In setting the AMDR for protein at 10-35% of daily energy, the Institute of Medicine acknowledged a lack of data regarding the safety of long-term intakes. The current study assessed the impact of chronic (17 months) protein consumption at the upper end of the AMDR on renal function, histology, and inflammation. Using plant and animal whole protein sources, female Sprague-Dawley rats (70 days old; n=8-11 at 4, 8, 12, or 17 mo.) were randomized to either a normal (NP; 15% of energy) or high protein (HP; 35% of energy) diet. Egg albumen and skim milk replaced carbohydrates in the HP diet. Diets were balanced for energy, fat, vitamins and minerals, and offered ad libitum. Renal function was analyzed by creatinine clearance and urinary protein levels. Glomerular hypertrophy, glomerulosclerosis and tubulointerstitial fibrosis were assessed on kidney sections. Kidney disease progression was determined by the measurement of transforming growth factor beta-1 (TGF-β1) and renal inflammation by the measurement of chemokines monocyte chemoattractant protein-1 (MCP-1) and regulated upon activation normal T-cell expressed and secreted (RANTES). Rats consuming the HP compared to NP diet had ~17% higher kidney weights (P<0.0001) and ~4.8 times higher proteinuria (P<0.0001). There was a trend towards higher creatinine clearance with HP (P=0.055). Consistent with this, HP compared to NP rats had ~22% larger glomeruli (P<0.0001) and ~33% more glomerulosclerosis (P=0.0003). The HP diet had no significant effect on tubulointerstitial fibrosis and renal TGF-β1 levels and did not result in higher renal levels of MCP-1 and RANTES. In fact, per mg renal protein, HP rats had ~16% lower MCP-1 (P<0.0001) and ~34% lower levels of RANTES (P<0.0001) than NP. The absence of an increase in cytokine levels may be a reflection of the moderate changes in renal pathology observed in rats offered HP diets. These data in normal female rats suggest that protein intakes at the upper end of the AMDR are detrimental to kidney health in the long-term. While modest, this may have implications for individuals whose kidney function is compromised, especially given the prevalence of those unaware of their kidney disease within North America.

Cardiomyocyte perinatal development is characterized by the transition from a hyperplastic to a hypertrophic growth. We hypothesize that genetic factors and processes in the cardiac perinatal transitional program can be identified by a systematic analysis of different stages in heart development. Microarray expression patterning of mRNAs and microRNAs uncovered a perinatal cardiogenomic switch between 5 and 7 days post-birth. Gene ontology analysis revealed cellular and metabolic processes as highly representative Biological Processes. Moreover, approximately 40% of known mice transcription factors are significantly (p<0.05) fluctuating between embryonic day 19 and 10 days post-birth. As the heart matures, cardiomyocytes progressively exit cell cycle with day 5 as a pivotal point. Hypertrophy entails cardiomyocyte binucleation which may be promoted by Protein Regulator of Cytokinesis (Prc1) and its interactors. Temporal cardiac transcription expression analysis provides insight into underlining effectors within the cardiac perinatal transitional program as well as cardiac pathology.

Aerobic exercise (AE) may interfere with muscle adaptations induced by resistance exercise (RE). Three experimental campaigns were conducted to explore the influence of AE on molecular, functional and muscular adaptations to acute and chronic RE. Twenty-nine men performed unilateral knee extensor RE preceded by AE (AE+RE). The contralateral leg did RE only. First, the influence of acute AE on muscle molecular responses to RE performed 6 h later was studied. Subsequently, this exercise regimen was implemented over 5 weeks training. The relationships between acute and chronic outcomes were examined and molecular responses to acute exercise were assessed in untrained and trained muscle. Finally, acute and chronic responses to AE+RE, interspersed by only 15 min recovery, were investigated.Phosphorylation of mTOR and p70S6K was greater after AE+RE than after RE. In parallel, myostatin was suppressed for a longer time after AE+RE. These results suggest that AE+RE enhance skeletal muscle anabolic environment more than RE alone (Paper I). After 5 weeks training, improvements in muscle strength and power were similar across legs. However, AE+RE prompted a greater increase in muscle size than RE, suggesting that AE potentiates the hypertrophic stimulus to RE training without altering muscle function progress (Paper II). Consistent with changes in whole-muscle size, AE+RE showed greater anabolic molecular responses than RE. As chronic training blunted this effect, it appears that AE offers a synergistic hypertrophic stimulus to RE only during short-term training (Paper III). Although putative regulators of hypertrophy such as p70S6K, myostatin and PGC-1a4 were examined, no molecular marker correlated with changes in muscle size, strength or power induced by training. Hence, this study challenges the concept that single molecular markers are viable predictors of training-induced muscle adaptations (Paper III–IV). When recovery time between exercise bouts was reduced to 15 min, AE+RE still produced a more substantial increase in muscle size than RE. However, progression of concentric strength was blunted. Thus, while restored muscle function between exercise bouts is a prerequisite for achieving maximal gains in strength and power, incomplete recovery appears not to compromise muscle hypertrophy (Paper V).Collectively, the results suggest that outcomes of AE+RE are impacted by chronic training and time allowed for recovery between exercise modes. Yet, the current study offers no support to the view that AE interferes with muscle hypertrophy induced by RE.

