Context: Several recovery strategies have been used, with limited effectiveness, to reduce the muscle discomfort or pain and the diminished muscle performance following a bout of unaccustomed physical activity, a condition known as delayed onset of muscle soreness (DOMS). Muscle damage in this condition is associated with mechanical disruption of the muscle and connective tissue and inflammation and increased oxidative stress. Low frequency, low intensity, whole body periodic acceleration (WBPA) that increases nitric oxide (NO) release from vascular endothelium into the circulation through increased pulsatile shear stress offers a potential solution. This is because endothelial derived nitric oxide has anti-inflammatory, antioxidant and anti-nociceptive properties. Objective: The purpose of this study was to examine the effects of WBPA on the pain and diminished muscle performance associated with DOMS induced by unaccustomed eccentric arm exercise in young male subjects. Design: Longitudinal. Setting: University Exercise Physiology Laboratory. Participants: Seventeen active men, 23.4 +/- 4.6 yr of age. Intervention: Subjects made six visits to the research facility over a two-week period. On day one, the subject performed a 1RM elbow flexion test and was then randomly assigned to the WBPA or control group. Criterion measurements were taken on Day 2, prior to and immediately following performance of the eccentric exercise protocol (10 sets of 10 repetitions using 120% of 1RM) and after the recovery period. During all subsequent sessions (24, 48, 72, and 96 h) these data were collected before the WBPA or passive recovery was provided. Main Outcome Measures: Isometric strength (MVC), blood markers (CPK, MYO, IL-6, TNF-alpha and Uric Acid), soreness, pain, circumference, and range of motion (ROM). Results: Significantly higher MVC values were seen for the WBPA group across the entire 96 h recovery period. Additionally, within group differences were seen in CPK, MYO, IL-6, soreness, pain, circumference, and ROM showing a smaller impact and more rapid recovery by the WBPA group. Conclusion: Application of WBPA hastens recovery from DOMS after eccentric exercise. Given the lack of other potential mechanisms, these effects appear to be mediated by the increased NO release with WBPA.

Introduction: The effect of electrical stimulation on muscle degeneration and regeneration is largely unknown and it has not been studied in conjunction with telomeres. The consumption of non-steroidal anti-inflammatory drugs (NSAIDs) is widespread in athletes and the general population when faced with muscle soreness or injury. Furthermore, the effect of NSAIDs on muscle regeneration is controversial and its effect on telomere lengths is also unknown. Methods: Young adult males performed 200 electrically stimulated maximal isokinetic contractions with one leg (ES) and the other worked as a control (CON). They received either 1200mg ibuprofen (IBU) per day or placebo (PLA) from 21 days pre- to 30 days post-exercise. Muscle biopsies were obtained from the vastus lateralis of the CON leg at baseline (H0) and ES leg at 2.5h (H2.5) and both legs at 2, 7 and 30 days post-exercise. Blood samples were obtained at the same time points and at day 4 post-exercise. Afterwards the muscle and blood specimen were analysed for skeletal muscle and peripheral blood telomere lengths by Southern blot and signs of muscle degeneration and regeneration were quantified histologically. Results: Histological changes occurred in the ES leg, including; increased proportion of damaged myofibres (2.1±2.8%) and infiltrated myofibres (5.0±6.0%) at day 7, small myofibres (3.0±4.4%) and internally located myonuclei (2.9±3.1%) at day 30. The IBU group had significantly less internally located myonuclei at day 30 compared to PLA (1.7±2.4% vs. 4.1±3.8%). No significant differences were observed in skeletal muscle mean and minimum telomere lengths between ES and CON leg, between IBU and PLA group or between time points. Peripheral blood mean telomere lengths were not significantly different between IBU and PLA group, but between time points; H0 (9.6±1.2kb) and H2.5 (9.1±1.1kb) were significantly shorter than day 4 (10.3±1.6kb) and day 7 (10.1±1.5kb) (P<0.05). Conclusion: Electrically stimulated contractions caused significant muscle degeneration and regeneration in the 30 days post-exercise. Electrical stimulation also appeared to cause fluctuations in peripheral blood telomere lengths, but not skeletal muscle telomeres. The intake of ibuprofen appeared to interfere with muscle regeneration, but did not seem to affect the peripheral blood or skeletal muscle telomeres. However, due to marked individual variations and the small participant group it is difficult to conclude on the effects of electrical stimulation and ibuprofen on proliferative potential. Further studies are warranted to elucidate the effects of electrical stimulation and ibuprofen on blood and skeletal muscle telomeres.

