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Treinamento de Contra Resistência - Hipertrofia, Quebra de Paradigmas, Saúde, Eletromiografias e Biomecânica/VIAS DE SINALIZAÇÃO PARA EVITAR A ATROFIA MUSCULAR MTOR, AKT, P70.pdf VIAS DE SINALIZAÇÃO INTRACELULAR NA ATROFIA MUSCULAR E NO TREINAMENTO RESISTIDO título Intracellular pathways signaling in muscle atrophy and resistance training Juliano Machado[a], Kleverton Krinski[b], Hassan Mohamed Elsangedy[c], Fabricio Cieslak[d], Greicely Lopes[e], Anna Raquel Silveira Gomes[f] [a]Educador Físico graduado pela Universidade da Região de Joinville (UNIVILLE), Mestrando em Fisiologia do Exercício da Universidade Federal do Paraná (UFPR), Curitiba, PR - Brasil, e-mail: jumachado17@yahoo.com.br [b]Educador Físico graduado pela Universidade Paranaense (UNIPAR), Mestrando em Atividade Física e Saúde da Universidade Federal do Paraná (UFPR), Curitiba, PR - Brasil, e-mail: klevertonkrinski@hotmail.com [c]Educador Físico graduado pela Universidade Paranaense (UNIPAR), Mestrando em Atividade Física Saúde pela Universidade Federal do Paraná (UFPR), Curitiba, PR - Brasil, e-mail: hassanme20@hotmail.com [d]Educador Físico graduado pela Universidade Estadual de Ponta Grossa (UEPG), Mestrando em Atividade Física e Saúde da Universidade Federal do Paraná (UFPR), Curitiba, PR - Brasil, e-mail: facieslak@gmail.com [e]Educadora Física graduada pela Universidade Federal do Paraná (UFPR), Mestrando em Fisiologia do Exercício pela Universidade Federal do Paraná (UFPR), Curitiba, PR - Brasil, e-mail: greicielylopes@hotmail.com [f]Fisioterapeuta graduada pela Pontifícia Universidade Católica do Paraná (PUCPR), Doutorado em Ciências Fisiológicas pela Universidade Federal de São Carlos (UFSCAR), Professora do curso de Fisioterapia e do Programa de Mestrado e Doutorado em Educação Física da Universidade Federal do Paraná (UFPR), Curitiba, PR - Brasil, e-mail: annaraquelsg@gmail.com Resumo INTRODUÇÃO: A atrofia muscular é caracterizada como um decréscimo da área de secção transversa da fibra muscular e conteúdo de proteína muscular, reduzida produção de força, aumentada resistência à insulina tão bem como, na maioria das vezes, transição do tipo de fibras lentas para rápidas. Os decréscimos na taxa de síntese proteica e aumento na taxa de degradação são responsáveis pela perda de massa muscular induzida pelo desuso, no entanto, esses mecanismos estão começando a ser elucidados por causa da evolução das técnicas de biologia molecular, as quais permitiram um melhor entendimento das vias de sinalização e as proteínas-chave envolvidas no processo de atrofia muscular induzida pelo desuso. OBJETIVO: o presente estudo realizou uma revisão de literatura referente à atrofia muscular induzida pelo desuso e suas vias de sinalização. METODOLOGIA: realizou-se uma busca de estudos indexados às bases de dados Lilacs, Pubmed/Medline e Scielo, entre o período de 01/01/1997 a 30/06/2008, utilizando as combinações das seguintes palavras-chave: atrophy AND skeletal muscle AND disuse AND lysosomal; atrophy AND skeletal muscle AND disuse AND calpain; atrophy AND skeletal muscle AND disuse AND caspase; atrophy AND skeletal muscle AND disuse AND ubiquitin-proteasome. RESULTADOS E CONCLUSÃO: a partir dessa busca, selecionaram-se cinco artigos e, após sua leitura, buscou-se 35 artigos referenciados por estes, que além das palavras-chave anteriormente descritas incluíam o exercício resistido como terapêutica para a atrofia muscular induzida pelo desuso. Verificou-se de acordo com os estudos apresentados na revisão atual, que o treinamento contra a resistência pode atuar como uma importante modalidade terapêutica para atenuar ou reverter a atrofia muscular induzida pelo desuso. Palavras-chave: Atrofia muscular. Síntese proteica. Proteólise. Exercício. ISSN 0103-5150 Fisioter. Mov., Curitiba, v. 22, n. 3, p. 383-393, jul./set. 2009 Licenciado sob uma Licença Creative Commons Fisioter Mov. 2009 jul/set;22(3):383-393 384 Machado J, Krinski K, Elsangedy HM, Cieslak F, Lopes G, Gomes ARS. Fisioter Mov. 2009 jul/set;22(3):383-393 Abstract INTRODUCTION: The muscular atrophy is characterized as a decrease in cross-sectional area of muscle fiber and protein content of muscle, reduced production of strength, increased resistance to insulin as well as, commonly, transition from slow to fast fibers. The decreases in the rate of protein synthesis and increase in the rate of degradation are responsible for loss of muscular mass induced by disuse, however, these mechanisms are beginning to be elucidated due to of developments in the molecular biology techniques which enabled a better understanding of signaling pathways and the key proteins involved in muscle atrophy induced by disuse. OBJECTIVE: this study was to make a review of literature concerning the muscular atrophy induced by disuse and their pathways of signaling. METHODOLOGY: the search was carried in the Lilacs, Pubmed/Medline and Scielo, limited 01/01/1997 to 30/06/2008, with the terms atrophy AND skeletal muscle AND disuse AND lysosomal; atrophy AND skeletal muscle AND disuse AND calpain; atrophy AND skeletal muscle AND disuse AND caspase; atrophy AND skeletal muscle AND disuse AND ubiquitin- proteasome. RESULTS AND CONCLUSION: It was found 5 articles and after reading it was searched 35 papers referred from them that presented resistance exercise as therapeutic to skeletal muscle atrophy induced by disuse beyond the key-words described above. It was verified according to studies presented in the current review that the resistance training can serve as an important therapeutic tool to attenuate or reverse muscle atrophy induced by disuse. Keywords: Muscle atrophy. Protein synthesis. Proteolysis. Exercise. SIGLAS E ABREVIAÇÕES 4E-BP1 – proteína de ligação 1 do fator de iniciação eucariótico 4; Akt – proteína quinase B, também conhecida como Akt; Bak – antagonista/matador homólogo do Bcl-2; Bax – proteína X associada ao Bcl-2; Bcl-2 – linfoma 2 da célula B; eIF – fator de iniciação eucariótico; FoxO – fatores de transcrição “Forkhead” da família da FoxO; GSK-3β - proteína quinase da glicogênio-3β; IGF-1 – fator de crescimento semelhante à insulina 1; IKB – inibidor do NF-kB; IKKβ – proteína quinase do IKB; IGF-1Ea – fator de crescimento semelhante à insulina sistêmica; IGF-BP – proteína de ligação do IGF; MAFbx – muscle atrophy F-box; MGF – fator de crescimento mecânico; MIKK – IKK específico do músculo; MuRF1 – muscle RING-finger protein-1 ou atrogina; mTOR – alvo da rapamicina de mamíferos; MyoD – membro da família dos fatores de diferenciação miogênicos; NF-kB – família do fator de transcrição nuclear kappa-B; PI3K – fosfatidilinositol 3 quinase; p70S6k – proteína quinase S6 ribossômica; p21-Waf1 – inibidor das quinases dependentes das ciclinas; TNF-α – fator de necrose tumoral alfa. 385Vias de sinalização intracelular na atrofia muscular e no treinamento resistido Fisioter Mov. 2009 jul/set;22(3):383-393 INTRODUÇÃO Condições como redução nos padrões habituais de atividade física, repouso no leito, permanência em cadeira de rodas, imobilização, câncer, sepsis, doenças autoimunes, desnervação, exposição à microgravidade podem levar à perda de massa e capacidade músculo-esquelética (1). A proteólise músculo esquelética induzida por estas condições é um fenômeno conhecido como atrofia muscular, e as consequências funcionais e morfológicas comuns em todas estas formas de atrofia são: diminuída área de secção transversa da fibra muscular e do conteúdo proteico, reduzida produção de força e potência, aumentada fatigabilidade e aumentada resistência à insulina (2-6). O desuso da musculatura esquelética por causa da diminuição da sobrecarga imposta leva a um decréscimo na taxa de síntese proteica e um aumento na taxa de degradação proteica (1, 7, 8), no entanto, muitas moléculas ativadoras que estão envolvidas na atrofia muscular são pouco conhecidas. Muitos avanços têm ocorrido recentemente para elucidar os mecanismos envolvidos na degradação