Cardiac hypertrophy is a compensatory response to increased work load or stress on the heart, but over time can lead to heart failure and death. The molecular mechanisms underlying this disease are still not completely understood, however the Rho/Rho kinase pathway has been shown to play a role. N-[11C]-methyl-hydroxyfasudil, a PET radiotracer, binds to active Rho kinase and could be a possible tracer for hypertrophy. Hypertrophy was induced in vitro using the β-adrenergic receptor agonist isoproterenol to evaluate optimal Rho kinase activity. Rho kinase activity data was correlated to N-[11C]-methyl-hydroxyfasudil binding. Cardiac hypertrophy was verified with an increase in nuclear size (1.74 fold) and cell size (~2 fold), activation of hypertrophic signalling pathways, and increased Rho kinase activity (1.64 fold). This correlated to a 10.3% increase in N-[11C]-methyl-hydroxyfasudil binding. This data suggests that N-[11C]-methyl-hydroxyfasudil may be useful as a radiotracer for detecting cardiac hypertrophy and merits further in vivo investigation.

Thesis (M.Sc.)--Memorial University of Newfoundland, Faculty of Medicine, 2001. / Typescript. Bibliography: leaves 95-112.

Le muscle cardiaque est un organe qui s'adapte à différents stress hémodynamiques en activant la synthèse protéique et en augmentant la taille des cardiomyocytes, résultant sur le développement d'une hypertrophie cardiaque. L'objectif de cette thèse est d'étudier le rôle potentiel du canal TRPM4 dans différents types d'hypertrophie cardiaque. Une altération du Ca2+ diastolique est à l'origine du signal initial activant les voies de signalisation d'une hypertrophie cardiaque délétère de type pathologique telle que la voie de la calcineurine-NFAT et la ré-expression de gènes fœtaux. Cette hypertrophie est alors compensatrice et vise à préserver la fonction de pompe du myocarde. Cette altération peut être conduite par divers stimulis tels qu'une augmentation de l'angiotensine II ou par des pathologies cardiovasculaires telles que l'infarctus du myocarde et l'hypertension. Cependant, une hypertrophie cardiaque bénéfique est également décrite dans la littérature, notamment lors des stades de développement du myocarde lors de l'embryogénèse ou en encore en réponse à une activité physique modérée régulière. Elle se caractérise par l'activation d'une toute autre voie de signalisation qu'est la voie de l'IGF-1-PI3K-Akt engendrée par une augmentation du taux de facteur de croissance qu'est l'insulin growth factor-1. Ces voies de signalisation ont été largement décrites dans la littérature et s'entrecroisent. Le canal TRPM4 est un canal cationique non sélectif perméable de manière égale aux ions Na+ et au K+, imperméables au Ca2+, mais activé par le Ca2+ intracellulaire. Dans le système immunitaire, il régule négativement l'entrée de Ca2+ et ce canal apparaît donc impliqué dans de nombreuses fonctions cellulaires dépendantes du Ca2+ dans différents types cellulaires. Par l'utilisation de deux modèles d'hypertrophie cardiaque, un physiologique généré par quatre semaines d'entraînement en endurance et un pathologique suite à un infarctus du myocarde induit par la ligature de l'artère coronaire gauche sur des souris wild-type et knock-out (KO) pour le canal TRPM4, nous avons mis en évidence une augmentation d'expression fonctionnelle du canal TRPM4 au sein du ventricule gauche associée à une régulation négative d'entrée de Ca2+. Le canal TRPM4 étant un régulateur de l'homéostasie calcique des cardiomyocytes, son expression fonctionelle après l'infarctus du myocarde ainsi que l'entraînement favorise l'activation de la voie de l'IGF-1-PI3K-Akt et prévient partiellement l'activation de la voie de la Calcineurine-NFAT et le développement d'une hypertrophie cardiaque pathologique, notamment dans le modèle d'infarctus du myocarde. En effet, en absence d'expression du canal, l'entrée de Ca2+ n'étant plus régulée, la voie de la Calcineurin-NFAT est favorisée. Mots clés : TRPM4, hypertrophie cardiaque, entraînement, IGF-1-PI3K-Akt, Calcineurine / Abstract: Cardiac muscle is an organ that adapts to different hemodynamic stress by activating protein synthesis and increasing cardiomyocytes size, resulting in cardiac hypertrophy. The objective of this PhD is to study the potential role of TRPM4 channel in different types of cardiac hypertrophy. Impaired diastolic Ca2+ is responsible for the initial signal activating signaling pathways in a deleterious cardiac hypertrophy pathological type such as Calcineurin-NFAT pathway and