The purpose of this study was to investigate the effects of 6 weeks of hydroxytyrosol (HT) supplementation on markers of muscle damage in healthy, recreationally active men before and throughout acute aerobic exercise bouts. Using a randomized, double-blind, repeated-measures, placebo-controlled design, sixty-one (n = 61) subjects (21.46 ± 0.22 yrs, 179.46 ± 0.79 cm, 78.91 ± 1.19 kg) consumed either a high dose (HI) HT supplement (150 mg HT), a low dose (LO) HT supplement (50 mg HT), or a placebo (PLA) every day for 6 weeks. Throughout the course of the study, the subjects performed four time trial rides (TT1-TT4) on a cycle ergometer. TT1 occurred before supplementation, TT2 halfway through the supplementation period, and TT3 and TT4 occurred in the sixth week and final two days of supplementation. Blood was drawn prior to (pre) and just before termination (end) of each time trial to measure markers of muscle damage during exercise. We observed that endurance exercise increased indicators of muscle damage, CPK and myoglobin, but an association between HT treatment and reduced muscle damage indicators during exercise were not demonstrated. However, the HT supplementation for 6 weeks in recreationally-active males improved time trial performance in the HT treatment groups over the course of the study and this improvement was accompanied by a lower increase in myoglobin concentration in blood in the HI treatment group than in the LO treatment group. Also, performance was improved after 6 weeks in the PLA group. This improvement was associated with an increase in rating of perceived exertion (RPE). RPE was not increased in either the LO and HI treatment groups, although time trial performance was significantly improved. It is possible that HT can improve performance by altering perception of effort. We conclude that chronic and acute HT supplementation did not reduce markers of muscle damage in this population at rest, during, or following exercise, but improved aerobic performance. / text

The mechanism and subsequent patterns of Heat shock protein (Hsp) expression in skeletal muscle specific to contraction type was determined. Rat tibialis anterior (TA) muscle was forcibly lengthened (LC) or shortened (SC) in 5 sets of 20 repetitions before being removed at 2, 8, 24, 48, 72, or 168 hours and analyzed for muscle damage and Hsp25 and Hsp72 expression. Isometric peak torque was reduced to 63% and 33% (P<0.001) at 3-minutes after SC and LC, respectively. Muscle fibre damage appeared at 8h and beyond following LCs, but no damage was observed after SCs. Hsp25 content in LC muscle increased by 3.1±0.53 fold (P<0.01) at 48h and remained elevated. Hsp72 content increased by 3.8±0.66 fold at 24h and remained elevated. Neither Hsp25 nor Hsp72 content was elevated following SCs. Muscle damage associated with LCs results in a greater Hsp accumulation than SCs and 100 SCs do not result in increased Hsp content.

The mechanism and subsequent patterns of Heat shock protein (Hsp) expression in skeletal muscle specific to contraction type was determined. Rat tibialis anterior (TA) muscle was forcibly lengthened (LC) or shortened (SC) in 5 sets of 20 repetitions before being removed at 2, 8, 24, 48, 72, or 168 hours and analyzed for muscle damage and Hsp25 and Hsp72 expression. Isometric peak torque was reduced to 63% and 33% (P<0.001) at 3-minutes after SC and LC, respectively. Muscle fibre damage appeared at 8h and beyond following LCs, but no damage was observed after SCs. Hsp25 content in LC muscle increased by 3.1±0.53 fold (P<0.01) at 48h and remained elevated. Hsp72 content increased by 3.8±0.66 fold at 24h and remained elevated. Neither Hsp25 nor Hsp72 content was elevated following SCs. Muscle damage associated with LCs results in a greater Hsp accumulation than SCs and 100 SCs do not result in increased Hsp content.

