Submitted by Nadir Basilio (nadirsb@uninove.br) on 2018-07-16T21:41:44Z No. of bitstreams: 1 Manoel Carneiro de Oliveira Junior.pdf: 2899222 bytes, checksum: 9b2b796a4ed66d8af915bf5458411bad (MD5) / Made available in DSpace on 2018-07-16T21:41:44Z (GMT). No. of bitstreams: 1 Manoel Carneiro de Oliveira Junior.pdf: 2899222 bytes, checksum: 9b2b796a4ed66d8af915bf5458411bad (MD5) Previous issue date: 2017-03-07 / Asthma is a chronic inflammatory airway disease, in which purinergic signaling has a central role, controlling activation of structural and hematopoietic cells. Aerobic exercise (AE) present anti-inflammatory effects to the airways, but no cellular and molecular mechanisms are known. Thus, this project evaluated the effects of AE on purinergic signaling response in a model of asthma induced by house dust mite (HDM). AE was performed in a treadmill at moderate intensity, 5x/week, during 4 weeks, after 3 weeks of prior HDM administration. HDM (dermatophagoides pteronyssinus; 100mg/mouse) was administered 3x/week, during 7 weeks. The results demonstrated that AE reduced adenosine triphosphate (ATP) accumulation (p<0.001), IL-1beta, IL-4, IL-5, CXCL1/KC, IL-13, IL-17, IL-23, IL-33 and TNF-alpha (p<0.001), while increased IL-1ra, IL-2 and IL-10 in bronchoalveolar lavage (BAL). Total number of leukocytes, eosinophils, lymphocytes and neutrophils in BAL and the number of eosinophils, neutrophils and lymphocytes in the airway wall (p<0.01) were reduced by AE. Airway collagen, elastin, smooth muscle and mucus were reduced by AE (p<0.01). TGF-beta, IGF-1 and VEGF levels was reduced by AE (p<0.001). Lung mechanics (Resistance, Elastance, GTIS, HTIS, RAW) and airway hyperresponsiveness (AHR) to methacholine was ameliorated by AE (p<0.01). IL-4, IL-5 and IL-13 production by lymph nodes, splenocytes and bone marrow cells was also reduced by AE. The expression of P2X7, P2Y2 and P2Y6 by peribronchial leukocytes (p<0.01) and by airway epithelial cells (p<0.01) were reduced by AE. AE reduces asthma phenotype by inhibiting purinergic signaling in a model of HDM-induce asthma. / A asma é uma doença inflamatória crônica das vias aéreas, na qual a sinalização purinérgica tem um papel central, controlando a ativação de células estruturais e hematopoiéticas. O treinamento físico aeróbio (TFA) apresenta efeitos anti-inflamatórios nas vias aéreas, mas não são conhecidos mecanismos celulares e moleculares. Assim, este projeto avaliou os efeitos da TFA sobre a resposta de sinalização purinérgica em um modelo de asma induzida pelo ácaro da poeira doméstica (HDM). TFA foi realizada numa esteira em intensidade moderada, 5x / semana, durante 4 semanas, após 3 semanas de administração anterior de HDM. Foi administrado HDM (dermatophagoides pteronyssinus, 100 mg / camundongo) 3x / semana, durante 7 semanas. Os resultados demonstraram que TFA reduziu a acumulação de adenosina trifosfato (ATP) (p <0,001), IL-1beta, IL-4, IL-5, CXCL1 / KC, IL-13, IL-17, IL-23, IL-33 e TNF-alfa (p <0,001), enquanto aumentou IL-1ra, IL-2 e IL-10 no lavado broncoalveolar (LBA). O número total de leucócitos, eosinófilos, linfócitos e neutrófilos na LBA e o número de eosinófilos, neutrófilos e linfócitos na parede das vias aéreas (p <0,01) foram reduzidos por EA. Colágeno da via aérea, elastina, músculo liso e muco foram reduzidos por EA (p <0,01). Os níveis de TGF-beta, IGF-1 e VEGF foram reduzidos pelo EA (p <0,001). A mecânica pulmonar (resistência, elastância, GTIS, HTIS, RAW) e a hiperreatividade das vias aéreas (AHR) à metacolina foi melhorada pelo EA (p <0,01). A produção de IL-4, IL-5 e IL-13 por nódulos linfáticos, esplenócitos e células da medula óssea também foi reduzida por EA. A expressão de P2X7, P2Y2 e P2Y6 por leucócitos peribronquiais (p <0,01) e por células epiteliais das vias aéreas (p <0,01) foram reduzidas pelo TFA. TFA reduziu o fenótipo de asma inibindo a sinalização purinérgica num modelo de HDM induzindo asma.