the re-expression of fetal genes. This hypertrophy is first compensatory and preserves the myocardial pump function. This alteration can be carried out by various stimuli such as increased angiotensin II or by cardiovascular diseases such as myocardial infarction and hypertension.However, a beneficial cardiac hypertrophy is also described in the literature, especially during development stages during embryogenesis or even in response to regular moderate physical activity. It is characterized by the activation one different signaling pathway, the IGF-1 - PI3K –Akt, generated by an increase in growth factor levels that is the insulin growth factor -1. These signaling pathways have been widely described in the literature and cross-talking. TRPM4 channel is a nonselective cation channel permeable equally to Na+ and K+, impermeable to Ca2+ but activated by the intracellular Ca2+. In the immune system, it downregulates Ca2+ entry and therefore appears to be involve in many Ca2+-dependent cellular functions in different cell types. By the use of two models of cardiac hypertrophy, a physiological generated by four weeks of training in endurance and pathological after myocardial infarction induced by ligation of the left coronary artery on wild-type and knockout mice -out (KO) for TRPM4 channel, we have demonstrated a functional expression increased TRPM4 channel within the left ventricle associated with down-regulation of Ca2 + entry. TRPM4 the channel being a regulator of calcium homeostasis in cardiomyocytes functional expression after myocardial infarction as well as the drive promotes the activation of the pathway of IGF-1-PI3K-Akt and partially prevents the pathway activation of the NFAT-calcineurin and the development of pathological cardiac hypertrophy, in particular myocardial infarction model. Indeed, in the absence of expression of the channel, the Ca2 + is not regulated, the path of Calcineurin-NFAT is favored. Keywords: TRPM4, cardiac hypertrophy, training, IGF-1-PI3K-Akt, calcineurin

O Cor pulmonale induzido pela administração intraperitoneal de monocrotalina é um dos modelos mais utilizados para estudar os efeitos dessa síndrome sobre o sistema cardiovascular. Essa síndrome é caracterizada por um desequilíbrio no estado redox celular e uma consequente alteração no imunoconteúdo de proteínas sinalizadoras para a hipertrofia e insuficiência cardíaca. Normalmente, o peróxido de hidrogênio caracteriza-se como a espécie reativa do oxigênio mais estável, e por isso, a molécula mais envolvida com a modulação dessa sinalização. O exercício físico aeróbio tem sido extensamente estudado devido ao fato de ser uma prática que altera o estado redox celular e, consequentemente, a sinalização nos cardiomiócitos. Dessa forma, o objetivo deste estudo foi testar a hipótese de que o exercício físico poderia modular o estado redox no ventrículo direito em animais tratados com monocrotalina e, ao mesmo tempo, provocar alterações na sinalização celular, estrutura e função cardíaca. Ratos Wistar machos com aproximadamente 180 gramas de massa corporal foram treinados por quatro semanas após a injeção de monocrotalina ou solução salina. Os grupos experimentais (n=6-9 animais/grupo) foram: controle sedentário (CS) – ratos sedentários que receberam uma dose única de solução salina (i.p), monocrotalina sedentário (MS) – ratos sedentários que receberam uma dose única de monocrotalina (i.p), controle treinado (CT) - ratos treinados que receberam uma dose única de solução salina (i.p) e monocrotalina treinado (MT) - ratos treinados que receberam uma dose única de monocrotalina (i.p). As medidas hemodinâmicas foram realizadas após 24 horas da última sessão de exercício físico aeróbio. Os dados de pressão diastólica final do ventrículo direito (PDFVD), pressão sistólica do ventrículo direito (PSVD), derivada pressão/tempo máxima (dP/dtmax) e derivada pressão/tempo mínima (dP/dtmin) foram analisados. Após a análise hemodinâmica, os ratos foram mortos por deslocamento cervical e seus órgãos (coração, pulmão e fígado) foram coletados para análises morfométricas, bioquímicas e moleculares. As concentrações de peróxido de hidrogênio e a relação GSH/GSSG foram medidas obtidas com o objetivo de verificar o estado redox nos diferentes grupos experimentais. A massa dos órgãos foi utilizada para analisar a hipertrofia cardíaca, congestão pulmonar e hepática. A massa ventricular direita foi utlizada em cortes histológicos e para a análise de proteínas relacionadas com o remodelamento cardíaco pela técnica de