O dano muscular induzido pelo exercício (DMIE) e os diferentes elementos envolvidos em seu processo têm sido amplamente estudados. A doença periodontal (DP), por sua vez, tem sido indicada como um possível fator de risco para várias condições sistêmicas, como diabetes, doenças cardiovasculares, partos prematuros, obesidade, entre outros. Tais associações têm sido atribuídas à possibilidade de que a DP possa induzir um processo de inflamação sistêmica de baixa intensidade, caracterizado pela elevação de biomarcadores sanguíneos que também estão envolvidos no mecanismo de dano muscular induzido pelo exercício (DMIE). O objetivo do presente estudo é investigar se a doença periodontal pode atuar como um modificador do DMIE em homens saudáveis. Foram avaliados 40 indivíduos, com idade entre 25 e 45 anos, que buscaram atendimento na faculdade de odontologia da UFRGS ou eram praticantes de atividades físicas. Questionário estruturado para obtenção de dados demográficos e comportamentais e o IPAQ (International Physical Activity Questionnaire) foram aplicados. Dois periodontistas examinaram perda de inserção (PI), profundidade de sondagem, sangramento à sondagem e índices de placa e sangramento gengival no exame basal, juntamente com avaliações antropométricas. Os participantes então realizaram um protocolo de indução de dano muscular que incluiu cinco séries de 15 contrações excêntricas máximas dos quadríceps de uma perna, em um dinamômetro isocinético. Força muscular (contrações isométricas voluntárias máximas - CIVM), espessura e ecogenicidade muscular (ultrassonografia) e dor (escala visual analógica) foram avaliadas em diferentes momentos em relação ao protocolo. Modelos de regressão logística multivariados foram ajustados para idade, educação, índice de massa corporal, fumo, consumo de álcool, proteína C reativa e nível de atividade física. Nessa amostra, PI esteve associada a maiores reduções de força muscular após o protocolo, com um aumento de 1 mm na média de PI representando 7% a mais de redução na CIVM. Pode-se concluir, a partir dessa análise preliminar, que a doença periodontal pode ser considerada um modificador do processo de dano muscular, aumentando a deterioração da força muscular. / Exercise-induced muscle damage (EIMD) and the different elements involved in it´s process has been largely studied. Periodontal diseases (PD) has been pointed out as a possible risk fator for a number of systemic conditions, like diabetes, cardiovascular diseases, preterm birth, obesity, and others. Such associations has been atribbuted to the fact that PD can lead to a low-grade inflammatory process, characterized by elevated blood concentrations of biomarkers that are also involved in the EIMD mechanisms. The aim of this study is to assess whether PD can act as a EIMD modifier in healthy men. This study included 40 healthy males with 25-45 yrs that seek for treatment at Dentistry Faculty or are physical activiy practitioners. A structured questionnaire to obtain demographic and comportamental data and the IPAQ (International Physical Activity Questionnaire) were applied. Two periodontists assessed attachment loss (AL), probing depth (PD), bleeding on probing (BOP), plaque and bleeding index in the baseline exam, together with anthropometrical evaluation. The participants then performed a muscle damage protocol comprising five sets of 15 maximum eccentric contractions of the quadriceps muscles of one leg in a isokinetic dynamometer. Evaluations of muscle strength (maximal voluntary isometric contraction), muscle thickness and echo intensity (ultrasonography images) and soreness (visual analogue scale) were made at different periods in relation to the protocol. Multivariable logistic models were fitted adjusting for age, education, body mass index (BMI), smoking, alcohol consumption, C-reactive protein (CRP) and physical activiy level. In this sample, AL was associated with higher reductions of muscle force, with a 1- mm increment in AL mean significantly decreased CIVM by 7%. It can be concuded, based on this preliminar analysis, that PD may be considered as a modifier of EIMD, increasing muscle strenght deterioration.