proteica intracelular, possibilitando um maior entendimento dos ativadores ligantes, e dos mecanotransdutores de sinais das vias de sinalização que levam à proteólise muscular (1, 9, 10). Diante disso, o objetivo desta revisão é relatar os achados mais recentes dos artigos publicados nos últimos dez anos, bem como alguns estudos clássicos que permitiram construir o conhecimento atual, sobre as moléculas de sinalização intracelular envolvidas na atrofia muscular induzida pelo desuso e na caquexia, assim como os efeitos da terapêutica relacionada ao treinamento contra resistência sobre estas vias de sinalização. METODOLOGIA O presente estudo foi realizado mediante uma pesquisa de estudos indexados às bases de dados Lilacs, Medline, Pubmed e SciELO entre 01/01/1997 a 30/06/2008. Para seleção dos artigos utilizaram-se parâmetros relacionados às vias de sinalização para atrofia muscular induzida pelo desuso, perfazendo as seguintes combinações de palavras: atrofia e vias lisossomais “atrophy and skeletal muscle and disuse and lysosomal”, atrofia e vias calpaínas “atrophy and skeletal muscle and disuse and calpain”, atrofia e vias das caspases “atrophy and skeletal muscle and disuse and caspase” e atrofia e ubiquitina-proteasoma “atrophy and skeletal muscle and disuse and ubiquitin-proteasome”. Como critérios de inclusão foram utilizados artigos que continham em seu título alguma das palavras-chave das combinações descritas e que não se repetiam em outra base de dados. Desta forma, foram encontrados 35 artigos no Pubmed e selecionados apenas quatro artigos, já no Medline foram encontrados 43 artigos e selecionado apenas um. Não foram encontrados artigos nas bases de dados Lilacs e SciELO com esses critérios. Diante disto, os 5 artigos encontrados nas bases anteriormente descritas apresentavam citações literárias que estavam de acordo com os critérios da revisão atual e que também apresentavam o exercício contra resistência como forma terapêutica para o tratamento da atrofia muscular induzida pelo desuso. Assim, outros 35 artigos, retirados de referências dos 5 artigos encontrados nas bases, foram pesquisados, lidos e incluídos nesta revisão. RESULTADOS E DISCUSSÃO Vias de sinalização envolvidas na atrofia muscular induzida pelo desuso Existem quatro vias proteolíticas conhecidas que levam à atrofia muscular: a via de sinalização das catepsinas ou lisossomais, via de sinalização das calpaínas dependentes de cálcio (Ca2+), via de sinalização das caspases e da ubiquitina proteassoma ATP-dependente (1, 9, 10). De maneira geral, parece 386 que as proteínas clivadas são degradadas no proteassoma, no entanto, o entendimento sobre as moléculas ativadoras envolvidas no decréscimo da síntese proteica, como o IGF-1, FoxO, os sinais de mecanotransdução da titina e os fatores de transcrição NF-kB estão começando a ser conhecidas. Via de sinalização lisossomal Os lisossomos são organelas encapsuladas que contêm grande número de proteases conhecidas como catepsinas B, D, H e L, tão bem como outras hidrolases ácidas. Tem-se verificado que nove dias de suspensão da pata traseira de ratos resulta em atrofia muscular e acentuada proteólise no sóleo (11). Além do mais, as medidas in vitro mostraram que a atividade das catepsinas B, B+L e calpaína-m aumentaram em 111%, 92% e 180% respectivamente, juntamente com uma aumentada concentração do RNAm destas proteinases (11). No entanto, as vias proteolíticas, tanto dependentes de cálcio como a lisossomal, apresentam uma pequena influência sobre a proteólise total, ou seja, 9% nos músculos controle e 18% nos atrofiados (11). Essas observações são consistentes com a atual visão de que as catepsinas não degradam proteínas citosólicas, como às proteínas miofibrilares, ao invés disso, seu maior papel está na degradação de proteínas de membrana tais como receptores, canais de íons, transportadores (1). Recentemente (12), demonstrou-se o que a proteólise dependente da autofagia/lisossomal apresenta mecanismos mais complexos após examinarem músculos de ratos que estão se atrofiando pela desnervação. Neste contexto, observou-se diminuída atividade da via de sinalização do IGF1/PI3K/ Akt e aumentada autofagia por meio do fator de transcrição FoxO3, mostrando uma regulação coordenada entre os sistemas proteassomal e lisossomal (12). Essas evidências nos mostram o quanto os mecanismos indutores de atrofia operam harmonicamente um com o outro, contudo, pouco se sabe sobre como todos esses mecanismos operam. Via de sinalização das calpaínas dependentes de Ca2+ As calpaínas são proteases cisteínas dependentes de Ca2+ que constituem uma grande e diversa família. As fibras músculo-esqueléticas contêm as calpaínas-1 e -2, e uma calpaína específica do músculo conhecida como calpaína -3 ou p94 (13). Pouco se sabe sobre os precisos papéis das calpaínas na regulação normal da musculatura esquelética, embora provavelmente elas estejam envolvidas na organização do citoesqueleto, ciclo celular e apoptose (13). O aumento nas concentrações de Ca2+ intracelulares pode ativar as calpaínas concentradas no disco-Z (9). Além do mais, as calpaínas degradam proteínas como a fodrina, um substrato bem caracterizado das calpaínas, a nebulina, uma importante proteína da arquitetura do sarcômero (14), a titina, proteína-C, vinculina, entre outras, nos quais são substratos conhecidos das calpaínas (1). Assim, a clivagem da titina, proteína que mantém o alinhamento do sarcômero, permite a liberação das miofibrilas para serem ubiquitinadas e, subsequentemente, degradadas no proteassoma (9), pois o proteassoma não é capaz de degradar proteínas intactas. Tem-se mostrado recentemente em ratos com a pata traseira imobilizada, que as calpaínas-1 e -2 estão envolvidas no desenvolvimento da atrofia em músculos com a característica predominantemente oxidativa e que as vias proteolíticas parecem diferir em músculos predominantemente lentos e rápidos (14). Via de sinalização das caspases As caspases constituem um grupo de família de proteases de cisteína – peptidases que usam um resíduo de cisteína como nucleófilo catalítico – que dividem uma especificidade para clivar proteínas alvos nos sítios próximos ao ácido aspártico. As caspases são responsáveis pela apoptose ou morte celular programada, que é essencial para o desenvolvimento embrionário e de muitas doenças (15). Machado J, Krinski K, Elsangedy HM, Cieslak F, Lopes G, Gomes ARS. Fisioter Mov. 2009 jul/set;22(3):383-393 387 A ativação da caspase-3 por meio da conexão entre a via de sinalização da PI3K/Akt e ativação das vias proteolíticas tem sido mostrado recentemente, e esta, têm um importante papel na atrofia muscular induzida por doenças como o câncer e o diabetes (16, 17). Sabe-se que o sistema proteolítico ubiquitina proteassoma é capaz de degradar monômeros de actina ou miosina, no entanto, esse sistema não é capaz de quebrar os complexos actomiosina intactos (10). Neste sentido, as caspases podem ter ações similares às calpaínas em tornar as proteínas miofibrilares disponíveis para a ubiquitinação (1). Assim, foi mostrado que o tratamento dos complexos de actomiosina solúveis da musculatura esquelética de ratos diabéticos com caspase-3 recombinante levava a uma acentuada proteólise (17). Embora prévios estudos tenham buscado investigar elucidar os mecanismos das caspases, não existem evidências mostrando o seu papel na atrofia muscular induzida pelo desuso. Via de sinalização da ubiquitina proteassoma O proteassoma 26S é um grande complexo multiproteico que consiste do centro proteolítico 20S e dois “anéis” o 19S, nos quais regulam a ligação e a degradação das proteínas ubiquitinadas (1). A degradação da maioria das proteínas miofibrilares decorrente da atrofia ocorre no proteassoma, e o processo de ubiquitinação envolve a cooperativa interação das três classes de proteínas determinadas E1 ou ativante de ubiquitina, E2 ou conjugante de ubiquitina e a E3 ou ligante de ubiquitina (1, 9, 18). A ubiquitina é primeiramente ativada por meio da ação da E1 num