Western Blot. A administração de monocrotalina provocou hipertrofia do ventrículo direito, congestão pulmonar, aumento da PDFVD, da PSVD, da dP/dtmax e da dP/dtmin nos animais MS e MT. Além disso, nos animais MS e CT, notamos uma redução nas concentrações de peróxido de hidrogênio, sugerindo uma modificação do sistema de defesa antioxidante provocada pela monocrotalina e pelo exercício físico. Já quanto ao volume de vasos, no grupo MS tivemos uma diminuição dessa variável em relação ao seu controle (CS), sendo que, o exercício físico preveniu este efeito nos animais MT em relação ao grupo MS. O exercício físico aeróbio promoveu uma redução no volume intersticial e na espessura da túnica média da artéria pulmonar nos animais MT. A monocrotalina provocou uma redução na relação p-GSK-3β/GSK-3β no grupo MT, sendo que que o exercício físico foi capaz de provocar um aumento nessa relação. Dessa forma, acreditamos que o exercício físico aeróbio possa alterar a função de proteínas redox-sensíveis e, dessa forma, modular a hipertrofia cardíaca nos animais que receberam a monocrotalina. / The Cor pulmonale induced by monocrotaline intraperitoneal administration is one of the most widel used models to study the effects of this syndrome on the cardiovascular system. This syndrome is characterized by an imbalance in cellular redox state and a consequent change in immunocontent of signaling proteins for hypertrophy and heart failure. Mostly, hydrogen peroxide is characterized as the most stable reactive oxygen species, and therefore the most involved molecule in the modulation of these signaling pathways. The aerobic exercise has been extensively studied due to the fact that it is a practice that alters the cellular redox state and thus signaling in cardiomyocytes. Thus, the aim of this study was to test the hypothesis that exercise could modulate the redox state of the right ventricle in animals treated with monocrotaline and, at the same time, cause changes in cell signaling, structure and cardiac function. Male Wistar rats approximately 180 grams of body mass were trained for four weeks after injection of monocrotaline or saline. The experimental groups (n = 6-9 animals / group) were: sedentary control (SC) - sedentary rats that received a single dose of saline (ip), sedentary monocrotaline (SM) - sedentary rats that received a single dose of monocrotaline (ip), trained control (TC) - trained rats that received a single dose of saline (ip) and trained monocrotaline (TM) - trained rats that received a single dose of monocrotaline (ip). Hemodynamic measurements were performed 24 hours after the last session of aerobic exercise. Data for end-diastolic pressure of the right ventricle (EDPRV), right ventricular systolic pressure (RVSP), maximum derived from pressure/time (dP/ dtmax) and minimum derived pressure/time (dP/dtmin) were analyzed. After hemodynamic analysis, mice were killed by cervical dislocation and their organs (heart, lung and liver) were colected. The hydrogen peroxide concentrations and GSH/GSSG are measurements with the aim of verifying the redox state in different experimental groups. The organ weights was used to analyze cardiac hypertrophy, pulmonary and hepatic congestion. A portion of the right ventricular mass was utilized for histological examination and other part fot analyze proteins related to cardiac remodeling, by Western blot. Morphometric analysis were performed after the removal of organs. Administration of monocrotaline caused right ventricular hypertrophy, pulmonary congestion, increased EDPRV, RVSP, dP/dtmax and dP/dtmin in SM and TM animals. Furthermore, in animals and SM and TC, we visualized a reduction in the concentrations of hydrogen peroxide, suggesting a change in the antioxidant defense system caused by monocrotaline and by exercise. Already for the volume of vessels in the SM group, we note a decrease of this variable in relation to its control (SC). At the same time, TM animals had an increase in the volume of vessels in relation to the SM group, showing that exercise promotes an increase in this item. The aerobic exercise promoted a decrease in interstitial volume and thickness of the muscle layer of the pulmonary artery in animals TM. The monocrotaline caused a decrease in the p-GSK-3β/GSK-3β in the TM group, showed that exercise was able to cause an increase in this ratio. Thus, we believe that aerobic exercise can alter the function of signaling proteins and thereby modulate cardiac hypertrophy in animals that received monocrotaline.