Magister Artium (Sport, Recreation and Exercise Science) - MA(SRES) / Obesity is recognised as a risk factor for non-communicable diseases which has reached epidemic proportions globally. South Africa is one of the developing countries with significant statistical representation reported for these conditions. Obesity is associated with other conditions such as type 2 diabetes, hypertension and dyslipidaemia which are all part of what is called metabolic syndrome. As a strategy to reduce the levels of obesity, physical activity has been introduced to compliment clients who are on medication for diabetes.

Myotonic dystrophy type 1 (DM1) is an autosomal dominant and progressive neuromuscular disorder caused by the CTG trinucleotide repeat expansion in the 3’ untranslated region of the DMPK gene. Clinical manifestations include extensive atrophy of skeletal muscle (SkM) concomitant with muscle weakness, that develops in a distal to proximal fashion. Central to muscle plasticity is the satellite cell (SC), a muscle specific stem cell that, upon activation, facilitates muscle repair and regeneration. To date, SCs have yet to be elucidated in DM1; therefore, the aim of the present study was to extensively characterize the PAX7+ SC population, along with other indices of muscle quality in SkM. DM1 patients (6 women, 5 men) performed stationary cycling 3 times per week for 12wks, with biopsies taken from the Vastus lateralis pre- (PRE) and post-endurance exercise intervention (POST). Age-matched, healthy controls (CTRL) were used for comparison of baseline measures. Type 1 and 2 myofiber-specific PAX7+ cells were significantly greater in DM1 patients (PRE), in comparison to CTRL (2.24- and 1.84-fold, respectively), with type 2 SC content further increasing following training (p<0.05). In addition, protein expression of myogenic regulatory factors PAX7 and myogenin were significantly higher in DM1 compared to CTRL, with no training effects observed. Both immunohistochemical and immunoblotting analysis showed that activated MYOD+/PAX7+ cells did not significantly differ in DM1 vs. CTRL. FISH- IF analysis of CUG repeats show that 30% of SCs in DM1 were positive for these inclusions. Muscle capillarization was significantly lower in type 2 fibers in DM1 vs CTRL, which was fully rescued with training (p<0.05). At baseline, DM1 muscle showed the presence of de novo and fat infiltrated fibres, as well as fibrosis, that were relatively non-existent in the CTRL. In vitro results show patient-derived myoblasts exhibit a proliferation defect. Furthermore, myoblasts showed impairments in both glycolysis and mitochondrial respiration, with the latter being completely normalized to CTRL in myotubes. Our novel findings display an increased, albeit non-functional, SC pool in DM1 SkM indicated by disturbances in the myogenic program and overall poor muscle quality. We show that both SCs and SkM remain responsive to exercise training, suggesting therapeutic potential. We also suggest that mitochondrial dysfunction may underpin these impairments in the myogenic program. / Thesis / Master of Science (MSc) / Myotonic dystrophy type 1 (DM1) is the most common muscular dystrophy in adults worldwide affecting 1:8000 individuals, with certain areas in northeastern Quebec having a higher prevalence of 1:600 individuals. DM1 is caused by an autosomal dominant genetic mutation that leads to muscle weakness, respiratory insufficiency, cataracts and cardiac conduction block, ultimately resulting in poor quality of life and shortened lifespan. Preliminary evidence suggests that the maintenance of muscle health can greatly improve quality of life and life-span of these individuals, making an in-depth research focus on this therapeutic intervention extremely important. Optimal muscle health is maintained by the functionality of muscle stem cells, that aid in muscle repair and facilitate adaptations in muscle following exercise interventions. These cells are shown to be dys- or non-functional in various muscular dystrophies which coincide with the observation of poor muscle health. Therefore, the aim of this study was to examine the number and functionality of muscle stem cells, and physiological factors of muscle health in DM1. In addition, we also aimed to explore whether exercise has therapeutic potential to alleviate poor muscle quality in DM1. In general, we found that DM1 patients have a higher proportion of muscle stem cells; however, they are inherently dysfunctional but did respond to exercise. Consistent with the latter observation, we found poor muscle quality metrics in DM1 patients, with aerobic training leading to improvements in muscle health. Altogether, our results provide in-depth analysis that underscores muscle dysfunction observed in DM1 and the benefits of exercise interventions.