processo dependente de ATP. A ubiquitina ativada é então transferida para a E2, e em seguida a enzima E3, a qual encontra-se ligada à proteína substrato que será marcada para ser degradada, se liga à E2. Neste sentido, a E2 transfere a ubiquitina para a proteína-alvo ligada na E3 marcando-a para a posterior morte no proteassoma. Esse processo é repetido até uma cadeia de quatro ou mais moléculas de ubiquitina ter sido formada, para que seguidamente a proteína-alvo seja degrada em pequenos peptídeos no proteassoma (9). TRANSDUÇÃO DE SINAL E PROTEÓLISE NA ATROFIA MUSCULAR Relação entre a via da PI3K-Akt e FoxO na atrofia muscular Tem-se mostrado que miotúbulos em cultura no estado de atrofia, a atividade da via da PI3K/ Akt diminui, levando a ativação dos fatores de transcrição FoxO e ativação da atrogin-1/MAFbx, e que o tratamento com IGF-1 ou a expressão exacerbada da Akt inibe a expressão da atrogin-1 (19). Assim, os fatores de transcrição FoxO têm papel crítico no desenvolvimento da atrofia muscular, e a inibição desses fatores é uma atrativa abordagem para combater o processo de atrofia induzida pelo desuso. Em um estudo foi mostrado que ratos transgênicos, hiper-expressando a FoxO1, mostraram um decréscimo significativo no tamanho das fibras do tipo I e do tipo II, além de um decréscimo no número de fibras do tipo I (20). Por outro lado, a atividade de corrida realizada na esteira significativamente reduziu a atividade da FoxO1 nos ratos transgênicos em comparação aos ratos controle (20). Verificou-se recentemente que humanos com doença pulmonar obstrutiva crônica, tanto em estado de atrofia muscular como em estado normal (controle), os níveis das proteínas FoxO1, Akt e 4E- BP1 estavam aumentados (21). Além disto, as concentrações do RNAm das ubiquitinas ligases atrogin- 1 e MuRF1 estavam aumentadas em sujeitos com atrofia em comparação aos sujeitos controle (21). Neste sentido, a regulação transcricional das ubiquitinas ligases ocorrem via FoxO1, porém, parece ser independente da Akt, mostrando que estes indivíduos apresentam elevada expressão das vias de sinalização hipertróficas na tentativa de restaurar massa muscular perdida (21). Contudo, essas respostas intracelulares ainda não foram verificadas em humanos saudáveis com atrofia muscular. Isso mostra que os modelos de atrofia muscular induzida pelo desuso precisam ser construídos utilizando como base os estudos experimentais com modelos animais, pois pouco se sabe sobre os mecanismos ativadores desta via, principalmente em humanos. Vias de sinalização intracelular na atrofia muscular e no treinamento resistido Fisioter Mov. 2009 jul/set;22(3):383-393 388 NF-kB como molécula de sinalização na atrofia muscular O fator de transcrição nuclear kappa-B (NF-kB) é um complexo proteico o qual foi mostrado que está envolvido no processo de atrofia por desuso. Em mamíferos, existem cinco tipos diferentes de NF-kB (p65 ou Rel A, Rel B, c-Rel, p52 e a p50), nos quais medeiam uma variedade de processos de acordo com o tipo de célula e dos ativadores específicos (10). A ativação do NF-kB se dá por meio da ubiquitinação e degradação de sua proteína inibitória IkB, que em estado normal encontra-se ligada ao NF-kB mantendo-o no citoplasma (10). Por exemplo, na via clássica ou canônica, o TNFá ativa a fosforilação de uma quinase do IkB, IKKâ, que por sua vez estimula a degradação do IkB, permitindo a translocação do heterodímero p65/p50 para o núcleo, porém, quando o IkB é ativado pelo IKKá, a via de ativação é a não-canônica do NF-kB (10). Tem-se mostrado que sete dias de suspensão da pata traseira de ratos, marcadamente autorregula os níveis nucleares da p50, enquanto a c-Rel é moderadamente autorregulada, a Rel B baixo- regulada, e a p52 e p65 não sofreram mudanças (22). Foi verificado também que durante esse período, os membros da família do NF-kB ativados pelo desuso são completamente diferentes dos membros ativados pela caquexia (22). Outro fator que vale ressaltar é que as concentrações da proteína anti- apoptótica Bcl-2 estavam aumentadas em quatro vezes, enquanto as proteínas pró-apoptóticas Bax e Bak demonstravam concentrações reduzidas (22). Recentemente demonstrou-se que um período de três a sete dias de suspensão da pata traseira ativa genes envolvidos na atrofia como a atrogin-1, FoxO3a entre outros, nos quais parecem ser alvos dos fatores de transcrição NF-kB (23). Neste sentido, a degradação do IkBá é um fator necessário para atrofia induzida pelo desuso, por meio do aumento na ubiquitinação da proteína IkB e ativação da via de sinalização do NF-kB e a expressão de genes alvos envolvidos na atrofia muscular (23). Porém, é possível que a ativação das vias de sinalização canônica e não-canônica do NF-kB na atrofia muscular induzida pelo desuso sejam ativadas de forma tempo dependente. Pois o NF-kB é ativado bifasicamente na musculatura esquelética de ratos tanto jovens como idosos durante quatro semanas de imobilização, com um decréscimo na atividade da via clássica do heterodímero p65/p50 nas primeiras duas semanas, seguido por um aumento na atividade deste heterodímero nas próximas duas semanas (24). Estes achados são consistentes com os achados publicados previamente nos quais mostraram uma ativação da via alternativa do NF-kB seguindo a atrofia por desuso (22, 23). Um estudo recente mostrou existir um componente acima do NF-kB, a IkB quinase-â (MIKK), o qual causa intensa proteólise (25). Foi verificada uma perda de massa muscular através da proteólise dependente da ubiquitina, pois a expressão da ubiquitina ligase MuRF1 estava aumentada em ratos com a forma constitutivamente ativa do MIKK (25). Além do mais, a inibição farmacológica do eixo IKKâ/NF-kB/MuRF1 reverteu a atrofia, levando a uma atenuada proteólise induzida pela desnervação ou tumor seguido de uma aumentada taxa de sobrevivência (25). Neste sentido, a sinalização do NF-kB é um componente central do processo de atrofia e pode estar envolvida na ativação dos processos proteolíticos. A partir desses achados, pode-se sugerir que os músculos imobilizados ou aqueles que estão em estado de atrofia por desuso, sofram um processo inflamatório, o qual pode apresentar uma variação tempo dependente levando à ativação da via do NF-kB. Efeitos do treinamento contra resistência sobre a atrofia muscular Tem-se mostrado que a aumentada sobrecarga, resultante do exercício crônico, conduz a uma aumentada expressão do gene que codifica o IGF-1 tanto em modelos animais (26) como em humanos (27). Além do mais, duas seletivas isoformas do IGF, o IGF-1Ea e o fator de crescimento mecânico (MGF) parecem ser seletivamente expressos na musculatura esquelética e regulados pela sobrecarga mecânica, nos quais apresentam efeitos parácrino e autócrino (28). Machado J, Krinski K, Elsangedy HM, Cieslak F, Lopes G, Gomes ARS. Fisioter Mov. 2009 jul/set;22(3):383-393 389 Desta forma, a ativação da PI3K por meio de um ligante em seu receptor específico, tal como o IGF-1, fosforila o fosfolipídeo de membrana fosfatidilinositol-4,5-bifosfato para fosfatilinositol- 3,4,5-trifosfato, criando um sítio de ligação na membrana plasmática para a proteína serina/treonina Akt (29, 30). A Akt em seu estado ativado/fosforilado, fosforila a proteína quinase alvo da rapamicina dos mamíferos (mTOR), produz um aumento na síntese proteica por meio da ativação da p70S6K e da 4E-BP1, os quais são reguladores-chave envolvidos na tradução e síntese proteica (29, 30). A ativação das vias de sinalização do mTOR tem importante papel em regular o crescimento muscular e a hipertrofia músculo-esquelética (31). O treinamento resistido de alta intensidade tem mostrado alterar o perfil dos polissomos, sugerindo que a taxa de iniciação da tradução é aumentada por esse tipo de treinamento (32). Além do mais, existe uma forte correlação entre a ativação da p70S6K, um regulador da iniciação da tradução, com os aumentos na massa muscular (32). Neste sentido, é possível inferir que realizar um treinamento com intensidades superiores à