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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
        <publisher-loc>S&#227;o Paulo, SP, Brazil</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">9yBfqgqLRjnVsk53FhhyGJx</article-id>
      <article-id pub-id-type="other">00008</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2007001600008</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(07)08900408</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2007001600008</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigo de Revis&#227;o</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Efeitos hemodin&#226;micos e vasculares do treinamento resistido: implica&#231;&#245;es na doen&#231;a cardiovascular</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Umpierre</surname>
            <given-names>Daniel</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Stein</surname>
            <given-names>Ricardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Porto Alegre</named-content>
          <named-content content-type="state">Rio Grande do Sul</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade Federal do Rio Grande do Sul</institution>
        <institution content-type="orgdiv1">Hospital de Cl&#237;nicas de Porto Alegre </institution>
        <institution content-type="orgdiv2">Laborat&#243;rio de Fisiopatologia do Exerc&#237;cio</institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>10</month>
        <year>2007</year>
      </pub-date>
      <volume>89</volume>
      <issue>4</issue>
      <fpage>256</fpage>
      <lpage>262</lpage>
      <history>
        <date date-type="rev-recd">
          <day>10</day>
          <month>05</month>
          <year>2007</year>
        </date>
        <date date-type="received">
          <day>24</day>
          <month>03</month>
          <year>2007</year>
        </date>
        <date date-type="accepted">
          <day>10</day>
          <month>05</month>
          <year>2007</year>
        </date>
      </history>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>O treinamento resistido tem sido proposto como poss&#237;vel estrat&#233;gia para preven&#231;&#227;o e reabilita&#231;&#227;o cardiovascular, e nesse contexto esta revis&#227;o descreve os efeitos cardiovasculares mediados por esse tipo de interven&#231;&#227;o. O incremento tanto na for&#231;a muscular quanto na capacidade para realiza&#231;&#227;o de tarefas do dia-a-dia s&#227;o benef&#237;cios bem caracterizados ante esse tipo de treinamento. Mais recentemente, estudos que utilizaram a avalia&#231;&#227;o hemodin&#226;mica verificaram estabilidade cardiovascular em pacientes com doen&#231;a coronariana ou insufici&#234;ncia card&#237;aca durante a realiza&#231;&#227;o de exerc&#237;cio resistido, sem aparentes preju&#237;zos na fun&#231;&#227;o ventricular ou aumento exacerbado na press&#227;o arterial ao exerc&#237;cio. Adicionalmente, a press&#227;o arterial em repouso tamb&#233;m parece ser influenciada pelo treinamento resistido cr&#244;nico, apresentando leve redu&#231;&#227;o tanto para a press&#227;o arterial sist&#243;lica (PAS) quanto para a press&#227;o arterial diast&#243;lica (PAD). A mensura&#231;&#227;o dos n&#237;veis press&#243;ricos ap&#243;s uma &#250;nica sess&#227;o de exerc&#237;cio resistido demonstra ocorr&#234;ncia da hipotens&#227;o p&#243;s-exerc&#237;cio em indiv&#237;duos normais e hipertensos; contudo, h&#225; controv&#233;rsias quanto &#224; intensidade de esfor&#231;o necess&#225;ria para indu&#231;&#227;o desse efeito. Recentemente, estudos de interven&#231;&#227;o t&#234;m investigado o exerc&#237;cio resistido sob o prisma vascular, avaliando a complac&#234;ncia arterial, assim como a fun&#231;&#227;o endotelial. Apesar dos poucos experimentos dispon&#237;veis, evid&#234;ncias t&#234;m demonstrado uma potencial influ&#234;ncia do treinamento resistido sobre a redu&#231;&#227;o da complac&#234;ncia arterial. Por sua vez, o fluxo sang&#252;&#237;neo perif&#233;rico apresenta-se aumentado ap&#243;s o treinamento resistido, ao passo que a fun&#231;&#227;o endotelial parece melhorada especialmente ap&#243;s o treinamento combinado. Pesquisas adicionais s&#227;o necess&#225;rias para an&#225;lise da efic&#225;cia dessa interven&#231;&#227;o sobre desfechos validados, e para aprofundamento de mecanismos fisiol&#243;gicos respons&#225;veis pelas adapta&#231;&#245;es vasculares.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Exerc&#237;cio</kwd>
        <kwd>aptid&#227;o f&#237;sica</kwd>
        <kwd>avalia&#231;&#227;o hemodin&#226;mica</kwd>
        <kwd>doen&#231;as cardiovasculares</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>18</day>
        <month>04</month>
        <year>2008</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>ARTIGO DE REVIS&#195;O</bold>
    </p>
    <p>Efeitos hemodin&#226;micos e vasculares do treinamento resistido: implica&#231;&#245;es na doen&#231;a cardiovascular</p>
    <p>
      <bold>Daniel Umpierre; Ricardo Stein</bold>
    </p>
    <p> Laborat&#243;rio de Fisiopatologia do Exerc&#237;cio, Hospital de Cl&#237;nicas de Porto Alegre - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p>O treinamento resistido tem sido proposto como poss&#237;vel estrat&#233;gia para preven&#231;&#227;o e reabilita&#231;&#227;o cardiovascular, e nesse contexto esta revis&#227;o descreve os efeitos cardiovasculares mediados por esse tipo de interven&#231;&#227;o. O incremento tanto na for&#231;a muscular quanto na capacidade para realiza&#231;&#227;o de tarefas do dia-a-dia s&#227;o benef&#237;cios bem caracterizados ante esse tipo de treinamento. Mais recentemente, estudos que utilizaram a avalia&#231;&#227;o hemodin&#226;mica verificaram estabilidade cardiovascular em pacientes com doen&#231;a coronariana ou insufici&#234;ncia card&#237;aca durante a realiza&#231;&#227;o de exerc&#237;cio resistido, sem aparentes preju&#237;zos na fun&#231;&#227;o ventricular ou aumento exacerbado na press&#227;o arterial ao exerc&#237;cio. Adicionalmente, a press&#227;o arterial em repouso tamb&#233;m parece ser influenciada pelo treinamento resistido cr&#244;nico, apresentando leve redu&#231;&#227;o tanto para a press&#227;o arterial sist&#243;lica (PAS) quanto para a press&#227;o arterial diast&#243;lica (PAD). A mensura&#231;&#227;o dos n&#237;veis press&#243;ricos ap&#243;s uma &#250;nica sess&#227;o de exerc&#237;cio resistido demonstra ocorr&#234;ncia da hipotens&#227;o p&#243;s-exerc&#237;cio em indiv&#237;duos normais e hipertensos; contudo, h&#225; controv&#233;rsias quanto &#224; intensidade de esfor&#231;o necess&#225;ria para indu&#231;&#227;o desse efeito. Recentemente, estudos de interven&#231;&#227;o t&#234;m investigado o exerc&#237;cio resistido sob o prisma vascular, avaliando a complac&#234;ncia arterial, assim como a fun&#231;&#227;o endotelial. Apesar dos poucos experimentos dispon&#237;veis, evid&#234;ncias t&#234;m demonstrado uma potencial influ&#234;ncia do treinamento resistido sobre a redu&#231;&#227;o da complac&#234;ncia arterial. Por sua vez, o fluxo sang&#252;&#237;neo perif&#233;rico apresenta-se aumentado ap&#243;s o treinamento resistido, ao passo que a fun&#231;&#227;o endotelial parece melhorada especialmente ap&#243;s o treinamento combinado. Pesquisas adicionais s&#227;o necess&#225;rias para an&#225;lise da efic&#225;cia dessa interven&#231;&#227;o sobre desfechos validados, e para aprofundamento de mecanismos fisiol&#243;gicos respons&#225;veis pelas adapta&#231;&#245;es vasculares.</p>