Bibliographic record ONDRÁČKOVÁ, Radka. Application of physiotherapy in treating myasthenia gravis. Prague: Charles University, 2nd Faculty of Medicine, Department of Rehabilitation and Sports Medicine, 2015, p. 90, Supervisor of the work: Doc. PaedDr. Libuše Smolíková, Ph.D. Abstract Myasthenia gravis is an autoimmune disease affecting the neuromuscular transmission. It manifests in muscular weakness and tiredness, which characteristically fluctuate and change throughout the time. The most typically affected muscles are extraocular, mimic, oropharyngeal and the muscles of lower and upper extremities. The danger of respiratory difficulties is aggravated by worsening physical condition, which comes as a consequence of muscular weakness and with the onset of the myasthenic crisis. The work is focused on the use of respiratory physiotherapy and aerobic physical activity in patients with myasthenia gravis. The aim is to verify the effect of respiratory physiotherapy and aerobic physical activity to improve lung function and condition, and the disease stabilization. Keywords Myasthenia gravis, neuromuscular disease, physiotherapy, respiratory physiotherapy, aerobic training

A hiperatividade do Sistema Renina Angiotensina (SRA) está intimamente relacionada a hipertensão. Avaliamos os efeitos sequênciais do treinamento aeróbio e sedentarismo sobre a pressão arterial média (PAM), frequência cardíaca (FC) e o SRA vascular em ratos SHR e WKY. Ao início dos protocolos SHR vs WKY apresentaram elevada PAM e FC. Ang II era superior em SHR vs WKY nas artérias renais, femorais e carótidas. O conteúdo de Ang (1-7) em SHR vs WKY era inferior nas renais, superior nas femorais e nas carótidas. O treinamento promoveu já na primeira semana redução de Ang II nas renais e aorta de SHR e WKY, femorais e carótidas de SHR; redução de Ang (1-7) nas renais, carótidas e aorta de SHR e WKY, e femoral de SHR. Redução da PAM foi observada apenas nos SHR a partir da 8ª semana de treinamento, por outro lado SHR e WKY apresentaram bradicardia de repouso na 2ª e 8ª semanas respectivamente. Em linhas gerais o treinamento promoveu imediata, progressiva e mantida redução da Ang II e Ang (1-7) vascular, favorecendo a redução da PAM nos SHR e da FC em ambos os grupos. / Hyperactivity of the Renin Angiotensin System (RAS) is closely related to hypertension. We evaluated the effects of aerobic training and sedentarism on blood pressure (MBP), heart rate (HR) and vascular RAS in SHR and WKY. At the beginning of protocols SHR vs. WKY showed high MAP and HR. Ang II was higher in SHR vs. WKY renal, femoral and carotid arteries. The contents of Ang (1-7) in SHR vs. WKY was lower in renal than in the femoral and carotid arteries. The training caused a reduction in the first week of Ang II in renal artery and aorta of SHR and WKY, femoral and carotid arteries SHR. And reduction of Ang (1-7) in renal artery, carotid and aorta of SHR and WKY, with reduction only in SHR femoral artery. Reduction of MAP was observed only in SHR from 8 weeks of training, on the other hand SHR and WKY had resting bradycardia at 2 and 8 weeks respectively. In general the training caused immediate, sustained and progressive reduction of Ang II and Ang (1-7) vascular, favoring the reduction in MAP in SHR.