intensidade de treino observada em protocolos clássicos como o de De Lorme, possam causar melhores resultados sobre a atrofia muscular induzida pelo desuso, porém é preciso estudos que comprovem essa teoria. O exercício resistido também induz um transitório aumento na fosforilação do mTOR (33), PKB/Akt (34), 4E-BP (35) e S6K1 (32), assim como na atividade do eIF2 (36, 37). Além do mais, parece existir uma ativação dependente do tempo dos mecanismos anabólicos e miogênicos que levam ao aumento miofibrilar. Um único período de exercício de contrações isométricas máximas em humanos, por meio da estimulação elétrica neuromuscular do músculo vasto lateral, com estímulos de 5 segundos e repouso de 15 segundos durante 30 minutos, onde as contrações evocadas eram em séries de 50 Hz e pulsos bifásicos de 450 µs, com o intuito de mimetizar um período de exercício resistido, resultou em uma série de alterações anabólicas na musculatura exercitada (38). Este protocolo resultou em aumentados níveis do RNAm para a proteína de ligação-4 do IGF, a IGFBP-4 (84%), MyoD (83%), miogenina (aproximadamente 3 vezes), ciclina D1 (50%), p21-Waf1 (16 vezes), um transitório decréscimo no RNAm do IGF-1 (38). Já os RNAm para o MGF, IFGBP-5 e do receptor do IGF-1 não apresentaram alteração, no entanto, 72 horas após a sessão, todos estes RNAm estavam aumentados (38), mostrando um efeito anabólico do treinamento resistido. Outra característica importante do treinamento resistido é a combinação de ações musculares (concêntrica, excêntrica e isométrica) com o objetivo de reverter ou minimizar a atrofia muscular induzida pelo desuso. Tem-se mostrado que a combinação das ações dinâmicas com as isométricas com suficiente volume apresenta importante estímulo anabólico e miogênico que se contrapõem aos estágios inicias da atrofia muscular induzida pelo desuso. Além destes efeitos, o treinamento resistido também elevou a expressão e fosforilação das proteínas quinases envolvidas nas respostas anabólicas, como a Akt, mTOR e a proteína glicogênio sintase quinase-3b (GSK-3b), em paralelo com um decréscimo do conteúdo da FoxO1 no núcleo (fator de transcrição envolvido na atrofia muscular) (39). Esses resultados mostram a nível molecular que umas das adaptações do treinamento resistido são os aumentos nas alterações anabólicas juntamente com um leve decréscimo nas alterações catabólicas, resultando em um equilíbrio nitrogenado positivo e aumento da massa muscular. Diante de todas essas informações, é importante salientar também a necessidade de se manter os níveis de treinamento para que os ganhos positivos sobre a massa muscular esquelética sejam mantidos, pois o treinamento resistido de oito semanas em humanos resultou em hipertrofia muscular (10%) juntamente com um aumento no conteúdo das proteínas Akt, GSK-3b e mTOR em seus estados fosforilados, em paralelo com um decréscimo do conteúdo da FoxO1 nuclear (39). Porém um período de destreinamento de oito semana o qual simulou o desuso, causou 5% de atrofia muscular, um decréscimo na Akt e GSK-3b nos seus estados fosforilados e um aumento na FoxO1 nuclear, em relação aos resultados obtidos no período pós-treinamento (39). Além do mais, logo após o período de treinamento foi observado um aumento nas ubiquitinas ligases atrogina 1 e MuRF1 (fase de hipertrofia), no entanto, ocorreu um decréscimo destas ubiquitinas logo após o período de destreinamento (fase de atrofia) (39). Vias de sinalização intracelular na atrofia muscular e no treinamento resistido Fisioter Mov. 2009 jul/set;22(3):383-393 390 Uma atual teoria mostra que um decréscimo na atividade/sobrecarga muscular diminui a sinalização dos fatores de crescimento, resultando num decréscimo da fosforilação da FoxO pela Akt. Na sua forma hipofosforilada, a FoxO transloca para o núcleo e aumenta a expressão de genes da atrofia como as proteínas ubiquitinas ligases atrogin-1 e a MuRF1 (8), além do mais, esta última também é regulada pelo NF-kB (40). As proteínas MuRFs (-1, -2, -3) interagem com o domínio quinase da titina, num músculo ativo e, assim, mantendo-se fortemente ligada à titina, porém, quando a ligação é quebrada, tal como pela inatividade, a MuRF é liberada e lançada para o núcleo, aumentando a expressão de genes da degradação proteica (8). Isto justifica a importância de se manter os níveis de treinamento físico para autorregular a via de hipertrofia muscular, ou ao menos manter a massa muscular, principalmente se o organismo vir a se encontrar em estado de atrofia muscular induzida pelo desuso, pois ao contrário da caquexia, a atrofia pelo desuso pode ser completamente revertido pelo treinamento resistido. CONSIDERAÇÕES FINAIS A presente revisão demonstrou a interação dos mecanismos envolvidos nas vias de sinalização da atrofia muscular induzida pelo desuso bem como no treinamento resistido. Diante de todas as citações acima, é verificado que apesar de existirem diversas vias de sinalização intracelular que atuam na atrofia muscular induzida pelo desuso (lisossomal, calpaínas, apoptóticas e proteassomal), a autorregulação da via da PI3k/Akt é essencial para a manutenção da musculatura esquelética, pois ela proporciona um efeito cascata integrando as vias de hipertrofia e atrofia muscular no desuso (Figura 1). Desta forma, modalidades terapêuticas como o treinamento resistido têm mostrado ser eficaz em autorregular a via de síntese proteica, o qual está baixo-regulada em estado de atrofia muscular induzida pelo desuso, assim, o treinamento resistido estimula um aumento ou mantém a massa muscular esquelética, contrapondo-se aos efeitos negativos gerados pela atrofia muscular causada pelo desuso. FIGURA 1 - Comparação das vias ativadas pelo desuso e treinamento resistido Legenda – As setas apontadas para cima indicam um aumento na expressão, as setas apontadas para baixo indicam uma diminuição da expressão da respectiva proteína intracelular. Os sinais positivos representam ativação, já os sinais negativos inibição de uma dada proteína. No estado treinado, existe uma maior atividade das vias anabólicas em comparação com as vias catabólicas, porém no desuso, a proteólise predomina sobre a síntese protéica. Contudo, deve-se salientar que tanto em estado treinado como no desuso da musculatura esquelética, as vias de síntese e de degradação protéica são ativadas, a diferença está no grau de predomínio de uma sobre a outra. Machado J, Krinski K, Elsangedy HM, Cieslak F, Lopes G, Gomes ARS. Fisioter Mov. 2009 jul/set;22(3):383-393 391 REFERÊNCIAS 1. Jackman RW, Kandarian SC. The molecular basis of skeletal muscle atrophy. Am J Physiol Cell Physiol. 2004;287(4):C834-C843. 2. 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Recebido: 18/08/2008 Received: 08/18/2008 Aprovado: 21/05/2009 Approved: 05/21/2009 Revisado: 23/09/2009 Reviewed: 09/23/2009 Vias de sinalização intracelular na atrofia muscular e no treinamento resistido Fisioter Mov. 2009 jul/set;22(3):383-393 Treinamento de Contra Resistência - Hipertrofia, Quebra de Paradigmas, Saúde, Eletromiografias e Biomecânica/TREINAMENTO RESISTIDO COM DIFERENTES FREQUENCIAS SEMANAIS E RESULTADOS.pdf ISSN 1750-9823 (print) International Journal of Sports Science and Engineering Vol. 05 (2011) No. 02, pp. 112-118 Effects of 8 Weeks Equal-Volume Resistance Training with Different Workout Frequency on Maximal Strength, Endurance and Body Composition Hamid Arazi , Abbas Asadi Department of physical education and sport science, University of Guilan, Rasht, Iran (Received March 15, 2011, accepted May 9, 2011) Abstract. The purpose of this study was to determine the effects of short-term equal-volume resistance training with different workout frequency on maximal strength, endurance, and body composition in novice subjects. Thirty-nine healthy males comprised four groups; total-body resistance training (12 exercises for one session per week) (part I=10), total-body resistance training (12 exercises for two sessions per week) (part II=10), lower-body, upper-body, and upper-body resistance training (12 exercises for three sessions per week) (part III=9), and control group (CG=10). Assessments of body composition, leg and arm circumferences, body weight, strength (one repetition maximum in bench and leg press) and endurance (bench and leg press) were determined before and after 8 weeks of training. One repetition maximum in bench and leg press was improved significantly in all training groups (P < 0.05). All groups increased body weight, body composition, and bench and leg press endurance (P < 0.05), but PIII group showed a little improvement rather than other groups (P > 0.05). The PIII group not only increased thigh circumference but also improved arm circumference, whereas the PI and PII groups changed either arm circumference or thigh circumference (P < 0.05). It is concluded that in healthy young men, whole and split weight training routine produce similar results over the first 2 months of training, with minimal differences among groups. Keywords: split routine, exercise performance, resistance training. 