O objetivo deste estudo foi comparar o efeito do treinamento de força realizado unilateralmente e bilateralmente nos parâmetros neuromusculares dos músculos extensores de joelho. Completaram o estudo 45 sujeitos do sexo feminino, destreinados em força, que foram divididos entre o grupo controle (GC; n=16; 22,7 ± 2,8 anos; 58,0 ± 5,7 kg; 163,6 ± 6,2 cm), grupo unilateral (GUL; n=14; 24,8 ± 1,4 anos; 60,8 ± 6,4 kg; 163,0 ± 6,5 cm) e grupo bilateral (GBL; n=15; 24,3 ± 3,7 anos; 160,2 ± 5,8 cm). O GUL realizou o exercício extensão de joelhos com um membro de cada vez e o GBL realizou o exercício com os dois membros simultaneamente. Ambos os grupos, GUL e GBL, treinaram por 12 semanas, duas vezes por semana. Outros exercícios completaram o programa de treinamento e foram realizados de forma similar pelos dois grupos. O GC não realizou o treinamento. Todos os sujeitos realizaram as avaliações pré e pós 12 semanas. Para avaliação da força máxima, foram realizados os testes de uma repetição máxima (1RM), isocinético e isométrico de extensão de joelho. Todos os grupos foram avaliados nas condições de teste UL e BL. A espessura muscular foi mensurada por ultrassonografia do grupo muscular quadríceps femoral. Para mensurar a ativação muscular foi realizada a coleta do sinal eletromiográfico dos músculos vasto lateral e reto femoral, de ambos os membros inferiores, nos testes de força isocinético e isométrico. Os valores de índice bilateral (IB) para verificar presença ou não de déficit bilateral (DB) na força, foram calculados a partir dos valores do teste de 1RM (IBRM) e de pico de torque (PT), encontrados no teste isométrico (IBPT), enquanto para ativação muscular (IBEMG) foram calculados a partir do sinal eletromiográfico coletado no teste de força isométrico. Os resultados do presente estudo mostraram que o GBL e o GUL tiveram incrementos significativos (p<0,05) nos valores de 1RM em ambas as condições de teste (UL e BL), mas que os ganhos foram significativamente maiores (p<0,05) na condição que os sujeitos realizaram o treinamento, enquanto o GC não apresentou alteração(p>0,05). Os valores de PT isométrico e isocinético também apresentaram incrementos significativos (p<0,05) nos dois grupos, GUL e GBL, em ambas as condições de teste, mas não para o GC (p>0,05). Além disso, essas variáveis, nos dois grupos de treino, foram significativamente maiores (p<0,05) na condição de teste UL. O GUL e o GBL mostraram incrementos significativos (p<0,05) na EM, enquanto o GC mostrou redução significativa (p<0,05). Em relação à ativação muscular coletada no teste de força isométrico, os três grupos mostraram incrementos significativos (p<0,05) na ativação nas condições de teste UL e BL. Para a ativação muscular coletada durante teste de força isocinético, todos os grupos mostraram incremento significativo na ativação (p<0,05), para ambas as condições de teste, com exceção do GC na condição de teste UL, que mostrou decréscimo significativo (p<0,05). Nenhum dos grupos mostrou alteração significativa (p>0,05) nos valores de IBPT no momento pós. Quanto aos valores de IBRM, apenas o GUL alterou os valores significativamente (p<0,05) no momento pós, levando o déficit para uma direção negativa. Ainda, apenas o GC alterou significativamente (p<0,05) os valores de IBEMG, sendo que os sujeitos que possuíam DB no momento pré deixaram de possuir no momento pós. O GUL utilizou cargas de treino significativamente mais elevadas (p<0,05) que o GBL apenas no quarto mesociclo de treino. Os resultados desse estudo permitem concluir que ambas as formas de executar o treino de força, UL e BL, são similarmente eficientes para incrementar força, espessura muscular e ativação muscular, dos músculos extensores de joelho. / The aim of this study was to compare the effect of strength training performed uniterallity and bilaterallity in neuromuscular parameters of the knee extensor muscles. Completed the study 45 female subjects, untrained in force, which were divided into control group (CG; n = 16; 22.7 ± 2.8 years; 58.0 ± 5.7 kg; 163.6 ± 6.2 cm), unilateral group (ULG; n = 14; 24.8 ± 1,4 years; 60.8 ± 6.4 kg; 163.0 ± 6.5 cm) and bilateral group (BLG; n = 15; 24.3 ± 3.7 years; 160.2 ± 5.8 cm). The ULG performed the knee extension exercise with one member at a time and GBL performed the exercise with the two members simultaneously. Both groups were trained for 12 weeks, twice per week. Other exercises completed the training program and were performed similarly by both groups. The CG did not perform the training. All subjects performed the evaluations pre and post 12 weeks. For evaluate the maximum strength were performed one repetition maximum (1RM), isokinetic and isometric tests of the knee extension. All groups were evaluated in the UL and BL test conditions. The muscle thickness was assessed by ultrasonography