A hipertensão arterial cursa com disfunção autonômica e lesão da barreira hematoencefálica (BHE) em áreas de controle autonômico. Demonstramos recentemente que o treinamento aeróbio corrige a lesão da BHE, e a disfunção autonômica, a qual se encontra correlacionada com a integridade da BHE observada nos hipertensos treinados. O objetivo deste trabalho é avaliar a expressão gênica e proteica de componentes da BHE envolvidos na mediação das respostas cardiovasculares à hipertensão e ao treinamento aeróbio (T). Ratos espontaneamente hipertensos (SHR) e seus controles normotensos (WKY) (250-300g) foram submetidos ao protocolo de T em esteira ou mantido sedentários (S) por 4 semanas. Ao final do T os animais dos grupos experimentais foram canulados para aquisição das variáveis hemodinâmicas. A seguir procedeu-se à infusão intra-arterial de 2 corantes (Rodamina-d, 70 KD, e FITC-d,10 KD) e 20 min após os encéfalos foram coletados para realização de ensaios de fluorescência no Núcleo Paraventricular do Hipotálamo (PVN). Outros ratos dos grupos experimentais foram perfundidos com salina via transcardíaca e realizada a microdissecção do PVN. O mRNA foi extraído e sua concentração de foi analisada pela técnica de RT-PCR. Para investigar os efeitos da hipertensão e do T nos componentes da BHE, foram utilizados os seguintes primers: Occludina, Claudina-5, Zônula Ocludens 1 (proteínas da junção oclusiva), Caveolina-1 (indicador de transporte transcelular), Laminina alfa 1 e Colágeno 4 (componentes da membrana basal), PDGFR&beta; (marcador de pericitos)e Aquaporina-4 (indicador de podócitos de astrócitos), todos eles normalizados para o HPRT endógeno. Os dados de PCR em tempo real foram quantificados pelo método 2&Delta; &Delta;CT. Além disso, outros ratos dos mesmos grupos experimentais foram perfundidos com paraformaldeído 4% para a fixação do encéfalo. O tecido foi crioprotegido e seccionado em criostato, 30 um, os cortes foram incubados em anticorpos primários (Reca-1(marcador endotelial), Claudina-5, Caveolina-1, PDGFR&beta; e Aquaporina-4) e secundários (Alexa Flúor 488 e 594), e sua quantificação no PVN foi realizada através da densidade integrada. Não foi observada diferença na pressão arterial entre os grupos T e S, porém, houve bradicardia de repouso nos animais T (SHR-T:317±3 e WKY-T:308±2) comparados com os animais S (SHR-S: 344±4 e WKY-S: 323±3). A permeabilidade da BHE foi reduzida e normalizada pelo T nos animais hipertensos (SHR-S: 13,6±1,2% e SHR-T: 3,8±0,4%; WKY-S: 3,9±0,2% e WKY-T: 4,1±0,16%), e análise do RT-PCR não mostrou nenhuma diferença para Claudina, PDGFR&beta; e Aquaporina-4 entre os T e S. A expressão gênica de Caveolina-1 estava aumentada nos SHR comparado aos WKY, e o T foi capaz de reduzir sua expressão (SHR-T: 1,05±0,1). O que foi confirmado pela expressão proteica no PVN: a Caveolina-1 encontrava-se aumentada significativamente nos SHR-S em relação aos WKY, e o T reduziu sua expressão no PVN dos SHR. Conclusão: Nossos dados sugerem que o aumento da permeabilidade da BHE no PVN de hipertensos é devida ao aumento de transcitose, identificada pela expressão de Caveolina-1 e que o treinamento aeróbio reverte esta permeabilidade ao reduzir o transporte transcelular sem alterar o transporte paracelular. / The arterial hypertension courses with autonomic dysfunction and Blood Brain Barrier (BBB) damage in areas of autonomic control. We recently demonstrated that aerobic training corrects the damage to the BBB, and autonomic dysfunction, which is correlated with the integrity of the BBB observed in trained hypertense subjects. The objective of this work is to evaluate the gene and protein expression of BBB components involved in mediating cardiovascular responses to hypertension and aerobic training (T). Spontaneously hypertensive rats (SHR) and their normotensive controls (WKY) (250-300g) were submitted to treadmill protocol or maintained sedentary (S) for 4 weeks. At the end of the T, the animals of the experimental groups were cannulated to acquire the hemodynamic variables. Intra-arterial infusion of two dyes (Rhodamine-d, 70 KD, and FITC-d, 10 KD) and 20 min after brains were collected for fluorescence assays in the Paraventricular Nucleus of hypothalamus (PVN). Other rats from the