1. Introduction Resistance training, also known as strength or weight training, has become one of the most popular forms of exercise for enhancing and individual's physical fitness as well as for conditioning athletes. Resistance training has been used extensively to increase fitness and sport performance. It has been demonstrated to augment maximum strength, power, and jumping ability (1,2,3). It is well known that a variety of resistance training programs can stimulate an increase in one repetition maximum (1RM) strength (4,5,6). However, only few studies have attempted to make direct comparisons of different styles of resistance training programs to determine adaptational differences. With short-term training, Marcinik et al. (7) compared high intensity (i.e., 70% of 1-RM) versus low intensity (i.e., 40% of 1-RM) aerobic/circuit resistance training in women who were U.S. Naval recruits. After 8 wk, 1-RM bench press performance was significantly greater in the high-intensity group, whereas no difference was observed between groups in 1- RM leg press performances. American College of Sports Medicine (ACSM) recommends split routines to maximize strength gains among intermediate-advanced resistance-trained individuals and athletes. With split routine training paradigm, individuals train different body parts on each training session within a week to allow proper muscle recovery and to maximize training loads. The ACSM expands this recommendation suggesting that split training routines should also require the periodization of the training load (8). This has been shown to be an effective initial frequency whereas 1-2 d·wk_1 appears to be an effective maintenance frequency for those individuals already engaged in a resistance training program (9). In a few studies: 4-5 d·wk_1 were superior to 3, 3 d·wk_1 superior to 1 and 2 d, and 2 d·wk_1 superior to 1 for increasing maximal strength (9,10). Performing upper/lower body split or muscle groups split routines during a workout are common at this level of training in addition to total-body workouts (5). Hakkinen et al. (11) reported greater increases in muscle cross-sectional area and strength when training Corresponding author. Tel.: +98 911 139 9207; Fax: +98-131 6690675. E-mail address: h_arazi2003@yahoo.com. Published by World Academic Press, World Academic Union International Journal of Sports Science and Engineering, 5 (2011) 2, pp 112-118 113 volume was divided into two sessions rather than one. Previous studies designed resistance training to upper- body, lower-body and or total-body workouts. They reported that upper-body and total-body resistance training resulted in similar improvements in performances and or total conditioning program directed at development of muscle tissue mass (12,13). In our knowledge, no study compared the effects of designing resistance training, which divided into three parts; total-body resistance training one session per week (part I), total-body resistance training two sessions per week (part II), and upper-body, lower-body, and upper-body resistance training three sessions per week (part III), together. No data are available to address this question that; Is resistance training for 1 session better than 2, or 3 sessions, and or 3 sessions is better than 1, or 2 sessions with equal-volume in novice subjects? Are important exercise sessions to design resistance training for novices and beginners? Are differences among exercise sessions for increasing physical fitness? Those are current questions that we want to answer in this study. Therefore, the purpose of this investigation was to examine the effect of three differences periodized resistance training programs (part I, part II, and part III) on strength, endurance, and body composition in novice subjects. 2. Methods 2.1. Subjects Thirty-nine healthy males were volunteered to participate in this study. Subjects were randomly divided into four groups; part I group (PI; n=10), part II group (PII; n=10), part III group (PIII; n=9), and control group (CG; n=10). Subjects were informed as to the experimental procedures and signed informed consent statements and medical history forms in adherence with the human subjects’ guidelines of the University of Guilan Health Sciences Center before any data collection. Subjects had been never involved any type of resistance training and had normal dietary intake during the study. There were no significant differences among groups in age, height, weight, and percent body fat at pre training (Table 1). Table 1. Subjects characteristics. Data are mean ± SD. PI PII PIII CG Age (yr) 20.20±1.87 20.40±2.31 20.33±1.80 20.40±2.06 Height (cm) 173.60±3.80 174.20±5.18 175.67±5.29 174.40±5.05 Weight (kg) 70±4.49 72.15±8.28 73.33±7.63 74.15±5.61 Body fat (%) 13.54±2.72 13.74±2.92 14.13±2.86 13.20±3.49 2.2. Testing Procedures The subjects were familiarized with the resistance training program about one week before the start of training period. During the familiarization session, subject initial characteristics such as; age, height, body weight, percent body fat, thigh and arm circumference, one repetition maximum (1RM) and endurance (60% 1RM) for bench press and leg press, were obtained. Subjects were tested pre training and post training (8 weeks). The same researchers conducted all tests. Pre and post training anthropometric measures of weight, and percent body fat were taken. Height was measured to a nearest to 0.1 cm using height rod. Body weight with minimal clothing was measured to the nearest 0.1 kg on a lever-type balance in a fasted state after emptying the bladder. Subjects had 3 skin fold sites (chest, abdominal, and thigh) measured to determine body composition or percent body fat. The measurement was used the method of Jackson and Pollock (14). The circumference of mid thigh and mid upper arm of the dominant limbs was assessed. A bilateral leg press test was selected to provide data on maximal strength through the full range of motion of the muscles involved. Maximal strength of the lower extremity muscles was assessed using concentric 1RM leg press action. Bilateral leg press tests were completed using standard leg press equipment (NIROO, KING BODY, IRAN), with the subjects assuming a sitting position and the weight sliding obliquely at 45˚. On command, the subjects performed a concentric leg extension (as fast as possible) starting from the flexed position to reach the full extension against the resistance determined by the weight. Warm-up consisted of a set of 10 repetitions at loads of 40-60% of the perceived maximum. For the bench press, each participant lowered the bar until contact with the chest was achieved and subsequently lifted the bar back to the fully extended elbow position. Any trials failing to meet the standardized technique criteria were discarded. A warm-up consisting of 5-10 repetitions with approximately 40-60% of perceived maximum was performed. The rest period between the actions was always 2 minutes. SSci email for subscription: publishing@WAU.org.uk Hamid Arazi, et al: Effects of 8 Weeks Equal-Volume Resistance Training with Different Workout Frequency 114 Subjects were allowed to perform maximum 8 repetitions during bench press and leg press, and were used equation of Brzycki (15) for the determine of 1RM. )0278.0(0278.1 )( 1 srepetitionofnumber kgweight RM The local muscular endurance test was conducted 24 hours after maximal strength tests. The test was accomplished by execution of repetitions to exhaustion. After a short period of light aerobic warm-up, participants performed as many repetitions as possible without stopping or pausing between repetitions. The resistance comprised 60% of 1RM (16). The exercises selected for the application of this test were the bench and leg press. 