    <p><bold>Palavras-chave:</bold> Exerc&#237;cio/psicologia, aptid&#227;o f&#237;sica/psicologia; avalia&#231;&#227;o hemodin&#226;mica, doen&#231;as cardiovasculares.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>Desde meados da d&#233;cada de 1960, as respostas cardiovasculares ao exerc&#237;cio predominantemente de for&#231;a t&#234;m sido discutidas<bold><sup>1,2</sup></bold>. At&#233; o in&#237;cio dos anos 1990, o treinamento resistido (tamb&#233;m chamado de "treinamento de for&#231;a, com pesos, contra-resist&#234;ncia" ou "muscula&#231;&#227;o") n&#227;o era contemplado em diretrizes internacionais. No entanto, nos &#250;ltimos anos, essa modalidade passou a ser considerada como uma poss&#237;vel estrat&#233;gia para preven&#231;&#227;o prim&#225;ria e secund&#225;ria de diferentes cardiopatias<bold><sup>3,4</sup></bold>. Al&#233;m disso, diversas pesquisas t&#234;m sugerido que o exerc&#237;cio resistido, quando prescrito e supervisionado de forma apropriada, apresenta efeitos favor&#225;veis em diferentes aspectos da sa&#250;de (for&#231;a muscular, capacidade funcional, bem-estar psicossocial, al&#233;m de impacto positivo sobre fatores de risco cardiovasculares)<bold><sup>5</sup></bold>.</p>
    <p>Foi principalmente a partir de adapta&#231;&#245;es neuromusculares e em efeitos como aumento de for&#231;a e resist&#234;ncia muscular que foi baseado o racional que d&#225; suporte &#224; aplica&#231;&#227;o do treinamento resistido em programas de exerc&#237;cios para pacientes cardiopatas<bold><sup>4,6</sup></bold>. Dentre as diversas adapta&#231;&#245;es promovidas por esse tipo de treinamento podem-se citar o aumento na capacidade de realizar atividades de vida di&#225;ria<bold><sup>7</sup></bold>, o incremento na toler&#226;ncia ao exerc&#237;cio aer&#243;bico subm&#225;ximo<bold><sup>8,9</sup></bold>, a supress&#227;o da queda de for&#231;a relacionada &#224; idade<bold><sup>10</sup></bold> e a atenua&#231;&#227;o das respostas cardiovasculares ao esfor&#231;o<bold><sup>11</sup></bold>. Mesmo que ainda exista car&#234;ncia de grandes ensaios cl&#237;nicos que tenham avaliado a efic&#225;cia desse tipo de treinamento aplicado de forma exclusiva sobre desfechos cl&#237;nicos validados, dados observacionais indicam diminui&#231;&#227;o no risco coronariano em praticantes do exerc&#237;cio de for&#231;a. </p>
    <p>Na coorte do <italic>Health Professionals Follow-up Study<sup>12</sup></italic>, a pr&#225;tica semanal de 30 minutos ou mais de treinamento resistido esteve associado &#224; diminui&#231;&#227;o de 23% no risco para ocorr&#234;ncia de infarto agudo do mioc&#225;rdio n&#227;o-fatal e/ou doen&#231;a cardiovascular fatal (RR 0,77; IC 95%, 0,61-0,98; p=0,03). An&#225;lise multivariada ajustada para fatores como idade, consumo de &#225;lcool, tabaco, hist&#243;rico familiar, perfil alimentar e pr&#225;tica de outras atividades f&#237;sicas foi utilizada para diminuir a chance de erro sistem&#225;tico.</p>
    <p>Nos dias de hoje, emergem evid&#234;ncias adicionais acerca do exerc&#237;cio resistido na sa&#250;de e na doen&#231;a cardiovascular (DCV), as quais possibilitam maior entendimento de efeitos j&#225; conhecidos, ao mesmo tempo que refor&#231;am as perspectivas de utiliza&#231;&#227;o do treinamento resistido na preven&#231;&#227;o secund&#225;ria. Nesse contexto, discute-se nesta revis&#227;o a influ&#234;ncia desse tipo de exerc&#237;cio sobre aspectos importantes na DCV ou no seu desenvolvimento, abordando evid&#234;ncias recentes e/ou ainda pouco exploradas em outras revis&#245;es.</p>
    <p>
      <bold>Estabilidade hemodin&#226;mica durante o exerc&#237;cio resistido</bold>
    </p>
    <p>Conforme a intensidade do esfor&#231;o realizado, as respostas hemodin&#226;micas durante o exerc&#237;cio resistido podem se assemelhar &#224;quelas ocorridas em contra&#231;&#245;es din&#226;micas ou isom&#233;tricas (est&#225;ticas). Portanto, em esfor&#231;os realizados com cargas leves verificam-se aumento da freq&#252;&#234;ncia card&#237;aca (FC), press&#227;o arterial sist&#243;lica (PAS), volume sist&#243;lico e d&#233;bito card&#237;aco (DC), ao passo que, quando da utiliza&#231;&#227;o de cargas altas, observa-se tamb&#233;m aumento na press&#227;o arterial diast&#243;lica (PAD)<bold><sup>13</sup></bold>. Durante o exerc&#237;cio resistido, maiores valores de FC e PA s&#227;o obtidos nas &#250;ltimas repeti&#231;&#245;es de s&#233;ries realizadas at&#233; a fadiga<bold><sup>14</sup></bold>, as quais t&#234;m sido contra-indicadas como prescri&#231;&#227;o no trabalho de for&#231;a com hipertensos. Al&#233;m disso, dentre outros fatores que influenciam o comportamento press&#243;rico, observam-se respostas aumentadas quanto maior for a massa muscular envolvida no exerc&#237;cio<bold><sup>15</sup></bold>. Em fisiculturistas, MacDougall e cols. observaram aumentos press&#243;ricos extremos (&#187;320/250 mmHg), quando esses indiv&#237;duos foram expostos a cargas entre 80% e 100%<bold><sup>16</sup></bold>. Por sua vez, o n&#237;vel de condicionamento f&#237;sico em for&#231;a parece apresentar rela&#231;&#227;o inversa com as magnitudes das respostas de PA e FC ao exerc&#237;cio<bold><sup>14</sup></bold>. </p>
    <p>Em cardiopatas com disfun&#231;&#227;o ventricular esquerda, durante a realiza&#231;&#227;o de testes de for&#231;a e s&#233;ries em diferentes intensidades, verificou-se aumento de novas anormalidades segmentares da parede do ventr&#237;culo esquerdo, as quais ocorreram em maior propor&#231;&#227;o durante a s&#233;rie final ap&#243;s protocolo de intensidades crescentes (tr&#234;s s&#233;ries com cargas progressivas)<bold><sup>17</sup></bold>. Entretanto, as magnitudes desses achados foram pequenas e, mesmo que possam refletir algum grau de isquemia durante o esfor&#231;o, elas n&#227;o sugerem redu&#231;&#227;o do desempenho card&#237;aco. Ainda, em 6.653 indiv&#237;duos sem DCV que realizaram testes de for&#231;a &#150; em dinam&#244;metro isocin&#233;tico e por meio do teste com execu&#231;&#227;o de 1-repeti&#231;&#227;o m&#225;xima em exerc&#237;cios como supino e <italic>leg press</italic> &#150; n&#227;o ocorreram eventos cardiovasculares fatais ou n&#227;o-fatais<bold><sup>18</sup></bold>.</p>
    <p>Mais recentemente, estudos com variadas t&#233;cnicas de avalia&#231;&#227;o aprofundaram o conhecimento da fun&#231;&#227;o cardiovascular durante o exerc&#237;cio resistido. Meyer e cols.<bold><sup>19</sup></bold> avaliaram por cateterismo direito dois grupos de pacientes: a) IC com disfun&#231;&#227;o ventricular, e b) doen&#231;a arterial coronariana est&#225;vel com fun&#231;&#227;o ventricular preservada. Os autores encontraram aumento no &#237;ndice card&#237;aco e no volume sist&#243;lico durante a execu&#231;&#227;o de <italic>leg press</italic> em diferentes intensidades de esfor&#231;o. Na intensidade de 60% da contra&#231;&#227;o volunt&#225;ria m&#225;xima, o &#237;ndice de trabalho sist&#243;lico se manteve est&#225;vel, indicando mudan&#231;as semelhantes na press&#227;o arterial m&#233;dia (PAM) e na press&#227;o diast&#243;lica da art&#233;ria pulmonar, o que sugere balan&#231;o entre pr&#233; e p&#243;s-carga. </p>
    <p>Um aspecto interessante desse estudo denota que, durante o exerc&#237;cio com intensidade de 60% da carga m&#225;xima, a varia&#231;&#227;o no comportamento press&#243;rico (mensurado de forma invasiva) foi de pequena magnitude (<xref ref-type="fig" rid="fig01">fig. 1</xref>). Resultados similares ocorreram em outro estudo que arrolou pacientes com insufici&#234;ncia card&#237;aca (IC) grave, os quais n&#227;o apresentaram instabilidade hemodin&#226;mica durante exerc&#237;cio resistido de membros superiores e inferiores. Nesses indiv&#237;duos com IC classe III e IV (FE: 25&#177;2%, VO<sub>2pico</sub>: 12,4&#177;0,7ml.kg<sup>-1</sup>.min<sup>-1</sup>) ocorreu discreta diminui&#231;&#227;o do volume sist&#243;lico em exerc&#237;cio de membros inferiores, e manuten&#231;&#227;o no exerc&#237;cio com membros superiores (em rela&#231;&#227;o aos valores de repouso), enquanto o valor do DC esteve mantido em ambos os movimentos. </p>