experimental groups were perfused with transcardiacally with saline and the PVN was microdissected. The mRNA was extracted and its concentration was analyzed by the RT-PCR technique. To investigate the effects of hypertension and T in the BBB components, the following primers were used: Occludin, Claudin-5, Zonula Ocludens 1 (tight junction proteins), Caveolina-1 (indicator of transcellular transport), Laminin &alpha; 1 and Collagen-4 (basement membrane components), PDGFR&beta; (pericyte marker) and Aquaporin-4 (astrocyte podocyte indicator), all standardized for endogenous HPRT. Real-time PCR data were quantified by the method 2&Delta;&Delta;CT. In addition, other rats from the same experimental groups were perfused with 4% paraformaldehyde for fixation of the brain. The tissue was cryoprotected and cross-sectioned, 30 m, sections were incubated on primary (Reca-1 (endothelial marker), Claudin-5, Caveolin-1, PDGFR&beta; and Aquaporin-4) and secondary antibodies (Alexa Fluor 488 and 594), and its quantification in thePVN was performed through the integrated density. There was no difference in blood pressure between the T and S groups, but there was resting bradycardia in the T animals (SHR-T: 317 ± 3 and WKY-T: 308 ± 2) compared to S controls (SHR-S: 344 ± 4 and WKY-S: 323 ± 3). The permeability of BBB was reduced and normalized by T in hypertensive animals (SHR-S: 13.6 ± 1.2% and SHR-T: 3.8 ± 0.4%; WKY-S: 3.9 ± 0, 2% and WKY-T: 4.1 ± 0.16%), and RT-PCR analysis showed no difference for Claudin-5, PDGFR&beta; and Aquaporin-4 between T and S. Caveolin-1 gene expression was increased in SHR compared to WKY, and T was able to reduce its expression (SHR-T: 1.05 ± 0.1). This was confirmed by protein expression in PVN: Caveolin-1 was significantly increased in SHR-S relative to WKY, and T reduced its expression in the PVN of SHR. Conclusion: Our data suggest that increased permeability of BBB in the PVN of hypertense individuals is due to the increase transcytosis as identified by Caveolin-1 expression and that aerobic training reverses this permeability by reducing transcellular transport without altering the paracellular transport.

A hipertensão cursa com importante déficit autonômico e lesão da barreira hematoencefálica (BHE) enquanto que o treinamento aeróbio (T) de hipertensos reduz acentuadamente a lesão da BHE, mantendo sua integridade no PVN, NTS e RVLM mesmo na persistência de níveis pressóricos elevados. Esta rápida resposta ao T (2 semanas) é condicionada pela redução da disponibilidade de ANGII nas áreas encefálicas, simultâneo aumento da expressão de podócitos dos astrócitos e desativação da microglia, os quais ocorrem simultaneamente à redução do simpático vasomotor (2 semanas) e antes mesmo do aumento da variabilidade da frequência cardíaca, da atividade parassimpática ao coração, da instalação da bradicardia de repouso e queda parcial da pressão arterial, que se instalam a partir da 4ª semana de T. Alterações na permeabilidade da BHE de hipertensos (lesão com prejuízo estrutural/funcional) e treinados (manutenção da integridade estrutural/funcional) são importantes fatores a condicionar respectivamente a disfunção autonômica na hipertensão ou a sua correção pelo treinamento. / The arterial hypertension is accompanied by important autonomic dysfunction and blood-brain barrier (BBB) lesion while aerobic training (T) in hypertension strongly decreases the BBB lesion, maintaining its integrity on the PVN, NTS and RVLM even in the persistence of high blood pressure (BP) levels. This early response to T (2 weeks) is conditioned by the reduction of ANGII availability, increased expression of astrocytic podocytes and deactivation of the microglia in brain areas. These responses occurred simultaneously with the reduction of vasomotor sympathetic activity (2 weeks) and before the increase of both heart rate variability and parasympathetic activity, resting bradycardia and partial BP fall, appearing only at the 4th week. Changes on the BBB permeability in hypertension (lesion with structural/functional damage) and trained (maintenance of the structural/ functional integrity) are important factors to condition the autonomic dysfunction in hypertension or its correction by the training, respectively.