2.3. Resistance Training All workouts started with a general warm-up and included cool-down periods (i.e., low-intensity aerobic exercise, stretching, etc.) of approximately 5-10 min. A trainer supervised all subjects so that all essential program characteristics were strictly enforced. Specifically, trainers were responsible for seeing that exercise prescriptions were properly carried out and achieved during a workout (e.g., velocity of movement, appropriate spotting, appropriate safety considerations, prescribed rest periods, and proper hydration requirements). Also, it has been recently demonstrated that direct supervision of resistance training is vital to optimize strength performance adaptations (17). The 8 weeks program consisted of free weight and machine exercises. The part I group performed all upper- and lower-body exercises in one training session per week (Saturday) for 8 weeks. Resistance training program included; leg press, leg curl, leg extension, calf raise, lat pull-down, lat pull-row, bench press, pack fly, arm curl, dumbbell arm curl, triceps push-down, and dumbbell triceps extension (Table 2). The part II group performed upper- and lower-body exercises in two training sessions per week (Saturday and Tuesday) for 8 weeks. Resistance training program included; leg press, leg curl, lat pull-down, bench press, arm curl, and triceps push-down on Saturday; and leg extension, calf raise, lat pull-row, pack fly, dumbbell arm curl, and dumbbell triceps extension on Tuesday (Table 2). The part III group performed lower-body, upper-body and upper-body exercises in three training sessions per week (Saturday, Monday, and Wednesday) for 8 weeks. Resistance training program included; leg press, leg curl, leg extension, and calf raise on Saturday; lat pull-down, lat pull-row, triceps push-down, and dumbbell triceps extension on Monday; bench press, pack fly, arm curl, and dumbbell arm curl on Wednesday, (Table 2). Subjects were tested every 2 weeks, and resistance exercises were designed based on new 1RM for each exercise. Total training volume was not different among groups, yet training frequency was different among the three programs. Table 2. Resistance training for PI, PII, PIII groups. Group Exercises Week 1-2 Week 3-4 Week 5-6 Week 7-8 Rest periods Reps-intensity PI I 12-60% 1RM 10-12-70% 1RM 8-10-75% 1RM 6-8-80%1RM 2-3 min PII II 12-60% 1RM 10-12-70% 1RM 8-10-75% 1RM 6-8-80%1RM 2-3 min PIII III 12-60% 1RM 10-12-70% 1RM 8-10-75% 1RM 6-8-80%1RM 2-3 min I; 12 exercises on Saturday II; 12 exercises on Saturday and Tuesday III; 12 exercises on Saturday, Monday and Friday 1RM; one repetition maximum 2.4. Statistical Analysis All data are presented as mean ± SD. A one-way analysis of variance (ANOVA) was used to determine significant differences among groups. In the event of a significant F ratio, Scheffe post hoc tests were used for pairwise comparisons. Paired t-tests were used to identify any significant differences between the groups at the pre and post tests for the dependent variables. A criterion α level of P ≤ 0.05 was used to determine statistical significance. 3. Results The results of this study are presented in figure 1. There were significant changes in the percent body fat, weight, 1RM bench press and 1RM leg press after a 8-week resistance training for all training groups (P < 0.05). The PII and PIII groups showed significant improvements rather than baseline in the thigh SSci email for contribution: editor@SSCI.org.uk International Journal of Sports Science and Engineering, 5 (2011) 2, pp 112-118 115 circumference (P < 0.05). Whereas, The PI and PIII groups showed significantly increases rather than baseline in the arm circumference (P < 0.05). In the bench press and leg press endurance, all training groups increased significantly from corresponding pre training and control group (except bench press endurance for PI group) (P < 0.05). There were no significant differences among groups at pre and post training for the all variables (P > 0.05). Fig 1. Differences in weight, percent body fat, arm and thigh circumference, one repetition maximum (1RM) at leg and bench press, and leg and bench press endurance (mean ± SD). * Significant difference from corresponding pre-training † Significant difference from corresponding CG PI; part I, PII; part II, PIII; part III, CG; control group 4. Discussion SSci email for subscription: publishing@WAU.org.uk Hamid Arazi, et al: Effects of 8 Weeks Equal-Volume Resistance Training with Different Workout Frequency 116 The purpose of the present study was to compare the effect of three equal-volume resistance training programs on physiological abilities in novice subjects. We hypothesized that, resistance training for 3 days are better than 1 or 2 days. The main finding of the present study was that, there were no significant differences among groups on 1RM bench and leg press, and leg and bench press endurance. Also, the PIII and PII groups showed significant improvements than pre training on arm circumference, and PIII and PI groups indicated significant increases from corresponding pre values on thigh circumference. Upper and lower body strength increased significantly in all groups after a 8-week resistance training. In the contrast of our study, Berger (18) compared of one, two, and three sessions per week training the bench press or squat concluded that three sessions were superior to one or two sessions in bringing about strength increases. Another comparison of training frequency for the bench press also concluded that three sessions were superior to one or two sessions (19). The findings of the percent study are in line with Graves et al. (20) who reported that one session was equally as effective as two or three sessions per week when training for isolated lumbar extension strength. DeMichele et al. (21) found that two sessions per week was equivalent to three and superior to one session per week when training for torso rotation. These studies indicate that three sessions per week are superior to one or two sessions per week when training arm and leg musculature, whereas when training spine muscles, one or two sessions per week result in equivalent gains compared to three sessions per week. The training frequency of three sessions per week when training the arms and legs results in a 20 to 30% greater strength gain than a frequency of two sessions per week (22). Rhea et al. (23) determined the dose-response for strength development, reporting that untrained individuals see a consistent response as the training frequency increases up to 3 days/week. Strength coach and athletes believe that split routines allow individuals to train at a maximal effort level for given intensity, producing higher muscle strain on a specific session. These routines would facilitate recovery due to the alternation in the muscle group trained. But, it appears that split training routine were not more effective than whole body training routines used by other, irrespectively of the training status (24,25). Only the PIII training group significantly increased in the arm and thigh circumference, whereas the PI and PII training groups