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Agradecemos a compreensão. on 2016-06-28T13:13:49Z (GMT) / Submitted by BRYAN STEVE MARTÍNEZ GALÁN null (bryan.mg@hotmail.com) on 2016-06-28T13:21:20Z No. of bitstreams: 1 DOCUMENTO FINAL ENTREGAR NA POSGRADUACAO.pdf: 2577231 bytes, checksum: 52c769c1caab7d358e80d7de7dfa71f7 (MD5) / Approved for entry into archive by Ana Paula Grisoto (grisotoana@reitoria.unesp.br) on 2016-06-28T13:28:57Z (GMT) No. of bitstreams: 1 martinezgalan_bs_me_arafcf.pdf: 2577231 bytes, checksum: 52c769c1caab7d358e80d7de7dfa71f7 (MD5) / Made available in DSpace on 2016-06-28T13:28:57Z (GMT). No. of bitstreams: 1 martinezgalan_bs_me_arafcf.pdf: 2577231 bytes, checksum: 52c769c1caab7d358e80d7de7dfa71f7 (MD5) Previous issue date: 2016-02-19 / INTRODUÇÃO: A taurina é um aminoácido não essencial que atua principalmente no músculo esquelético evitando lesões musculares e auxiliando no tônus muscular. Visto a importância de um aporte nutricional adequado considerando calorias, carboidratos e proteínas, a fim de maximizar a recuperação após o treino e minimizar o risco de lesões musculares, a utilização de taurina seria uma alternativa para prevenir a inflamação e danos musculares, favorecer o processo de síntese proteica e reparo muscular e consequentemente melhorar a qualidade do treino sequencial dos triatletas. OBJETIVO: Analisar os efeitos de 8 semanas de suplementação de taurina e achocolatado sobre os marcadores de lesão muscular, resposta inflamatória e a capacidade aeróbia em triatletas. MÉTODOS: Foi realizado um estudo duplo cego, crossover, randomizado o qual contou com a participação de 9 triatletas da categoria de longa distância, do sexo masculino, com idade entre 25 a 35 anos. Foi realizada a suplementação de 3 gramas de taurina (TAU) ou placebo (PLA) associado a 400 ml de achocolatado de baixo de teor de gordura, durante o período de 8 semanas. Foram coletadas amostras de sangue antes (Pré) e após (Pós) cada período de suplementação para quantificação de marcadores de lesão muscular como lactato desidrogenase (LDH) e creatina quinase (CK), e também de marcadores inflamatórios como fatores de necrose tumoral-alfa (TNF-alfa) e interleucina-6 (IL-6). O desempenho físico dos triatletas foi avaliado por teste de exaustão em esteira. RESULTADOS: Foi constatado um aumento significativo nas concentrações de CK após a suplementação taurina (p=0,01). Entretanto as concentrações de LDH não apresentaram diferença significativa após as suplementações realizadas (TAU Pré; 270,13±141,3 U.L-1 e Pós 350±186 U.L-1); (PLA Pré 196,07±78,1 U.L-1 e Pós 230,2±98,5 U.L-1), assim como não foram encontradas alterações nos parâmetros de desempenho físico; limiar anaeróbio (TAU Pré 11,05±0,7 km/h e Pós 11,12±0,94 km/h); (PLA Pré 11,1±0,8 km/h e Pós 11,05±1,2), percepção subjetiva ao esforço (TAU Pré 5±1 u.a e Pós 5,7±1,3 u.a); (PLA Pré 4,9±1,5 u.a e Pós 5,3±1,4 u.a), frequência cardíaca (TAU Pré 170±9,5 bpm e Pós 160,4±26,01 