A hipertensão arterial é acompanhada de hiperatividade do sistema renina angiotensina (SRA). Demonstramos em ratos SHR que a hiperativação do SRA plasmático antecede o cardíaco. A hiperatividade do SRA foi acompanhada de aumento do estresse oxidativo, perfil inflamatório, hipertrofia cardíaca e deposição de colágeno no ventrículo esquerdo (VE) de SHR. O treinamento aeróbio de baixa a moderada promoveu pronta redução do SRA cardíaco e plasmático seguido por normalização do estresse oxidativo e redução da inflamação no VE. Embora não houve alteração na hipertrofia cardíaca, observamos redução da deposição de colágeno no VE de SHR treinados. Sugerimos que a redução do SRA foi determinante na modulação dos parâmetros analisados contribuindo para a manutenção das estruturas cardíacas e evitando remodelamento cardíaco deletério nos SHR treinados. / The hypertension is followed by renin angiotensin system hyperactivity (RAS). We have showed in SHR rats that plasma RAS hyperactivity precedes the cardiac RAS hyperactivity. Furthermore the RAS hyperactivity was followed by oxidative stress and inflammation increase as well as left ventricle (LV) collagen deposition in SHR. The aerobic training promoted prompt cardiac and plasma RAS activity reduction. It was followed by oxidative stress normalization and inflammatory reduction. Although we did not observe cardiac hypertrophy change, the collagen deposition was reduced in SHR trained group. We suggest the RAS activity reduction as a determinant condition to the beneficial adaptations occurred in the parameters analyzed. Thus contributing to maintenance of cardiac structures and avoids the deleterious cardiac remodeling in SHR.

O objetivo deste estudo foi averiguar se o metabolismo do tecido adiposo branco (TAB) de animais treinados sofre total reversibilidade em um longo período de destreinamento. Para isso, ratos wistar foram distribuídos em 3 grupos: treinado (T), destreinado (D) e sedentário (S). O grupo T apresentou redução de massa e diâmetro das células dos coxins adiposos SC, PE e RP, embora a celularidade apresentou-se semelhante entre os três grupos. Verificamos no grupo D, um quadro de resistência à insulina, representado pelo aumento de insulina plasmática e pelo índice de HOMAIR, em relação aos demais grupos (S e T). Na captação de 2-desoxi-D-glicose, o grupo D apresentou uma menor resposta à ação da insulina em relação ao grupo S. Com relação à capacidade de incorporação da glicose em TAG, o grupo T apresentou menor resposta quando as células foram estimuladas com insulina. O grupo D teve aumento na incorporação de glicose em ácidos graxos (AG) quando comparados ao T. Por outro lado, a atividade das enzimas lipogências não apresentou diferenças entre os grupos. Em suma, estes dados sugerem que a capacidade lipogênica do TAB sofre reversibilidade no destreino. Além disso, um quadro de resistência periférica à insulina é observado com a descontinuidade do treinamento físico. Nossos achados descartam a hipótese de que haveria aumento de massa adiposa após 8 semanas de destreino em relação ao estado sedentário. / The objective of this study was to determine whether the metabolism of white adipose tissue (TAB) of total reversibility trained animals suffer in a long period of detraining. Wistar rats were divided into three groups: trained (T), untrained (D) and sedentary (S). The T group showed a reduction in mass and diameter of cells from SC, PE and RP fat pads, although the cellularity showed similar results in the three groups. We found in group D, a part of insulin resistance, represented by the increase in plasma insulin and the HOMA index, compared to other groups (S and T). Uptake of 2-deoxy-D-glucose, D group had a lower response to insulin than in group S. Regarding the capacity to incorporate glucose into TAG, the group had a lower response when T cells were stimulated with insulin. Group D had an increase in the incorporation of glucose into fatty acids (FA) compared to T. On the other hand, the activity of enzymes lipogências not differ between groups. In short, these data suggest that the lipogenic capacity in untrained TAB undergoes reversible. In addition, a framework for peripheral insulin resistance is observed with the discontinuation of physical training. Our findings rule out the hypothesis that there would be an increase in fat mass after 8 weeks of detraining compared to sedentary status.