increased either arm circumference or thigh circumference. All of the subjects improved their body weight and percent body fat (except CG). Increases in thigh CSA were only observed for the total body groups in the kraemer's et al study (13). Hakkkinen et al. (11) reported greater increases in muscle CSA when training volume was divided into two sessions per day rather than one. Huffman et al. (26) examined the effects of 10 weeks varying self-selected training frequencies among collegiate football players using different body-part training programs, and reported significant changes in the chest and thigh circumference, and sum of skinfold following four or five session-per-week training. Previous study reported increases in lean tissue mass after 10 weeks of training (27). Changes in muscle mass and CSA can be increases in; myofilaments, actin and myosin filaments, sarcoplasm, and connective tissue (28). A comparison of total body training routine and split system routine in young women who were previously not weight trained demonstrated no significant differences between groups in fat-free mass, or percent body fat changes (29). The results indicated that total-body and split-routine systems using the same total training volume produce similar results in healthy young women (29). Additionally, Carroll et al. (30) reported that when resistance training was equated for both time and number of sessions, 2 days/week resulted in a significant increase in the proportion of myosin heavy chain IIa compared with 3 days/week. The rest period between sessions must be sufficient to allow for muscular recuperation and development while alleviating the potential for overtraining (31). Split routine can allow performance of more assistance exercises and so many also be useful for enhancing physiological development. All experimental groups improved significantly rather than pre training and control group in leg and bench press endurance (except bench press endurance for the PI group). Kraemer et al. (12) compared the effects of total-body and upper-body resistance training on endurance performance, and reported similar improvements in the squat endurance, push-ups, and sit-ups. A split routine system allows the training intensity for a particular body part or group of exercises to be higher than would be possible if the four to six sessions were combined into two or three long sessions of equivalent training volume. It is also possible to develop split routines in which the total training volume per body part is higher than that in a typical total body training session because in a split routine each training session is dedicated to a smaller number of body parts or muscle groups (5). In the present study, we not found any significant changes among groups, but part III showed minimal improvement rather than other groups. We think that, the lack of change in the anthropometric profiles suggests that neural factors may have been more important to the observed increases in strength and endurance than morphological adaptations. Moritani and DeVries (32) described that neural SSci email for contribution: editor@SSCI.org.uk International Journal of Sports Science and Engineering, 5 (2011) 2, pp 112-118 117 adaptations would occur during the first weeks of training, it has been suggested that strength increments due to neural adaptations should also occur in highly trained athletes (33). Collectively, we recommend that, novice individuals had better use the split routine training for improving performance and promoting muscular adaptations. 5. Acknowledgments The authors wish to thanks all the subjects for their participation and commitment to the study. 6. 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E-mail: kraemer@uconnvm.uconn.edu Current Sports Medicine Reports 2002, 1:165–171 Current Science Inc. ISSN 1537-890x Copyright © 2002 by Current Science Inc. Introduction Traditionally, strength athletes seeking to improve muscle strength, hypertrophy, power, and sports-specific fitness almost exclusively performed resistance training. Although it has been shown to have profound effects on these physical fitness components, only recently have the health- related benefits of resistance training been elucidated. It is now a popular form of exercise that is recommended by national health organizations such as the American College of Sports Medicine (ACSM), American Heart Association, and the American Association for Cardiovas- cular and Pulmonary Rehabilitation, in conjunction with other modalities of exercise (ie, aerobic, flexibility), for the maintenance and improvement of health and performance [1••,2]. Particularly when incorporated into a comprehen- sive fitness program, resistance training reduces several risk factors associated with many diseases and physical ailments, and improves the quality of life by preserving and improving functional capacity [2]. In addition, it can improve athletic performance by increasing muscular strength, power, speed, size, endurance, balance, and coordination [3••]. The vast body of literature examining resistance training supports its inclusion into the daily exercise regimens of the adolescent, adult, and elderly populations. However, it is important that each individual participating in a resistance training program has adequate understanding of fundamental principles and techniques, and in certain cases be supervised by qualified profession- als (eg, inexperienced trainees, children) for the prevention of injury and for maximizing the associated benefits [4•]. Important Qualities of Resistance Training Programs In order to maximize the benefits of resistance training, adherence to three basic principles is mandatory. These principles are 1) progressive overload, 2) specificity, and 3) variation. Progressive overload is the gradual increase of stress placed on the body during resistance training. In reality, resistance training is only effective for improving health and performance if the human body is continually required to exert a greater magnitude of force to meet higher physiologic demands. Thus, a gradual increase in demand of the resistance training program is necessary for long-term improvement in muscular fitness and health. Specificity refers to the body’s responses and subsequent adaptations to certain program variables. The physiologic adaptations to resistance training are specific to the muscle actions involved [5], velocity of movement [6], exercise range of motion [7], muscle groups trained [2], energy systems involved [2], and the intensity and volume of training [8]. The most effective resistance training programs are designed individually to bring about specific adaptations. Variation is the systematic alteration of the resistance training program over time to allow for the training stimulus to remain optimal. It has been shown that systematic program variation is most effective for long-term progression [9]. How much resistance training can improve health and performance depends on the individual’s genetic makeup, program design and implementation, and training status or level of fitness. The rate of performance enhancement differs considerably between previously untrained and Resistance training is recommended by national health organizations for incorporation into a comprehensive fitness program that includes aerobic and flexibility exercise. Its potential benefits on health and performance are numerous; it has been shown to reduce body fat, increase basal metabolic rate, decrease blood pressure and the cardiovascular demands to exercise, improve blood lipid profiles, glucose tolerance, and insulin sensitivity, increase muscle and connective tissue cross-sectional area, improve functional capacity, and relieve low back pain. Many improvements in physical function and athletic performance are associated with the increases in muscle strength, power, endurance, and hypertrophy observed during resistance training. The key element to effective resistance training is supervision by a qualified professional and the proper prescription of the program variables. Proper program design, ie, that which uses progressive overload, variation, and specificity, is essential to maximize the benefits associated with resistance training. 