    <fig id="fig01">
      <graphic xlink:href="1678-4170-abc-89-04-0256-00008-gf01.jpg"/></fig>
    <p>Os mecanismos que propiciam a manuten&#231;&#227;o da fun&#231;&#227;o ventricular nos indiv&#237;duos saud&#225;veis, cardiopatas isqu&#234;micos, e tamb&#233;m em pacientes em diferentes classes de IC ainda n&#227;o est&#227;o completamente elucidados. A despeito dessa inc&#243;gnita, cabe salientar que, embora alguns estudos tenham demonstrado aumento no inotropismo, parece ser a resposta cronotr&#243;pica a principal respons&#225;vel pela manuten&#231;&#227;o do DC<bold><sup>19-21</sup></bold>. </p>
    <p>O comportamento t&#237;pico de aumento da resist&#234;ncia vascular sist&#234;mica promovido pela contra&#231;&#227;o isom&#233;trica pura<bold><sup>22</sup></bold>, muitas vezes, n&#227;o &#233; desejado para indiv&#237;duos cardiopatas. Entretanto, ao contr&#225;rio do que ocorre na contra&#231;&#227;o isom&#233;trica, a resist&#234;ncia vascular dos cardiopatas parece n&#227;o se elevar durante a realiza&#231;&#227;o das s&#233;ries de exerc&#237;cio resistido (<xref ref-type="fig" rid="fig02">fig. 2</xref>)<bold><sup>19-21,23</sup></bold>. Esse efeito &#233; possivelmente proporcionado pelo componente din&#226;mico, o qual tamb&#233;m est&#225; presente nas contra&#231;&#245;es desse tipo de exerc&#237;cio. </p>
    <fig id="fig02">
      <graphic xlink:href="1678-4170-abc-89-04-0256-00008-gf02.jpg"/></fig>
    <p>
      <bold>Exerc&#237;cio resistido e press&#227;o arterial</bold>
    </p>
    <p>O exerc&#237;cio f&#237;sico regular auxilia no controle da press&#227;o arterial (PA) em curto e longo prazos e, em vista disso, &#233; indicado como interven&#231;&#227;o adjunta no manejo da hipertens&#227;o arterial<bold><sup>24</sup></bold>. Para uma discuss&#227;o mais ampla sobre os efeitos do exerc&#237;cio na PA, &#233; v&#225;lido ressaltar que essa pode ser influenciada n&#227;o s&#243; pelas adapta&#231;&#245;es decorrentes do treinamento f&#237;sico cr&#244;nico (adapta&#231;&#245;es cr&#244;nicas), mas tamb&#233;m pela influ&#234;ncia de uma &#250;nica sess&#227;o de exerc&#237;cio (efeitos sub-agudos ou p&#243;s-exerc&#237;cio).</p>
    <p>
      <bold>Treinamento resistido: efeitos cr&#244;nicos </bold>
    </p>
    <p>Evid&#234;ncias mais recentes v&#227;o de encontro ao antigo dogma de que o treinamento resistido poderia elevar a PA de repouso. Esse racioc&#237;nio foi originado a partir da id&#233;ia de que os maiores aumentos press&#243;ricos associados ao exerc&#237;cio resistido (por seu maior componente isom&#233;trico) acarretariam a eleva&#231;&#227;o cr&#244;nica da PA. </p>
    <p>Duas metan&#225;lises robustas demonstraram efeitos ben&#233;ficos do treinamento resistido sobre a PAS e PAD de repouso. Ambas analisaram estudos com as seguintes caracter&#237;sticas: 1) ensaios randomizados com grupo-controle sem exerc&#237;cio; 2) treinamento resistido como &#250;nica interven&#231;&#227;o; 3) sujeitos normotensos ou hipertensos previamente sedent&#225;rios; e 4) dura&#231;&#227;o m&#237;nima de quatro semanas. Kelley e Kelley<bold><sup>25</sup></bold> examinaram 11 estudos, com um total de 320 sujeitos (182 em exerc&#237;cio, e 138 controles), encontrando redu&#231;&#227;o da PAS (-3&#177;3 mmHg; Intervalo de confian&#231;a 95%: -4 a -1 mmHg) e PAD (-3&#177;2 mmHg; Intervalo de confian&#231;a 95%: -4 a -1 mmHg), o que representou queda aproximada de 2% e 4%, respectivamente. </p>
    <p>Posteriormente, a metan&#225;lise publicada por Cornelissen e Fagard<bold><sup>26</sup></bold>, composta por 12 estudos e 341 participantes, tamb&#233;m foi nessa dire&#231;&#227;o, evidenciando redu&#231;&#227;o dos valores de PAS (-3,2 mmHg; p=0,10) e PAD (-3,5 mmHg; p&lt;0,01) para os indiv&#237;duos que foram expostos ao treinamento resistido. Quando an&#225;lises de subgrupos foram efetuadas tamb&#233;m n&#227;o se observaram diferen&#231;as relacionadas &#224;s intensidades de exerc&#237;cio, bem como quanto &#224; utiliza&#231;&#227;o do treinamento resistido convencional ou em circuito. No treinamento convencional executam-se todas as s&#233;ries de determinado movimento antes de iniciar o exerc&#237;cio seguinte e, normalmente, t&#234;m-se maiores cargas e tempo de intervalo do que no treinamento em circuito. </p>
    <p>Por sua vez, nesse outro modo de treino a atividade &#233; mais cont&#237;nua e com menores tempos de intervalo, visto que a execu&#231;&#227;o &#233; de uma &#250;nica s&#233;rie em cada esta&#231;&#227;o, passando ao pr&#243;ximo exerc&#237;cio imediatamente, e repetindo o circuito mais vezes se necess&#225;rio. Ainda que o treinamento resistido, de forma semelhante ao treinamento aer&#243;bico<bold><sup>27</sup></bold>, proporcione apenas redu&#231;&#245;es discretas nos valores de PA, em termos populacionais isso pode ter impacto em uma menor incid&#234;ncia de doen&#231;a coronariana e acidente vascular cerebral<bold><sup>28</sup></bold>.</p>
    <p>
      <bold>Hipotens&#227;o ap&#243;s o exerc&#237;cio resistido </bold>
    </p>
    <p>O exerc&#237;cio f&#237;sico pode promover a queda sustentada dos n&#237;veis press&#243;ricos no p&#243;s-esfor&#231;o. Esse efeito cl&#225;ssico &#233; denominado hipotens&#227;o p&#243;s-exerc&#237;cio (HPE), o qual est&#225; bem demonstrado em rela&#231;&#227;o ao exerc&#237;cio aer&#243;bico<bold><sup>29</sup></bold>, e tem sido estudado tamb&#233;m diante do exerc&#237;cio de for&#231;a, tanto na avalia&#231;&#227;o ambulatorial de 24 horas, pela monitoriza&#231;&#227;o ambulatorial da press&#227;o arterial (MAPA), quanto em avalia&#231;&#245;es durante o per&#237;odo de recupera&#231;&#227;o (at&#233; aproximadamente 90 minutos ap&#243;s o exerc&#237;cio). Bermudes e cols.<bold><sup>30</sup></bold> n&#227;o verificaram diferen&#231;as na PAS e na PAD de 24 horas ap&#243;s uma sess&#227;o controle sem exerc&#237;cio e ap&#243;s uma sess&#227;o de exerc&#237;cios resistidos em circuito. No entanto, durante o per&#237;odo de sono, houve queda significativa da PA ap&#243;s a sess&#227;o de exerc&#237;cio resistido em compara&#231;&#227;o &#224; condi&#231;&#227;o controle. Da mesma forma, em indiv&#237;duos jovens e com diferentes tipos de condicionamento &#150; sedent&#225;rios, treinados em for&#231;a, e treinados em resist&#234;ncia &#150;, PAS, PAD e PAM tamb&#233;m n&#227;o estiveram diferentes ap&#243;s uma sess&#227;o de exerc&#237;cio ou sess&#227;o controle<bold><sup>31</sup></bold>. Muito recentemente, ao estudarem 20 mulheres hipertensas em uso de inibidor da enzima conversora de angiotensina (captopril), Melo e cols.<bold><sup>31</sup></bold> constataram redu&#231;&#227;o press&#243;rica importante (PAS:-12&#177;3 mmHg, PAD:-6&#177;2 mmHg) no per&#237;odo de recupera&#231;&#227;o at&#233; 120 minutos ap&#243;s uma sess&#227;o de exerc&#237;cio resistido de baixa intensidade. Adicionalmente, os valores observados pela MAPA permaneceram significativamente mais baixos at&#233; 10 horas ap&#243;s o exerc&#237;cio (durante o per&#237;odo de vig&#237;lia), o que n&#227;o ocorreu ap&#243;s a sess&#227;o controle<bold><sup>32</sup></bold>.</p>