bpm); (PLA Pré 167,2±10,2 bpm e Pós 168,2±8,5 bpm), e nas concentrações de citocinas inflamatórias de IL- 6 (TAU Pré ; 66,28±124,61 U.L-1 e Pós 70,51±130,59 U.L-1); (PLA Pré 71,39±146,26 U.L-1 e Pós 71,43±135,54 U.L-1), e TNF-α (TAU Pré 80,17±131,34 U.L-1 e Pós ; 83,82±148,35 U.L-1); (PLA Pré 90,21±149,23 U.L-1 e Pós 76,56±131,50 U.L-1). CONCLUSÕES: A suplementação de taurina não promoveu benefícios com relação aos marcadores de lesão muscular, inflamação e desempenho físico de triatletas. / INTRODUCTION: Taurine is an essential amino acid that acts primarily in skeletal muscle preventing muscle damage and improving muscle tone. Given the importance of an adequate nutritional supply considering calories, carbohydrates and proteins in order to maximize recovery after training and to minimize the risk of muscle damage, the use of taurine would be an alternative to prevent the inflammation and muscle damage, favor the process of protein synthesis and muscle repair and consequently improve the quality of triathlon training. In order to verify the effects of 8 weeks of taurine and chocolate milk supplementation, markers of muscle damage and inflammatory response, and aerobic capacity were quantified in triathletes. METHODS: A double-blind, crossover, randomized study was conducted with 9 male long distance triathletes, aged 25-35 years. Supplementation of 3 g of taurine was performed (TAU) or placebo (PLA) associated with 400 ml low fat chocolate milk during an 8-week period. Blood samples were collected before (Pre) and after (Post) each supplementation period for quantification of markers of muscle damage: Lactate dehydrogenase (LDH), creatine kinase (CK), inflammatory markers: tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), the physical performance of triathletes was evaluated by treadmill test until exhaustion. RESULTS: It was observed a significant increase in CK levels after TAU supplementation (p = 0.01). However, LDH concentrations did not differ significantly after the supplementations performed (TAU Pre; 270.13 ± 141.3 UL-1 and Post 350 ± 186 UL-1); (PLA Pre 196.07 ± 78.1 UL-1 and Post 230.2 ± 98.5 UL-1), and there were no changes in physical performance parameters; Anaerobic Threshold (TAU Pré 11,05±0,7 km/h e Pós 11,12±0,94 km/h); (PLA Pré 11,1±0,8 km/h e Pós 11,05±1,2), Perceived exertion (TAU Pré 5±1 u.a e Pós 5,7±1,3 u.a); (PLA Pré 4,9±1,5 u.a e Pós 5,3±1,4 u.a), (heart rate TAU pre 170± 9.5 bpm and post 160,4 ± 26.01 bpm); (PLA Pre 167.2 ± 10.2 bpm and Post 168.2 ± 8.5 bpm), and the concentrations of IL-6 (TAU Pre 66,28 ± 124,61 UL-1 and Post 70,51 ± 130.59 UL-1); (PLA Pre 70,39 ± 146.26 UL-1 and Post 71,43 ± 135,54 UL-1) and TNF-α (TAU Pre 80.17 ± 131.34 UL-1 and Post 83.82 ± 148,35 UL-1); (PLA Pre 90,21 ± 149,23 UL-1 and Post 76,56 ± 131,50 UL-1). CONCLUSIONS: The supplementation of taurine did not provide benefits with respect to muscle damage markers, inflammation and physical performance triathletes.