166 Training trained individuals, as trained individuals have shown much slower rates of improvement [10]. These data demonstrate the difficulty in improving with greater levels of fitness, and stress the importance of a proper resistance training program design in order to progress further. It is important to note that progression is not always the major goal. Once a certain level of fitness is attained, many individuals tailor their programs to maintain that level. In either scenario, training programs are designed accordingly through proper manipulation of program variables. The key quality to an individualized resistance training program is the acute manipulation of program variables targeting certain areas of muscular fitness. The program variables are 1) intensity (or loading), 2) volume (the number of sets and repetitions), 3) exercises selected, 4) the order of the exercises, 5) rest intervals between sets, 6) velocity of contraction, and 7) frequency. Altering one or more of these variables significantly affects the acute responses and subsequent physiologic adaptations to resistance training. Recently, the ACSM published a position stand on recommended progression models during resistance training [1••]. This document provides recommendations for novice, intermediate, and advanced levels of training for specific improvements in muscular strength, power, hypertrophy, endurance, and motor performance. Although it is beyond the scope of this article, we encourage readers to refer to this document [1••] for more information. Resistance Training and Health Improvements The potential health benefits associated with resistance train- ing have significant impact on the quality of life and func- tional capacity of individuals of all ages. The safe and proper prescription of resistance exercise has been shown to reduce body fat and increase basal metabolic rate, decrease blood pressure and cardiovascular demands to activity, improve blood lipid profiles, improve glucose tolerance and insulin sensitivity, attenuate muscle sarcopenia, reduce the risk of osteoporosis and colon cancer, and maintain long-term independence and functional capacity [2,11,12,13••]. These benefits, as well as the performance-related benefits, have been shown to improve the quality of life in the elderly and clinical populations, such as those with low back pain, osteoarthritis, cardiovascular disease, HIV, neuromuscular disease (eg, myasthenia gravis, myotonic dystrophy), obesity, renal failure, chronic obstructive pulmonary disease, and type 2 diabetes mellitus, and those recovering from a stroke, [13••,14–18]. Although research has clearly demonstrated the value of resistance training for improving muscular performance, the influence of resistance exercise on health and physical well-being continues to be elucidated. Resistance training and function in the elderly Advancing age, particularly in sedentary individuals, is associated with a number of changes detrimental to health and performance. Sarcopenia, or the loss of skeletal muscle with advancing age, results in a lower basal metabolic rate, weakness, reduced activity levels, decreased bone mineral density, and increased risk of falls or injury [11,18]. This reduction in skeletal muscle mass can result in frailty and physical disability, which contribute to escalating health care costs. Resistance training is considered a promising intervention for reversing the loss of muscle function and deterioration of muscle structure that is associated with sarcopenia. Increasing evidence now indicates that elderly subjects respond favorably to weight training in a qualitatively similar manner as younger individuals. For example, in a study of physically frail 76- to 92-year-old men and women, Yarasheski et al. [19] reported that muscle protein synthesis was significantly greater follow- ing 3 months of supervised weight training. Other studies have shown that resistance training significantly increases the mass and quality of skeletal muscle [18]. These findings indicate that elderly individuals can respond favorably to the increased contractile activity associated with progressive resistance training. Cross-sectional and longitudinal data indicate that muscle strength declines by approximately 15% per decade in the sixth and seventh decades of life, and by about 30% thereafter [2], leading to reductions in the ability to perform daily functions. Therefore, a resistance training intervention may be warranted to minimize these reductions in strength and performance in the elderly. A number of studies have demonstrated substantial increases in muscle strength in the elderly following resistance training [20,21]. For example, Charette et al. [20] reported increases in strength of 28% to 115% following 12 weeks of lower body resistance training in elderly women (mean age = 70 years). Pertinent to daily function in the elderly, other studies have shown significant improvements in local muscular endurance, balance, coordination, and functional ability (eg, ability to carry groceries, walk, and climb stairs, reduced risk of falls, and so forth) [22]. These studies indicate that resistance training can be performed safely by the elderly, and that such exercise significantly increases muscle strength and performance, due in part to the mechanisms associated with muscle hypertrophy. Such mechanisms serve to reverse the characteristic loss in lean body mass that is associated with sarcopenia. Body composition and weight loss Obesity is a chronic metabolic disorder that is associated with cardiovascular disease and increased morbidity and mortality. Multiple epidemiologic studies now show an association between body mass index and body fat with coronary heart disease, type 2 diabetes and insulin resis- tance, stroke, hypertension, and colon cancer [23]. The mortality rate increases by 50% to 100% when body mass index is equal to or greater than 30 kg/m2. Central obesity appears to serve as a platform for a cascade of events that can result in a variety of clinical health problems. Proper Resistance Training for Health and Performance • Kraemer et al. 167 diet and aerobic exercise are important to weight loss and body fat reductions. In addition, resistance training is beneficial to body fat reduction and increase in lean body mass. A review of the literature has shown that body fat reductions of 1% to 9% are possible following resistance training programs of various durations [24]. Increases in lean tissue mass and daily metabolic rates, in addition to greater energy expenditure while exercising, are observed during resistance training, which in turn may result in body fat reductions [3••]. For example, Van Etten et al. [25] reported a 9.5% increase in average daily metabolic rate after 18 weeks of resistance training. High-volume work- outs with short rest periods using a large muscle mass appear most conducive to body fat reductions [3••]. Weight loss, and the associated dieresis, aid in reducing blood pressure in both overweight hypertensive and nonhypertensive individuals, reducing serum triglyceride concentrations, increasing high-density lipoprotein (HDL) cholesterol concentrations, and producing reductions in low-density lipoprotein (LDL) cholesterol concentrations. Blood pressure Hypertension, defined as resting systolic or diastolic blood pressure greater than or equal to 140/90 mm Hg, is a major public health problem affecting approximately 24% of noninstitutionalized adults in the United States [26]. Increasing scientific evidence now indicates that progres- sive resistance training is an effective nonpharmacologic intervention that
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