in the quadriceps femoralis muscle group. For measure muscle activation the EMG signal was collected from the vastus lateralis muscle and rectus femoris muscle in both legs, in the isometric and isokinetic strength tests. The bilateral index (BI) values to verify the presence or absence of bilateral deficit (BD) in strength were calculated from the values of 1RM (BIRM) and peak torque (PT), obtained in isometric test (BIPT), while for muscle activation (BIEMG) were calculated from the EMG signal collected in isometric strength test. The results of this study showed that BLG and ULG significantly increased (p<0.05) the strength in 1RM in both test conditions (UL and BL), but the gains were significantly higher (p<0.05) in the condition which the subjects performed the training, while the GC not had significant increases (p>0.05). The isometric and isokinetic PT values also showed significant increases (p<0.05) for the ULG and BLG in both test conditions, but not for the CG (p>0.05). Moreover, these variables in both training groups, were significantly higher (p<0.05) in the UL test condition. The ULG and BLG showed significant increases (p<0.05) in the muscle thickness, whereas the CG showed a significant reduction (p<0.05). In relation to muscle activation obtained in isometric strength test, all three groups showed significant increases (p<0.05) in the activation in UL and BL test conditions. For the muscle activation collected during isokinetic strength test, all groups showed a significant increases in activation (p<0.05) for both test conditions, except the GC in the UL test condition, which showed a significant decrease (p<0.05). Neither group showed significant changes (p>0.05) in the BIPT values at post training. In relation to BIRM values, only the GUL changed the values significantly (p <0.05) at post training, leading to a negative direction. Furthermore, only the CG changed significantly (p<0.05) the BIEMG values, the subjects had DB at pre training period, but not at post training period. The GUL used training loads significantly higher (p<0.05) than GBL only during at fourth mesocycle training. The results of this study show that both forms of performing strength training, UL and BL, are effective similarly for increases in strength, muscle thickness and muscle activation in knee extensors muscles.

O processo de envelhecimento causa importantes prejuízos na função neuromuscular. O treinamento de força já demonstrou ser um eficiente método de exercício para amenizar em certo grau os efeitos do processo de envelhecimento. Porém, para isso algumas variáveis, como o volume de treinamento, precisam ser controladas. Assim, o objetivo desse estudo foi verificar o efeito de dois volumes de treinamento de força, série simples e séries múltiplas, nas adaptações neuromusculares dos membros inferiores e superiores de mulheres idosas. No primeiro estudo experimental, 27 sujeitos foram divididos em dois grupos de treinamento: grupo série simples (SS; n=14) e grupo séries múltiplas (SM; n=13). O grupo SS realizou uma série em exercício, enquanto que o grupo SM realizou três séries em cada exercício. O valor de uma-repetição máxima (1-RM) de extensão de joelho e flexão de cotovelo, a espessura muscular (EM) dos músculos extensores de joelho e flexores de cotovelo, bem como a força isométrica máxima e a ativação eletromiográfica (EMG) máxima dos membros inferiores e superiores foram avaliadas pré e após seis semanas de treinamento. Os resultados demonstraram que ambos os grupos incrementaram significativamente o 1-RM de extensão de joelho e flexão de cotovelo e a EM dos músculos extensores de joelho e flexores de cotovelo, sem diferença entre eles. No estudo experimental dois, 20 mulheres idosas foram divididas em dois grupos de treinamento: grupo SS (n=11) e grupo SM (n=9). O 1-RM de extensão de joelho e flexão de cotovelo, a EM dos músculos extensores de joelho e flexores de cotovelo, força isométrica máxima e ativação EMG máxima dos membros inferiores e superiores, bem como a qualidade muscular avaliada por echo intensity obtida por ultrassonografia (QMEI), por tensão específica (QMTE), e por tensão específica ajustando os valores de massa muscular por uma escala alométrica (QMEA). Após 13 semanas de treinamento, ambos os grupos incrementaram significativamente o 1-RM de extensão de joelho e a flexão de cotovelo, a EM dos membros inferiores e superiores e a EMG máxima dos músculos vasto medial e bíceps braquial, bem como a QMEI, QMTE, QMEA, sem diferença entre os grupos em nenhuma variável. No estudo experimental três, 20 sujeitos foram divididos em dois grupos de treinamento, grupo SS (n=11) e SM (n=9). O 1-RM de extensão de joelho e flexão de cotovelo, a EM dos músculos extensores de joelho e flexores de cotovelo, força isométrica máxima e ativação EMG máxima