    <p>Conforme ilustrado na <xref ref-type="fig" rid="fig03">figura 3</xref>, no exerc&#237;cio resistido a HPE &#233; mais marcada durante o per&#237;odo de recupera&#231;&#227;o (&#187;90 minutos ap&#243;s a sess&#227;o), e tende a voltar aos n&#237;veis basais nas horas subseq&#252;entes. Mesmo que esse efeito tenha sido constatado em indiv&#237;duos normotensos e hipertensos<bold><sup>31-34</sup></bold>, controv&#233;rsias ainda existem, especialmente aquelas relacionadas &#224; intensidade do exerc&#237;cio. Alguns autores documentaram redu&#231;&#227;o da PAS ap&#243;s sess&#245;es com utiliza&#231;&#227;o de cargas elevadas<bold><sup>35,36</sup>;</bold> por&#233;m, em outros estudos, protocolos com altas intensidades n&#227;o foram eficazes em promover quedas press&#243;ricas significativas<bold><sup>37-39</sup></bold>. </p>
    <fig id="fig03">
      <graphic xlink:href="1678-4170-abc-89-04-0256-00008-gf03.jpg"/></fig>
    <p>Recentemente, Rezk e cols. demonstraram que sess&#245;es a 40% e 80% da carga m&#225;xima foram seguidas de redu&#231;&#227;o da PAS no per&#237;odo de recupera&#231;&#227;o (-6&#177;1 mmHg e -8&#177;1 mmHg, p&lt;0,05, respectivamente), enquanto a PAD esteve reduzida somente ap&#243;s a sess&#227;o de menor intensidade (40% da carga m&#225;xima). De acordo com os autores, a hipotens&#227;o gerada por ambos os protocolos foi mediada pelo menor DC, sendo observadas apenas modestas eleva&#231;&#245;es, tanto na resist&#234;ncia vascular sist&#234;mica quanto na FC p&#243;s-esfor&#231;o<bold><sup>35</sup></bold>. A partir dos dados supracitados entende-se que o exerc&#237;cio resistido realizado de forma cr&#244;nica ou aguda n&#227;o parece oferecer riscos quanto ao aumento da PA, cabendo salientar ali&#225;s que tal interven&#231;&#227;o pode auxiliar no controle press&#243;rico a longo prazo.</p>
    <p>
      <bold>Influ&#234;ncia do treinamento resistido na complac&#234;ncia arterial: a evid&#234;ncia emergente</bold>
    </p>
    <p>A capacidade de distens&#227;o das art&#233;rias em respostas &#224;s diferen&#231;as de press&#227;o intravascular (complac&#234;ncia arterial) possibilita a redu&#231;&#227;o de flutua&#231;&#245;es press&#243;ricas na circula&#231;&#227;o central, e contribui ao adequado direcionamento de fluxo. Em idosos sedent&#225;rios observa-se eleva&#231;&#227;o da rigidez arterial (grandeza oposta &#224; complac&#234;ncia arterial), a qual tamb&#233;m est&#225; aumentada em condi&#231;&#245;es patol&#243;gicas como aterosclerose, resist&#234;ncia a insulina e diabete melito<bold><sup>40</sup></bold>. Outro fator de risco independente para o aumento da rigidez arterial &#233; a obesidade<bold><sup>41</sup></bold>. Al&#233;m disso, a rigidez a&#243;rtica &#233; preditora de mortalidade cardiovascular e por todas as causas em pacientes hipertensos<bold><sup>42</sup></bold>. Em vista disso, alguns experimentos t&#234;m avaliado a complac&#234;ncia e rigidez arterial ante a interven&#231;&#227;o pelo exerc&#237;cio f&#237;sico, uma vez que esse tem impacto salutar sobre diversos dos fatores de risco associados com rigidez arterial. </p>
    <p>Estudos observacionais e de interven&#231;&#227;o demonstraram que o exerc&#237;cio aer&#243;bico regular parece atenuar o enrijecimento arterial associado &#224; idade, e contribuir para o aumento de complac&#234;ncia arterial ap&#243;s treinamento f&#237;sico sistem&#225;tico<bold><sup>43-46</sup></bold>. Assim, nos &#250;ltimos anos, o interesse em investigar poss&#237;veis benef&#237;cios do exerc&#237;cio resistido sobre a distensibilidade vascular cresceu, por&#233;m as evid&#234;ncias n&#227;o t&#234;m confirmado essa hip&#243;tese. Estudos transversais observaram menor complac&#234;ncia arterial em adultos de diferentes faixas et&#225;rias treinados em for&#231;a quando comparados aos seus pares sedent&#225;rios<bold><sup>47,48</sup></bold>. Em mulheres jovens, Cortez-Cooper e cols. verificaram que 11 semanas de treinamento resistido de alta intensidade promoveram eleva&#231;&#227;o da rigidez arterial central (aumento no &#237;ndice de amplifica&#231;&#227;o da press&#227;o sist&#243;lica na art&#233;ria car&#243;tida e na velocidade da onda de pulso a&#243;rtico)<bold><sup>49</sup></bold>. </p>
    <p>Por sua vez, Miyachi e cols. randomizaram homens jovens em grupos controle e interven&#231;&#227;o, conduzindo um estudo com dura&#231;&#227;o de oito meses: treinamento resistido de alta intensidade (80% da carga m&#225;xima) durante quatro meses, seguido por um per&#237;odo de destreinamento (sem exerc&#237;cio) nos quatro meses subseq&#252;entes. Ao final do per&#237;odo de treinamento constataram-se complac&#234;ncia reduzida (p&lt;0,01), &#237;ndice de rigidez arterial aumentado (p&lt;0,01) e correla&#231;&#245;es significativas entre as altera&#231;&#245;es na complac&#234;ncia da car&#243;tida e os &#237;ndices de massa (r = -0,56, p&lt;0,001) e de hipertrofia ventricular esquerda (r = -0,68, p&lt;0,001). Ap&#243;s o destreinamento, as vari&#225;veis modificadas com o exerc&#237;cio retornaram aos valores basais (pr&#233;-estudo)<bold><sup>50</sup></bold>. </p>
    <p>Em contrapartida, outro estudo que tamb&#233;m arrolou homens jovens, os quais foram expostos a tr&#234;s meses de treinamento com sess&#245;es de volume e intensidade levemente menores, n&#227;o demonstrou altera&#231;&#245;es no enrijecimento arterial e nas dimens&#245;es card&#237;acas<bold><sup>51</sup></bold>. Outra publica&#231;&#227;o muito recente, que utilizou treinamento resistido de intensidade moderada (50% da carga m&#225;xima, quatro meses de treinamento) demonstrou diminui&#231;&#227;o na complac&#234;ncia arterial (p&lt;0,01) e aumento no &#237;ndice de rigidez arterial (p&lt;0,01), altera&#231;&#245;es que desapareceram ap&#243;s quatro meses subseq&#252;entes sem treinamento. Entretanto, para o grupo que realizou treinamento combinado (treino resistido a 80% da carga m&#225;xima acrescido de 30 minutos de exerc&#237;cio aer&#243;bico ao final da sess&#227;o) n&#227;o houve enrijecimento arterial; ao contr&#225;rio, esse tipo de treinamento tendeu a aumentar a complac&#234;ncia<bold><sup>52</sup></bold>. </p>
    <p>A partir desses achados &#233; importante mencionar que ainda n&#227;o s&#227;o conhecidos os mecanismos que explicam o enrijecimento arterial tempor&#225;rio observado na maioria dos estudos ap&#243;s o treinamento resistido exclusivo. A hip&#243;tese vigente parece ir na dire&#231;&#227;o de altera&#231;&#245;es do conte&#250;do estrutural das art&#233;rias (elastina e col&#225;geno).</p>
    <p>Se consideradas de forma isolada, as informa&#231;&#245;es descritas aqui podem sugerir potenciais malef&#237;cios do treinamento resistido, por&#233;m esses efeitos n&#227;o parecem suplantar as demais adapta&#231;&#245;es promovidas pelo treinamento resistido. Portanto, tais observa&#231;&#245;es n&#227;o devem servir como uma contra-indica&#231;&#227;o a esse. Por exemplo, um relato muito recente indicou que indiv&#237;duos idosos, os quais t&#234;m maior rigidez arterial, n&#227;o demonstraram enrijecimento arterial, al&#233;m de terem apresentado redu&#231;&#227;o da PA central, ap&#243;s 20 semanas de treinamento resistido<bold><sup>53</sup></bold>. Por fim, ainda que em homens jovens o exerc&#237;cio resistido pare&#231;a ocasionar diminui&#231;&#227;o da complac&#234;ncia, esse efeito parece ser perfeitamente neutralizado pelo exerc&#237;cio aer&#243;bico.</p>
    <p>
      <bold>Treinamento resistido e implica&#231;&#245;es na fun&#231;&#227;o vascular e fluxo sang&#252;&#237;neo basal</bold>
    </p>