O dano muscular induzido pelo exercício (DMIE) e os diferentes elementos envolvidos em seu processo têm sido amplamente estudados. A doença periodontal (DP), por sua vez, tem sido indicada como um possível fator de risco para várias condições sistêmicas, como diabetes, doenças cardiovasculares, partos prematuros, obesidade, entre outros. Tais associações têm sido atribuídas à possibilidade de que a DP possa induzir um processo de inflamação sistêmica de baixa intensidade, caracterizado pela elevação de biomarcadores sanguíneos que também estão envolvidos no mecanismo de dano muscular induzido pelo exercício (DMIE). O objetivo do presente estudo é investigar se a doença periodontal pode atuar como um modificador do DMIE em homens saudáveis. Foram avaliados 40 indivíduos, com idade entre 25 e 45 anos, que buscaram atendimento na faculdade de odontologia da UFRGS ou eram praticantes de atividades físicas. Questionário estruturado para obtenção de dados demográficos e comportamentais e o IPAQ (International Physical Activity Questionnaire) foram aplicados. Dois periodontistas examinaram perda de inserção (PI), profundidade de sondagem, sangramento à sondagem e índices de placa e sangramento gengival no exame basal, juntamente com avaliações antropométricas. Os participantes então realizaram um protocolo de indução de dano muscular que incluiu cinco séries de 15 contrações excêntricas máximas dos quadríceps de uma perna, em um dinamômetro isocinético. Força muscular (contrações isométricas voluntárias máximas - CIVM), espessura e ecogenicidade muscular (ultrassonografia) e dor (escala visual analógica) foram avaliadas em diferentes momentos em relação ao protocolo. Modelos de regressão logística multivariados foram ajustados para idade, educação, índice de massa corporal, fumo, consumo de álcool, proteína C reativa e nível de atividade física. Nessa amostra, PI esteve associada a maiores reduções de força muscular após o protocolo, com um aumento de 1 mm na média de PI representando 7% a mais de redução na CIVM. Pode-se concluir, a partir dessa análise preliminar, que a doença periodontal pode ser considerada um modificador do processo de dano muscular, aumentando a deterioração da força muscular. / Exercise-induced muscle damage (EIMD) and the different elements involved in it´s process has been largely studied. Periodontal diseases (PD) has been pointed out as a possible risk fator for a number of systemic conditions, like diabetes, cardiovascular diseases, preterm birth, obesity, and others. Such associations has been atribbuted to the fact that PD can lead to a low-grade inflammatory process, characterized by elevated blood concentrations of biomarkers that are also involved in the EIMD mechanisms. The aim of this study is to assess whether PD can act as a EIMD modifier in healthy men. This study included 40 healthy males with 25-45 yrs that seek for treatment at Dentistry Faculty or are physical activiy practitioners. A structured questionnaire to obtain demographic and comportamental data and the IPAQ (International Physical Activity Questionnaire) were applied. Two periodontists assessed attachment loss (AL), probing depth (PD), bleeding on probing (BOP), plaque and bleeding index in the baseline exam, together with anthropometrical evaluation. The participants then performed a muscle damage protocol comprising five sets of 15 maximum eccentric contractions of the quadriceps muscles of one leg in a isokinetic dynamometer. Evaluations of muscle strength (maximal voluntary isometric contraction), muscle thickness and echo intensity (ultrasonography images) and soreness (visual analogue scale) were made at different periods in relation to the protocol. Multivariable logistic models were fitted adjusting for age, education, body mass index (BMI), smoking, alcohol consumption, C-reactive protein (CRP) and physical activiy level. In this sample, AL was associated with higher reductions of muscle force, with a 1- mm increment in AL mean significantly decreased CIVM by 7%. It can be concuded, based on this preliminar analysis, that PD may be considered as a modifier of EIMD, increasing muscle strenght deterioration.

Background: Stretching may be viewed as an external/internal force influencing the range of motion of the connective tissue (muscles, tendons and the myotendon unit (MTU)) The magnitude and rate of stretching may potentially induce mechanical responses of the musculoskeletal system, such as increased range of motion (ROM). The degree of the intensity of stretch (low, medium, or high) may be used to optimize recovery from muscle damage via ameliorating inflammation; this is however, a plausible hypothesis that needs to be appropriately investigated. Aims: The present project aimed to investigate: 1) whether intense stretching (IS) causes an acute inflammatory response (study 1), 2) the effects of stretching intensity (low, medium, or high) in the onset of inflammation (study 2), and 3) investigate whether stretching intensity is responsible for aiding in the recovery of the muscle, post muscle damage (study 3). Methods: Studies one and two were randomized crossover trials consisting