dos membros inferiores e superiores, bem como a QMEI foram avaliadas após 6, 13 e 20 semanas de treinamento. Ambos os grupos incrementaram significativamente o 1-RM de extensão de joelho e flexão de cotovelo após 6, 13 e 20 semanas de treinamento, sendo que após 20 semanas o grupo SM apresentou um ganho significativamente maior. A força isométrica máxima dos membros inferiores apenas aumentou após 20 semanas de treinamento e a força isométrica máxima dos membros superiores aumentou após 13 e 20 semanas de treinamento. A EM dos membros inferiores e superiores aumentou em todos os momentos, de modo que após 20 semanas o grupo SM apresentou um ganho significativamente maior com relação a EM dos membros inferiores. Ambos os grupos apresentaram ganho significativo na EMG máxima dos membros inferiores e superiores apenas após 20 semanas de treinamento. A QMEI aumentou significativamente após 13 e 20 semanas de treinamento em ambos os grupos, de modo que o grupo SM apresentou um ganho significativamente maior. O resultado desse estudo demonstraram que mulheres idosas podem obter ganhos significativos com um pequeno e um grande volume de treinamento nos membros superiores, já os membros inferiores necessitam de um grande volume para obter ganhos durante longos períodos de treinamento. / The aging process results in important impairments in neuromuscular function. The strength training has been shown to be a safe and an efficient method for attenuate some effects of the aging process. However, the effectiveness of strength training is dependent of the control of acute variables such as the training volume. Therefore, the aim of present study was assess the effects of the two strength training volumes, single set and multiple sets, on neuromuscular adaptations of lower- and upper-body muscles in older women. In the first experimental study, 27 subjects were divided into two training groups: single set group (SS; n=14) and multiple sets group (SM; n=13). The SS group performed one set per exercise, while the SM group performed three sets per exercise. Knee extension and elbow flexion one-repetition maximal (1- RM), muscle thickness (MT) of the knee extensors and of the elbow flexors, as well maximal electromyography (EMG) activation of the lower- and upper-body muscles were evaluated before and after six weeks of training. The results showed that both groups significantly increased the knee extension and elbow flexion 1-RM and the knee extensors and elbow flexors MT, with no difference between groups. In the second experimental study, 20 subjects were divided into two training groups: SS group (n=11) and SM group (n=9). The knee extension and elbow flexion 1-RM, MT of the knee extensors and of the elbow flexors, maximal isometric strength and maximal EMG activation of the lowerand upper-body muscles, as well as muscle quality (MQ) of the lower-body muscles measured by echo intensity obtained by ultrasonography (MQEI), strength per unit of muscle mass (MQST), and strength per unit of muscle mass adjusted with an allometric scale (MQAS) were obtained. After 13 weeks of training, both groups significantly increased knee extension and elbow flexion 1- RM, MT of the knee extensors and elbow flexors, maximal EMG activation, as well QMEI, QMTE, QMEA, with no differences between groups. In the third experimental study, 20 subjects were divided in the two training groups, SS groups (n=11) and SM group (n=9). The knee extension and elbow flexion 1- RM, knee extensors and elbow flexors MT, maximal isometric strength and maximal EMG activation of the lower- and upper-body muscles and MQEI was measured after 6, 13 and 20 weeks of training. Both groups significantly increased knee extension and elbow flexion at after 6, 13 and 20 weeks of training, however after 20 weeks knee extension 1-RM gains were greater for SM group. The maximal isometric strength of the lower-body significantly increased only after 20 weeks and the maximal isometric strength of the upperbody increased after 13 and 20 weeks of training, with no difference between groups. Both groups showed significant increases in MT of the knee extensors and elbow flexors muscles after 6, 13 and 20 weeks of training, with greater gains for the SM group after 20 weeks in knee extensors MT. The MQEI significantly increased after 13 and 20 weeks of training in both groups, with a gain significantly higher in the SM group. The findings of this study showed that older women may obtain significant gains in upper-body muscles with a lower strength training volume during long period of the training. For lower-body muscles a lower and high volume strength training were similarly effective during the early period and until three months of training; nevertheless the highvolume resulted in gains substantially higher after long period of training.