    <p>A perda ou atenua&#231;&#227;o da vasodilata&#231;&#227;o fisiol&#243;gica mediada pelo endot&#233;lio &#150; disfun&#231;&#227;o endotelial &#150; &#233; um evento precoce no processo ateroscler&#243;tico, e est&#225; associado a diversos fatores de risco em adultos ou crian&#231;as<bold><sup>54,55</sup></bold>. Na presen&#231;a de IC (isqu&#234;mica ou n&#227;o-isqu&#234;mica) a disfun&#231;&#227;o endotelial est&#225; associada ao aumento da mortalidade<bold><sup>56</sup></bold>. Por sua vez, algumas evid&#234;ncias t&#234;m estabelecido melhora da fun&#231;&#227;o endotelial e aumento do fluxo sang&#252;&#237;neo em pacientes com IC ap&#243;s treinamento aer&#243;bico<bold><sup>57,58</sup></bold>. Essa adapta&#231;&#227;o vascular parece tamb&#233;m ocorrer ap&#243;s programas de exerc&#237;cios resistidos associados a est&#237;mulos aer&#243;bicos. Maiorana e cols.<bold><sup>59</sup></bold> verificaram aumento da vasodilata&#231;&#227;o dependente e independente do endot&#233;lio em pacientes com IC (FE: 26&#177;3%, VO<sub>2</sub>pico: 19,5&#177;1,2ml.kg<sup>-1</sup>.min<sup>-1</sup>) ap&#243;s um treinamento combinado de oito semanas<bold><sup>59</sup></bold>. Em cardiopatas isqu&#234;micos, o treinamento combinado predominantemente de membros inferiores aumentou a vasodilata&#231;&#227;o mediada pelo fluxo na art&#233;ria braquial, indicando adapta&#231;&#227;o endotelial sist&#234;mica proporcionada pelo exerc&#237;cio<bold><sup>60</sup></bold>, ao passo que a resposta independente do endot&#233;lio n&#227;o foi alterada. </p>
    <p>No que se referem ao treinamento resistido exclusivo, v&#225;rias evid&#234;ncias explicitam, em especial, efeitos sobre o aumento do fluxo sang&#252;&#237;neo basal. Inicialmente, um estudo piloto demonstrou que, ap&#243;s 11 semanas de treinamento em circuito, pacientes com IC classes II e III (FE: 26&#177;6 %) obtiveram aumento do fluxo sang&#252;&#237;neo em repouso (p&lt;0,01), por&#233;m sem altera&#231;&#245;es nas respostas de vasodilata&#231;&#227;o (resposta endotelial)<bold><sup>61</sup></bold>. No entanto, outro estudo evidenciou resultados como aumento de fluxo sang&#252;&#237;neo basal, al&#233;m de melhora na fun&#231;&#227;o endotelial<bold><sup>62</sup></bold>. Neste ensaio cl&#237;nico randomizado e controlado, os pacientes com IC que realizaram tr&#234;s meses de treinamento resistido em intensidade moderada, apresentaram aumento do fluxo sang&#252;&#237;neo, tanto em repouso quanto em resposta a est&#237;mulos de exerc&#237;cio ou isquemia (maior hiperemia ap&#243;s oclus&#227;o, indicando aumento da vasodilata&#231;&#227;o mediada pelo endot&#233;lio). </p>
    <p>O treinamento resistido tamb&#233;m parece elevar o fluxo sang&#252;&#237;neo basal de indiv&#237;duos saud&#225;veis. Em homens jovens saud&#225;veis que realizaram tr&#234;s meses de treinamento resistido, foi observado aumento do fluxo sang&#252;&#237;neo em repouso, bem como evid&#234;ncias de remodelamento arterial, achados esses constatados a partir do aumento do di&#226;metro da art&#233;ria braquial. Entretanto, esta amostra n&#227;o apresentou mudan&#231;as na fun&#231;&#227;o endotelial braquial. A explica&#231;&#227;o para esses achados pode estar relacionada ao fato de os participantes terem fun&#231;&#227;o vascular normal no in&#237;cio do estudo, o que n&#227;o propiciaria maior adapta&#231;&#227;o ao longo dos tr&#234;s meses de treinamento<bold><sup>63</sup></bold>. </p>
    <p>Por sua vez, no envelhecimento, o fluxo sang&#252;&#237;neo e a condut&#226;ncia vascular decrescem, o que pode contribuir para redu&#231;&#227;o na perfus&#227;o muscular e na capacidade funcional<bold><sup>64</sup></bold>. Enquanto o exerc&#237;cio aer&#243;bico parece n&#227;o atenuar a diminui&#231;&#227;o de fluxo ocorrida no envelhecimento, um estudo transversal sugeriu que homens treinados em for&#231;a n&#227;o apresentam diminui&#231;&#227;o de fluxo sang&#252;&#237;neo perif&#233;rica relacionado &#224; idade<bold><sup>65,66</sup></bold>. A partir disso, dados de um recente estudo prospectivo indicaram a aparente efic&#225;cia do treinamento resistido sobre a manuten&#231;&#227;o do fluxo sang&#252;&#237;neo perif&#233;rico em indiv&#237;duos de idades avan&#231;adas<bold><sup>67</sup></bold>. Nesse trabalho, idosos e adultos de meia-idade randomizados ao treinamento resistido com dura&#231;&#227;o de 13 semanas apresentaram aumento do fluxo sang&#252;&#237;neo e da condut&#226;ncia vascular na art&#233;ria femoral. </p>
    <p>Em suma, as informa&#231;&#245;es dispon&#237;veis na literatura indicam que o treinamento resistido, realizado de forma exclusiva ou em combina&#231;&#227;o aos exerc&#237;cios aer&#243;bicos, pode melhorar a fun&#231;&#227;o endotelial. Al&#233;m disso, as evid&#234;ncias tamb&#233;m apontam para um importante efeito do exerc&#237;cio resistido sobre o aumento de fluxo sang&#252;&#237;neo perif&#233;rico, o que pode contribuir para minimizar a limita&#231;&#227;o funcional presente no envelhecimento ou em diferentes condi&#231;&#245;es patol&#243;gicas. </p>
    <p>
      <bold>Considera&#231;&#245;es finais</bold>
    </p>
    <p>O exerc&#237;cio resistido tem se inserido progressivamente em programas de preven&#231;&#227;o e reabilita&#231;&#227;o cardiovascular. As perspectivas de poss&#237;veis estudos com avalia&#231;&#245;es de desfechos relevantes validados podem refor&#231;ar as informa&#231;&#245;es j&#225; consistentes que atualmente permitem prescri&#231;&#245;es seguras para pr&#225;tica desse tipo de exerc&#237;cio por diferentes popula&#231;&#245;es.</p>
    <p>A proposta desta revis&#227;o foi atualizar as evid&#234;ncias que concernem &#224;s respostas cardiovasculares ao exerc&#237;cio resistido cr&#244;nico e agudo. As informa&#231;&#245;es encontradas na literatura demonstram estabilidade hemodin&#226;mica durante o exerc&#237;cio, e potenciais efeitos que auxiliam para o controle press&#243;rico. Al&#233;m disso, esta revis&#227;o apresenta importantes particularidades da adapta&#231;&#227;o da distensibilidade arterial, da fun&#231;&#227;o vascular e do fluxo sang&#252;&#237;neo perif&#233;rico frente ao treinamento resistido. </p>
    <p>Por fim, o corpo de evid&#234;ncias dispon&#237;vel sobre a aplicabilidade e seguran&#231;a do treinamento resistido em cardiopatas vai ao encontro daquilo que j&#225; est&#225; estabelecido em rela&#231;&#227;o &#224; indica&#231;&#227;o do exerc&#237;cio aer&#243;bico.</p>
    <p>
      <bold>Potencial Conflito de Interesses</bold>
    </p>
    <p>Declaro n&#227;o haver conflitos de interesses pertinentes.</p>
    <p>
      <bold>Fontes de Financiamento</bold>
    </p>
    <p>O presente estudo n&#227;o teve fontes de financiamento externas.</p>
    <p>
      <bold>Vincula&#231;&#227;o Acad&#234;mica</bold>
    </p>
    <p>O artigo &#233; parte de tese de mestrado de Daniel Umpierre, pela Universidade Federal do Rio Grande do Sul - UFRGS, Laborat&#243;rio de Fisiopatologia do Exerc&#237;cio - LasiEx, Servi&#231;o de Cardiologia.</p>
    <p>
      <fn id="end" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Ricardo Stein </p>
        <p> Rua Jo&#227;o Caetano, 20/402 &#150; Tr&#234;s Figueiras </p>
        <p> 90460-270 - Porto Alegre, RS - Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="kuqui2@terra.com.br">kuqui2@terra.com.br</email> / </p>
        <p>
          <email xlink:href="rstein@cardiol.br">rstein@cardiol.br</email>
        </p>
      </fn>
    </p>
    <p> Artigo recebido em 24/03/07; revisado recebido em 10/05/07; aceito em 10/05/07.</p>
  </body>