of 12 and 11 recreational male athletes, respectively. The former investigated whether high intensity stretching can cause an acute inflammatory response, with study two examining the effects of different stretching intensities (30%, 60% and 90%) based on a participant’s perceived maximum range of motion (mROM). Blood for both studies was collected at pre-, post, and 24h post intervention, and analyzed for high sensitivity C-reactive protein (hsCRP) (study 1 and 2), and for interleukin (IL)-1β, IL-6, and tumour necrosis factor (TNF)-α (study 1). In study three, a randomized controlled trial investigated whether stretching intensity (low or high), can influence the recovery from muscle damage. Thirty participants were randomized into three groups, a) low intensity stretching (LiS) (30-40% ROM), b) high intensity stretching (HiS) (70-80% ROM) and c) Control group. All participants performed both eccentric (EPT) and isometric peak torque (IPT) tests prior to a muscle damage protocol (MDP) (baseline). Participants were then assessed for EPT and IPT for three consecutive days post MDP. Soreness levels were recorded immediately post muscle damage and at 24, 48, and 72h, with blood samples collected at pre, 24, 48, and 72h post muscle damage and analyzed for Creatine Kinase (CK) and hsCRP. Results: Study one revealed a significant increase in hsCRP (P = 0.006) when comparing IS to Control condition, also confirmed by the effect size analyses. In study two, low (30% of mROM), and medium (60% of mROM) intensity stretching did not elicit an inflammatory response while a pronounced inflammatory response was observed when comparing 30 to 90 and 60 to 90% mROM. In study three, LiS showed a significant increase in EPT compared to both HiS and Control, and these findings were confirmed by magnitude based inferences analyses (i.e. LiS was associated with a positive effect for both IPT and soreness levels compared to Control and HiS). Blood biomarkers were associated with inconsistent effects compared to Control and HiS for all three-time periods. Conclusions: This thesis provides preliminary results suggesting that increased stretching intensity may be responsible for causing an acute inflammatory response. In addition, it was observed that LiS might be associated with faster recovery from muscle damage with respect to muscle function (EPT and IPT) and soreness levels. More research is needed to investigate these findings further.

A realização de uma sessão com ações excêntricas provoca dano na estrutura muscular. Durante o processo de recuperação, essa estrutura sofre adaptações que a protegem da ocorrência de dano nas sessões subseqüentes. Essas adaptações são chamadas de Efeito da Carga Repetida (ECR). Esse efeito foi estudado com a realização de apenas duas sessões de exercícios. A velocidade da ação excêntrica também pode contribuir para a variabilidade do dano induzido. O objetivo desse estudo foi investigar através da análise dos indicadores indiretos, creatina quinase (CK), força, dor, circunferência e amplitude de movimento (ADM), o dano induzido por diferentes velocidades da ação excêntrica e o efeito da carga repetida com a realização das diferentes velocidades (60ºs-1 (Exc60) e 180ºs-1 (Exc180)); e verificar se o efeito da carga repetida seria maior com a realização de três sessões de exercícios. Os resultados dos indicadores analisados tiveram alterações semelhantes nos grupos Exc60 e Exc180, sugerindo que as diferentes velocidades parecem não interferir na magnitude do dano induzido. O ECR não foi diferente entre as velocidades, pois o comportamento das variáveis analisadas foi semelhante entre os dois grupos nas duas sessões iniciais. A realização da terceira sessão de exercícios excêntricos não promove o aumento do efeito protetor, visto que não houve diferenças significantes entre a segunda e a terceira sessão. Indicando que o ECR advém principalmente da realização da primeira sessão / Performing a bout of eccentric exercise causes muscle damage. During recovery, some adaptations occur that can protect muscle structure. These adaptations are known as Repeated Bout Effect. However, this phenomenon has been studied with two bouts. Velocity of eccentric action has been referred as one possible factor which can affect the extension of muscle damage. The aim of this study was to investigate muscle damage induced by different velocities, the repeated bout effect with different velocities and to verify if the repeated bout effect could be larger if three bouts of eccentric exercise were performed. Results of indirect markers of muscle damage (CK, DOR, upper-arm circumference, maximal isometric force) showed similar alterations in groups Exc60 and Exc180, suggesting that different velocities do not affect the extension of muscle damage. Repeated bout effect is not different between velocities, because changes in markers were comparable in both groups after the first two bouts. After performing a third bout of eccentric exercise, there was not any significant differences between second and third bouts. It indicates that the first bout is responsible for the adaptations of the repeated bout effect