clinical orthotopic model of prostate cancer, echocardiography was utilized to test the hypothesis that exercise training will mitigate prostate cancer induced-cardiac and skeletal muscle atrophy and improve LV function versus sedentary tumor-bearing counterparts. Methods: Dunning R-3327 AT-1 prostate cancer cells were injected orthotopically in male Copenhagen rats aged (n=39; ~5 mo. old). Animals were randomized into four groups, exercise-trained tumor-bearing (EXTB) or control (EXCON) and sedentary tumor-bearing (SEDTB), or control (SEDCON). Exercise training was performed via a rodent treadmill set at 15m/min with a 15° incline for 60 min/day for ~30 days. Animals underwent echocardiographic evaluation using the parasternal short axis view to examine ventricle dimensions pre-cancer or exercise (PRE) and 15 (Post 1) and 30 (Post 2) days post cancer cell injection and/or exercise training with tissues collected immediately after Post 2. Results: Cardiac and LV mass of SEDTB animals were significantly lower than all groups (p<0.05). Tumor mass was significantly negatively correlated with LV mass in EXTB (-0.75, p<0.02) and SEDTB animals (-0.72, p<0.02). EXCON group had significantly higher stroke volume Post 2 assessment compared to both sedentary groups (p<0.05), but not EXTB animals. Conclusion: The current investigation demonstrates prostate cancer independent of anti-cancer treatment significantly reduces cardiac mass, and LV mass as well as locomotor muscle masses. However, moderate intensity exercise training can mitigate cardiac and skeletal muscle atrophy with prostate cancer.

Desde seu desenvolvimento na década de 60, a fototerapia têm sido utilizada no tratamento de diversas condições patológicas, havendo um considerável corpo de evidências acerca de sua ação regenerativa, analgésica e anti-inflamatória. Tais efeitos terapêuticos podem ser explicados pela capacidade que a energia luminosa possui de ser absorvida pelos tecidos e estimular ou inibir processos intracelulares. Estudos recentes têm apresentado resultados promissores desta terapia também sobre a redução da fadiga e do dano muscular induzido pelo exercício. A fadiga muscular é um fenômeno multifacetado caracterizado por uma progressiva redução da capacidade de produção de força do músculo. O dano muscular, causado principalmente pelas ações excêntricas do exercício, é caracterizado pela desorganização da estrutura microscópica do músculo e redução da capacidade contrátil deste tecido. Assim, o objetivo do presente trabalho foi verificar o efeito da fototerapia aplicada imediatamente antes do exercício sobre: (1) a fadiga muscular de extensores de joelho submetidos a exercício isocinético concêntrico; (2) o dano muscular de extensores de joelho submetidos a exercício isocinético excêntrico. No primeiro estudo, 17 homens saudáveis e fisicamente ativos participaram de um desenho experimental cruzado no qual foram submetidos a 30 repetições concêntricas máximas de flexo-extensão do joelho, precedidas de tratamento com fototerapia ou placebo. A fototerapia foi aplicada através de um equipamento de light emitting diodes therapy (LEDT) composto por 35 diodos infravermelhos de 850 nm e 34 diodos vermelhos de 660 nm. O tratamento foi realizado em três pontos do quadríceps com aplicação de uma dose total de 125,1 J. Mensurações da função muscular dos extensores de joelho foram realizadas antes e imediatamente após o exercício através de contrações voluntárias máximas (CVM) de extensores de joelho a 60º de flexão da articulação. Como resultado, observou-se que os voluntários apresentaram um decréscimo de torque significativamente menor quando tratados com fototerapia em comparação ao tratamento placebo. No segundo estudo, 36 homens saudáveis e fisicamente ativos foram randomizados em grupo fototerapia (n=18) e grupo placebo (n=18), e submetidos a cinco séries de 15 contrações excêntricas máximas de extensores de joelho. Avaliações de dor muscular e níveis séricos das enzimas lactato desidrogenase (LDH) e creatina kinase (CK) foram mensuradas pré-exercício, 24 e 48 horas pós-exercício. Avaliações da função muscular (CVM de extensores de joelho) foram realizadas pré-exercício, imediatamente após, 24 e 48 horas após o exercício. Um equipamento de low level laser therapy (LLLT) composto por cinco diodos infravermelhos de 810 nm foi utilizado para aplicar o tratamento em seis pontos do quadríceps e transmitir uma dose total de 180 J. Como resultado, observou-se que o grupo fototerapia apresentou: (1) menores incrementos de LDH 48 horas após o exercício; (2) menores incrementos de CK 24 e 48 horas após o exercício; e (3) menor decréscimo do torque de extensores de joelho imediatamente após, 24 e 48 horas após o exercício, em comparação ao grupo placebo. Os achados destes estudos permitem concluir que o tratamento com fototerapia foi capaz de atenuar os efeitos da fadiga e do dano muscular induzidos por exercício em dinamômetro isocinético. / Since its development in the 60’s, phototherapy has been used in the treatment of several pathological conditions, with a considerable body of evidence with respect to its regenerative, analgesic and anti-inflammatory action. These therapeutic effects may be explained by the capacity that the light energy has of being absorbed by soft tissues and stimulate or inhibit intracellular processes. Recent studies have also shown promising results regarding the reduction of muscle fatigue and exercise induced muscle damage. Muscle fatigue is a multifaceted phenomenon characterized by a progressive reduction in muscle force production capacity. Muscle damage, mainly caused by eccentric exercise, is characterized by the microscopic disorganization of muscle structure and reduction of the contractile capacity of this tissue. Thus, the purpose of this study was to verify the effect of phototherapy applied immediately before exercise on: (1) knee extensors muscle fatigue after isokinetic concentric exercise; (2) knee extensor muscle damage after isokinetic eccentric exercise. In the first study 17 healthy and physically active male subjects participated of a cross-over design trial. Subjects were subjected to 30 maximal concentric repetitions of knee flexion-extension, preceded by placebo or phototherapy treatment. Phototherapy was applied with a light emitting diodes therapy (LEDT) equipment composed by 35 infrared diodes of 850 nm wavelength and 34 red diodes of 660 nm. Treatment was applied in three different points of the quadriceps muscle with a total dose of 125.1 J. Measurements of knee extensor muscle function were obtained before and immediately after exercise by maximal voluntary contractions (MVC) at a knee angle of 60º of joint flexion. Subjects showed a significant smaller decrease in torque when treated with phototherapy compared to placebo treatment. On the second study, 36 healthy and physically active male subjects were randomized into a phototherapy (n=18) and a placebo (n=18) group, and subjected to five series of 15 maximal knee extensor eccentric contractions. Measurements of pain and serum levels of lactate dehydrogenase (LDH) and creatine kinase (CK) enzymes were obtained pre-exercise, 24 and 48 hours postexercise. Evaluations of muscle function (knee extensor MVC) were obtained preexercise, immediately after, and 24 and 48 hours after exercise. A low level laser therapy (LLLT) equipment composed by five infrared diodes of 810 nm wavelength was used to apply the treatment on six different points of the quadriceps muscle with a total dose of 180 J. The phototherapy group showed: (1) smaller increments of LDH 48 hours after exercise; (2) smaller increments of CK 24 and 48 hours after exercise; and (3) smaller decrease on knee extensor torque immediately after, 24 and 48 hours after exercise compared to the placebo group. These findings allow us to conclude that the phototherapy treatment was able to attenuate the effects of fatigue and muscle damage induced by isokinetic exercise.