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  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Review Update</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Hemodynamic and vascular effects of resistance training: implications for cardiovascular disease</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>Resistance training has been proposed as a possible strategy for cardiovascular prevention and rehabilitation, and in this context, this review describes the cardiovascular effects mediated by this type of intervention. Increments in both muscular strength and capacity to perform daily tasks are well-characterized benefits of this type of training. More recently, studies using hemodynamic evaluation have shown cardiovascular stability in patients with coronary disease or heart failure during the performance of resistance exercise, with no apparent detriment to ventricular function or exacerbated increase in exercise blood pressure. Additionally, resting blood pressure also seems to be influenced by chronic resistance training, with a slight reduction in both systolic blood pressure (SBP) and diastolic blood pressure (DBP). The measurement of pressure levels after a single resistance exercise session shows the occurrence of post-exercise hypotension in normal and hypertensive individuals; however, there is controversy as to the intensity of the effort necessary to induce this effect. Recently, intervention studies have investigated resistance exercise effects on vascular variables as arterial compliance and endothelial function. Despite the small number of experiments available, evidence has shown a potential influence of resistance training on the reduction of arterial compliance. On the other hand, peripheral blood flow is increased after resistance training, whereas the endothelial function seems to be improved especially after combined aerobic and resistance training. Additional research is necessary for an analysis of the efficacy of this intervention on validated outcomes, and for a greater understanding of the physiological mechanisms responsible for vascular adaptations.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Exercise</kwd>
        <kwd>physical fitness</kwd>
        <kwd>hemodynamic evaluation</kwd>
        <kwd>cardiovascular diseases</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>REVIEW ARTICLE</bold>
      </p>
      <p>Hemodynamic and vascular effects of resistance training: implications for cardiovascular disease</p>
      <p>
        <bold>Daniel Umpierre; Ricardo Stein</bold>
      </p>
      <p> Laborat&#243;rio de Fisiopatologia do Exerc&#237;cio, Hospital de Cl&#237;nicas de Porto Alegre - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brazil</p>
      <p>
        <xref ref-type="corresp" rid="end-body2">Mailing address</xref>
      </p>
      <p>
        <bold>SUMMARY</bold>
      </p>
      <p>Resistance training has been proposed as a possible strategy for cardiovascular prevention and rehabilitation, and in this context, this review describes the cardiovascular effects mediated by this type of intervention. Increments in both muscular strength and capacity to perform daily tasks are well-characterized benefits of this type of training. More recently, studies using hemodynamic evaluation have shown cardiovascular stability in patients with coronary disease or heart failure during the performance of resistance exercise, with no apparent detriment to ventricular function or exacerbated increase in exercise blood pressure. Additionally, resting blood pressure also seems to be influenced by chronic resistance training, with a slight reduction in both systolic blood pressure (SBP) and diastolic blood pressure (DBP). The measurement of pressure levels after a single resistance exercise session shows the occurrence of post-exercise hypotension in normal and hypertensive individuals; however, there is controversy as to the intensity of the effort necessary to induce this effect. Recently, intervention studies have investigated resistance exercise effects on vascular variables as arterial compliance and endothelial function. Despite the small number of experiments available, evidence has shown a potential influence of resistance training on the reduction of arterial compliance. On the other hand, peripheral blood flow is increased after resistance training, whereas the endothelial function seems to be improved especially after combined aerobic and resistance training. Additional research is necessary for an analysis of the efficacy of this intervention on validated outcomes, and for a greater understanding of the physiological mechanisms responsible for vascular adaptations.</p>
      <p><bold>Key words:</bold> Exercise/psychology; physical fitness/psychology; hemodynamic evaluation; cardiovascular diseases.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>Since the mid 1960s, cardiovascular responses to predominantly strength-based exercise have been discussed<bold><sup>1,2</sup></bold>. Until the early 1990s, resistance training (also called strength training) was not included in international guidelines. However, over the last years, this modality has come to be considered as a possible strategy for primary and secondary prevention of different heart diseases<bold><sup>3,4</sup></bold>. Furthermore, several research projects have suggested that resistance exercise, when appropriately prescribed and supervised, has favorable effects on different aspects of health (muscular strength, functional capacity, psychosocial well-being, besides the positive impact on cardiovascular risk factors)<bold><sup>5</sup></bold>.</p>
      <p>Neuromuscular adaptations and effects such as an increase in muscular strength and resistance have been the primary basis for the rationale that supports the application of resistance training in exercise programs for heart patients<bold><sup>4,6</sup></bold>. Among the different adaptations promoted for this type of training are the increased capacity to carry out daily activities<bold><sup>7</sup></bold>, an increment in tolerance to submaximal aerobic exercise<bold><sup>8,9</sup></bold>, a suppression of age-related strength decline<bold><sup>10</sup>,</bold> and an attenuation of cardiovascular responses to effort<bold><sup>11</sup></bold>. Even in the absence of large clinical studies evaluating the efficacy of this type of training applied exclusively on validated clinical outcomes, observation data indicate a reduced coronary risk for resistance exercise practioners. </p>
      <p>In the Health Professionals Follow-up Study cohort<bold><sup>12</sup></bold>, weekly participation in 30 minutes or more of resistance training was associated with a 23% decrease in risk of a non-fatal acute myocardial infarct and/or fatal cardiovascular disease (RR 0.77; 95% CI, 0.61-0.98; p=0.03). Multivariate analysis was used, adjusted for factors such as age, alcohol consumption, smoking, family history, food profile, and engagement in other physical activities to decrease the chance of systematic error. </p>
      <p>Currently, there is further evidence as to resistance exercise in health and in cardiovascular disease (CVD) which allows a better understanding of known effects and reinforces the perspective of using resistance training in secondary prevention. In this review we discuss the influence of this type of exercise on important aspects of CVD or its development, covering evidence that is recent and/or yet unexplored in other reviews.</p>
      <p>
        <bold>Hemodynamic stability during resistance exercise</bold>
      </p>