O objetivo desse estudo foi verificar o efeito de diferentes volumes de treinamento de força na força máxima de membros inferiores e na hipertrofia do reto femoral e do vasto lateral após quatro, oito e doze semanas em indivíduos treinados em força. Vinte e seis indivíduos jovens saudáveis do sexo masculino (idade 23,6 ± 4,6 anos, massa corporal 76,6 ± 7,5 kg, estatura 1,75 ± 0,1 cm), com tempo médio de treinamento de força (4,7 ± 4,1 anos) foram divididos em três grupos experimentais, treinamento de força alto volume (TFAV, n = 8), treinamento de força médio volume (TFMV, n = 9) e treinamento de força baixo volume (TFBV, n = 9). As medidas de força dinâmica máxima (1RM) e de área de secção transversa muscular (ASTM) do reto femoral (RF) e do vasto lateral (VL) foram realizadas nos momentos pré- treinamento, pós quatro semanas, pós oito semanas e pós-treinamento. O volume total de treinamento apresentou aumento estatístico para todos os grupos TFAV (p < 0,0001), TFMV (p < 0,0001) e TFBV (p < 0,0001) ao longo do período experimental. Os valores de 1RM aumentaram de maneira significativa após a oitava semana de treinamento TFAV (11,8 ± 4,7%; p < 0,0001) e TFMV (12,1 ± 8,5%; p < 0,0001) e TFBV (9,6 ± 7,3%; p < 0,001) e no pós-treinamento TFAV (13,9 ± 3,9%; p < 0,0001), TFMV (16,7 ± 10,8%; p < 0,0001) e TFBV (14,0 ± 8,1%; p < 0,0001) para todos os grupos, porém não foi observado diferença entre os grupos. A ASTM do RF apresentou aumento estatístico no pós-treinamento somente para o grupo TFAV (15,0 ± 11,9%; p < 0,0001). Apenas o grupo TFAV aumentou estatisticamente a ASTM do VL após quatro semanas de treinamento (7,71 ± 4,42%; p < 0,0001), porém todos os grupos aumentaram significativamente a ASTM do VL após oito semanas de treinamento TFAV (11,37 ± 3,88%; p < 0,0001), TFMV (9,68 ± 9,36%; p < 0,0001) e TFBV (7,26 ± 3,15%; p < 0,01) e no pós-treinamento TFAV (14,54 ± 4,07%; p < 0,0001), TFMV (14,77 ± 8,24%; p < 0,0001) e TFBV (8,66 ± 3,97%; p < 0,001), porém não foi observado diferença entre os grupos. Os resultados do presente estudo demonstraram que, independente do volume adotado, os ganhos de força máxima foram semelhantes. Por outro lado, a ASTM foi influenciada pelo volume de treinamento, dado que o grupo TFAV foi o único que apresentou aumento significativo da ASTM do RF no pós-treinamento e aumentou a ASTM do VL com apenas quatro semanas de treinamento / The aim of this study was to investigate the effects of different strength training volumes on muscle strength and hypertrophy of the lower limbs after four, eight and twelve weeks of strength training in strength-trained individuals. Twenty-six healthy young males (age 23.6 ± 4.6 years, body mass 76.6 ± 7.5 kg, height 1.75 ± 0.1 cm), with an average experience of strength training (4.7 ± 4.1 years) were divided into three groups, high-volume strength training (TFAV, n = 8), mid-volume strength training (TFMV, n = 9) and low-volume strength training (TFBV, n = 9). Maximum dynamic strength (1RM) and muscle cross-sectional area (MCSA) of the rectus femoris (RF) and vastus lateralis (VL) were measured at baseline, after four weeks, after eight weeks and post-training. The total training volume significantly increased for the groups TFAV (p < 0.0001), TFMV (p < 0.0001) and TFBV (p < 0.0001) throughout the experimental period. The 1RM values increased after the eighth weeks of training, compared to baseline values, for the TFAV (11.8 ± 4.7%; p < 0.0001), TFMV (12.1 ± 8.5%; p < 0.0001), and TFBV (9.6 ± 7.3%; p < 0.001) groups, and post-training TFAV (13.9 ± 3.9%; p < 0.0001), TFMV (16.7 ± 10.8%; p < 0.0001) and TFBV (14.0 ± 8.1%; p < 0.0001) for all groups, with no difference between groups. Only TFAV group presented higher RF MCSA values at post-training (15.0 ± 11.9%; p < 0.0001). Furthermore, only TFAV significantly increased the VL MCSA after four weeks of training (7.71 ± 4.42%; p < 0.0001). All of the groups presented significantly greater VL MCSA than baseline values at eight weeks TFAV (11.37 ± 3.88%; p < 0.0001), TFMV (9.68 ± 9.36%; p < 0.0001) and TFBV (7.26 ± 3.15%; p < 0.01) and at post-training TFAV (14.54 ± 4.07%; p < 0.0001), TFMV (14.77 ± 8.24% ; p < 0.0001) and TFBV (8.66 ± 3.97%; p < 0.001), with no difference between groups. The results of this study demonstrated that, regardless of the adopted volume, the muscle strength gains were similar. On the other hand , MCSA was influenced by the training volume, since the TFAV was the only group that showed significant increase of RF MCSA post- training and increased VL MCSA with only four weeks of training