O objetivo deste estudo foi investigar os efeitos de dois programas de exercício físico na composição corporal de adolescentes obesos submetidos ao tratamento multidisciplinar e verificar qual programa de exercício físico foi mais eficaz para reduzir a gordura corporal e aumentar a massa magra nos dois gêneros. Foram selecionados 60 adolescentes obesos, sendo 36 do gênero feminino e 20 do gênero masculino, com índice de massa corporal (IMC) igual ou acima do percentil 95, na faixa etária de 15 a 19 anos. A amostra foi dividida em dois grupos: grupo aeróbio e grupo força. Os adolescentes foram submetidos a avaliação antropométrica, clínica, de composição corporal e da aptidão física. Além disso, receberam orientação para mudança no estilo de vida e consultas nutricional, psicológica e médica. As sessões de exercícios físicos ocorriam três vezes por semana, em dias alternados, com duração de 60 minutos. A composição corporal foi avaliada pela absortometria de duplo feixe de energia (DEXA) nos momentos inicial e final do estudo. A duração da intervenção foi de 12 semanas. Os principais resultados demonstraram que os grupos aeróbio e força apresentaram redução significante na massa corporal e no IMC e, quando analisados por gênero, verificou-se que no gênero feminino não houve diferença significante, enquanto que o gênero masculino apresentou redução significante no grupo força. Na massa magra observou-se aumento significante apenas no grupo força, tanto sem distinção de gênero quanto diferenciando por gênero. Os dois grupos apresentaram redução significante na massa de gordura, no percentual de gordura corporal total e no percentual de gordura de tronco tanto sem distinção de gênero quanto diferenciando por gênero. Verificou-se correlação positiva na redução do percentual de gordura de tronco com o percentual de gordura periférica. Concluiu-se que o treinamento de força foi mais efetivo para aumentar a massa magra e, levando em consideração a maior redução na variação percentual entre os momentos inicial e final, o grupo aeróbio foi mais efetivo para reduzir a massa de gordura e o grupo força para reduzir o percentual de gordura corporal total dos adolescentes obesos submetidos ao tratamento multidisciplinar de doze semanas. / The objective of this study was to investigate the effects of two physical exercises programs applied to obese adolescents submitted to multidisciplinary treatment in order to establish which program is more effective to reduce body fat and increase lean mass in both gender. 60 obese adolescents aged between 15 and 19 years were selected, comprising 36 girls and 20 boys with body mass index (BMI) equal to or above the 95th percentile. The sample was divided into two groups: aerobic and strength. The adolescents were submitted to anthropometric, clinical, body composition and physical fitness evaluation. In addition, they were oriented to change their lifestyle and received nutritional, psychological and medical assistance. 60 minute physical exercise sessions occurred three times a week on alternate days. Body composition was evaluated by dual-energy X-ray absorptiometry (DEXA) twice: at the beginning and at the end of the program. The program lasted for 12 weeks. The main results show that both aerobic and the strength groups had significant reduction of body weight and of the BMI, and when analyzed by gender, no significant difference was observed among girls of both groups, while boys of the strength groups had a significant reduction. Lean mass increased significantly in the strength group only. Participants of both physical training groups had significant reduction of their fat mass, percentage of total body fat and percentage of trunk fat. A positive correlation was established between the reduction in the percentage of trunk fat and the percentage of peripheral fat. In conclusion, strength training was more effective to increase lean mass. Considering the greater reduction in the percentage variation between the beginning and the end of the period, aerobic training was more effective to reduce the fat mass while strength training was more effective to reduce the percentage of total body fat of obese adolescents submitted to multidisciplinary treatment during twelve weeks.