      <p>According to the intensity of the effort put forth, hemodynamic responses during resistance exercise can be similar to those that occur in dynamic or isometric (static) contractions. Therefore, in efforts with low loads, there is an increase in heart rate (HR), systolic blood pressure (SBP), systolic volume, and cardiac output (CO), whereas with high loads, there is also an increase in diastolic blood pressure (DBP)<bold><sup>13</sup></bold>. During resistance exercise, greater HR e BP values are obtained in the last repetitions of the series performed to exhaustion<bold><sup>14</sup></bold>, and this training design has been contraindicated for hypertensive patients. Additionally, among other factors that influence blood pressure response, the greater the muscle mass involved in the exercise, the greater the response<bold><sup>15</sup></bold>. MacDougall et al observed extreme pressure rises (&#187;320/250 mmHg) in body-builders when these individuals were exposed to loads between 80% and 100%<bold><sup>16</sup></bold>. On the other hand, the level of physical strength conditioning seems to maintain an inverse relationship with the magnitude of the BP and HR responses to exercise<bold><sup>14</sup></bold>. </p>
      <p>In cardiac patients with left ventricular dysfunction, during strength tests and in series with different intensities, an increase in new segment abnormalities of the left ventricular wall was observed which occurred in greater proportions during the final series after a protocol of growing intensities (three series with progressive loads)<bold><sup>17</sup></bold>. However, these were small-magnitude findings and even if they can reflect some degree of ischemia during effort, they do not suggest a reduction in cardiac performance. Indeed, in 6,653 individuals without CVD who performed strength tests &#150; on isokinetic dynamometer as well as in 1-maximum repetition test in exercises as bench press and leg press &#150; there were no fatal or non-fatal cardiovascular events<bold><sup>18</sup></bold>.</p>
      <p>More recently, studies with different evaluation techniques have broadened our knowledge of cardiovascular function during resistance exercise. Meyer et al<bold><sup>19</sup></bold> used direct catheterization of two groups of patients: a) HF with ventricular dysfunction, and b) stable coronary artery disease with preserved ventricular function. The authors identified an increase in the cardiac index and in the systolic volume during the leg press at different effort intensities. At the 60% intensity of maximum voluntary contraction, the systolic work index remained stable, indicating similar changes in the mean blood pressure (MBP) and in the diastolic pressure of the pulmonary artery, suggesting a balance between pre- and post-load. </p>
      <p>One interesting aspect of this study is that during exercise with 60% of the maximum load, the variation in blood pressure levels (measured invasively) was of a small magnitude (<xref ref-type="fig" rid="fig01-body2">Figure 1</xref>). Similar results occurred in another study that enrolled patients with severe heart failure (HF) who did not present hemodynamic instability during resistance exercises of the upper and lower limbs. In this individuals with HF class III and IV (EF: 25&#177;2%, VO<sub>2peak</sub>: 12.4&#177;0.7ml.kg<sup>-1</sup>.min<sup>-1</sup>), there was a slight decrease in the stroke volume with lower limb exercises, and maintenance of the stroke volume during upper limb exercises (relative to resting values), while the value of the CO was unchanged during both exercises. </p>
      <fig id="fig01-body2">
        <graphic xlink:href="1678-4170-abc-89-04-0256-00008-gf01-en.jpg"/></fig>
      <p>The mechanisms that afford maintenance of ventricular function in healthy individuals, in ischemic cardiomyopathy patients, and in patients from different HF classes are not fully elucidated. Even so, it is important to note that, although some studies have demonstrated an increase in inotropism, the chronotropic response seems to be the main factor responsible for maintaining the CO<bold><sup>19-21</sup></bold>. </p>
      <p>The typical behavior of increased systemic vascular resistance caused by pure isometric contraction<bold><sup>22</sup></bold> many times is not desirable for cardiac patients. Nonetheless, contrary to what happens in isometric contractions, vascular resistance in cardiac patients is not elevated during the performance of a resistance exercise series (<xref ref-type="fig" rid="fig02-body2">Figure 2</xref>)<bold><sup>19-21,23</sup></bold>. This effect is possibly brought about by the dynamic component which is also present in the contractions of this type of exercise.</p>
      <fig id="fig02-body2">
        <graphic xlink:href="1678-4170-abc-89-04-0256-00008-gf02-en.jpg"/></fig>
      <p>
        <bold>Resistance exercise and blood pressure</bold>
      </p>
      <p>Regular physical exercise helps in the short-term and long-term control of blood pressure (BP) and is therefore indicated as coadjuvant intervention in managing hypertension<bold><sup>24</sup></bold>. For a wider discussion of the effects of exercise on BP, it is important to note that this may be influenced not only by adaptations resulting from chronic physical training (chronic adaptations), but also by the effects of a single exercise session (subacute or post-exercise effects).</p>
      <p>
        <bold>Resistance training: Chronic effects</bold>
      </p>
      <p>More recent evidence does not support the ancient dogma that resistance training could elevate resting BP. This reasoning originated from the idea that greater pressure gains associated with resistance exercise (due to the greater isometric component) would lead to a chronic elevation of the BP. </p>
      <p>Two robust meta-analyses demonstrated beneficial effects of resistance training on resting SAP and DAP. Both reviews included studies with the following characteristics: 1) randomized studies using a control group without exercise; 2) resistance training as a single intervention; 3) previously sedentary normotensive or hypertensive individuals; and 4) a minimum duration of four weeks. Kelley and Kelley<bold><sup>25</sup></bold> examined 11 studies, with a total of 320 subjects (182 with exercise and 138 controls), and found a reduction in SAP (-3&#177;3 mmHg; 95% Confidence Interval: -4 to -1 mmHg) and DAP (-3&#177;2 mmHg; 95% Confidence Interval: -4 to -1 mmHg), which represented an approximate drop of 2% and 4%, respectively. </p>
      <p>Posteriorly, a meta-analysis published by Cornelissen and Fagard<bold><sup>26</sup></bold>, composed by 12 studies and 341 participants, showed the same tendency with reductions in SAP (-3.2 mmHg; p=0.10) and DAP (-3.5 mmHg; p&lt;0.01) for the individuals exposed to resistance training. When the analyses of subgroups were carried out, again there were no differences related to the intensity of exercise, as well as when conventional or circuit resistance training was used. In conventional training, all sets of a certain movement are executed before initiating the following exercise, and there are normally higher loads and longer intervals than in circuit training. </p>
      <p>On the other hand, in this other training mode, activity is more continuous and intervals are shorter since only one series is executed at each station, with immediate progression to the next station, and the circuit is repeated more times if necessary. Even if resistance training, similar to aerobic training<bold><sup>27</sup></bold>, provides merely mild changes in the BP values, in terms of the population, this can have an impact in terms of a lower incidence of coronary disease and strokes<bold><sup>28</sup></bold>.</p>
      <p>
        <bold>Hypotension after resistance exercise</bold>
      </p>
      <p>Physical exercise can promote a sustained drop in post-exercise blood pressure levels. Called post-exercise hypotension (PEH), this classic effect has been well demonstrated with aerobic exercise<bold><sup>29</sup></bold> and has been studied in strength training both in ambulatory 24-hour evaluations (ABPM) and assessments made during the period of recovery (up to approximately 90 minutes after exercise). Bermudes et al<bold><sup>30</sup></bold> did not observe differences in 24-hour SAP and DAP values after one control session without exercise, and after one session of circuit resistance exercises. However, during the sleep period, there was a significant drop in BP after the resistance exercise session in comparison with the period after the control condition. Likewise, in young individuals with different levels of physical conditioning &#150; sedentary, resistance-trained, and endurance-trained. SAP, DAP, and MAP were not different after one session of exercise or one control session<bold><sup>31</sup></bold>. Very recently, when studying 20 hypertensive women who use an angiotensin-converting enzyme inhibitor (captopril), Melo et al<bold><sup>31</sup></bold> noted a significant reduction in blood pressure (SAP:-12&#177;3 mmHg, DAP:-6&#177;2 mmHg) during the recovery period up to 120 minutes after a low-intensity resistance exercise session. Additionally, the values observed by ABPM remained significantly lower for up to 10 hours after exercise (during the awake period), which did not occur after the control session<bold><sup>32</sup></bold>.</p>
      <p>According to what is illustrated in <xref ref-type="fig" rid="fig03-body2">Figure 3</xref>, in resistance exercise, PEH is more accentuated during recovery (&#187;90 minutes after the session), and tends to return to basal levels in the subsequent hours. Even though this effect was verified in normotensive and hypertensive individuals<bold><sup>31-34</sup></bold>, controversy still exists, especially related to the intensity of the exercise. Some authors have documented a reduction in SAP after sessions using high loads<bold><sup>35,36</sup>;</bold> in other studies, however, high-intensity protocols were not effective in promoting significant pressure reductions<bold><sup>37-39</sup></bold>. </p>
      <fig id="fig03-body2">
        <graphic xlink:href="1678-4170-abc-89-04-0256-00008-gf03-en.jpg"/></fig>
      <p>Recently, Rezk et al<bold><sup>35</sup></bold> demonstrated that sessions at 40% and 80% of the maximum load were followed by a reduction in SAP during the recovery (-6&#177;1 mmHg and -8&#177;1 mmHg, p&lt;0.05, respectively), while the DAP was reduced only after the lowest intensity session (40% of the maximum load). According to the authors, the hypotension generated by both protocols was mediated by the lower CO, and only modest elevations were noted in both systemic vascular resistance and post-exercise HR<bold><sup>35</sup></bold>. Based on the abovementioned data, it is clear that resistance exercise performed chronically or acutely does not seem to offer risks as to an increase in BP, and this intervention may facilitate long-term pressure control.</p>
      <p>
        <bold>Influence of resistance training in arterial compliance: emerging evidence</bold>
      </p>
      <p>The distension capacity of arteries in response to differences in intravascular pressure (arterial compliance) enables the reduction of pressure fluctuations in the central circulation and contributes towards an adequate direction of flow. In sedentary elderly individuals, increased arterial stiffness is noted (the quality opposite of arterial compliance), which is also increased in pathological conditions such as atherosclerosis, insulin resistance, and diabetes mellitus<bold><sup>40</sup></bold>. Another independent risk factor for increased arterial stiffness is obesity<bold><sup>41</sup></bold>. Moreover, aortic stiffness is a predictor of cardiovascular mortality and all-cause mortality in hypertensive patients<bold><sup>42</sup></bold>. Since regular exercise has a healthy impact on several risk factors associated with arterial stiffness, some studies have tested this intervention to possible changes in the distensibility parameters. </p>
      <p>Observational and interventional studies have shown that regular aerobic exercise seems to attenuate age-related arterial stiffening and contribute to an increase in arterial compliance after systematic physical training<bold><sup>43-46</sup></bold>. Thus, over the last years, interest in investigating possible benefits of resistance exercise on vascular distensibility has grown, but evidence has not yet confirmed this hypothesis. Cross-sectional studies have noted less arterial compliance in adults from different age groups who are resistance-trained when compared to their sedentary peers<bold><sup>47,48</sup></bold>. In young women, Cortez-Cooper et al verified that 11 weeks of high-intensity resistance training led to an elevation of central arterial stiffness (an increase in the augmentation index of systolic in the carotid artery and in the aortic pulse wave velocity)<bold><sup>49</sup></bold>. </p>
      <p>In as elegant study design with duration of 8 months, Miyachi et al randomized young men in control and intervention groups; high-intensity resistance training (80% of the maximum load) was used for four months, followed by a period of detraining (no exercise) in the four subsequent months. At the end of the training period, reduced compliance (p&lt;0.01) and increased arterial stiffness (p&lt;0.01) were noted, with significant correlations between the changes in carotid compliance and mass indexes (r = -0.56, p&lt;0.001) and left ventricular hypertrophy (r = -0.68, p&lt;0.001). After the detraining, the variables modified by exercise returned to the basal (pre-study) values<bold><sup>50</sup></bold>. </p>
      <p>In contrast, another study that also enrolled young men who were exposed to three months of training with slightly lower volume and intensity sessions, showed no changes in arterial stiffening and cardiac dimensions<bold><sup>51</sup></bold>. Another very recently published study using moderate-intensity resistance training (50% of the maximum load, four months of training) showed a decrease in arterial compliance (p&lt;0.01) and in increase in the arterial stiffness index (p&lt;0.01), alterations that disappeared after four subsequent months without training. Nevertheless, for the group that performed a combined training (resistance training at 80% of the maximum load plus 30 minutes of aerobic exercise at the end of the session), there was no arterial stiffening; on the contrary, this type of training tended to increase compliance<bold><sup>52</sup></bold>. </p>
      <p>Based on these findings, it is important to mention that the mechanisms that explain temporary arterial hardening observed in most studies after the exclusive use of resistance training are not yet known. The currently adopted hypothesis seems to tend towards changes in the structural content of arteries (elastin and collagen).</p>
      <p>If considered alone, the information described here could suggest potential ill effects of resistance training, but these effects do not seem to supplant the other adaptations afforded by resistance training. Therefore, these observations should not serve as a contraindication for this type of exercise. For example, a very recent report indicated that elderly individuals, who usually have greater arterial stiffness, did not demonstrate arterial hardening although they did show a reduction in central BP after 20 weeks of resistance training<bold><sup>53</sup></bold>. Finally, even though in young men resistance exercise may seem to cause a decrease in compliance, this result seems to be perfectly neutralized by aerobic exercise.</p>
      <p>
        <bold>Resistance training and its implications for vascular function and basal blood flow</bold>
      </p>
      <p>The loss or attenuation of physiological endothelium-mediated vasodilation &#150; endothelial dysfunction &#150; is an early event in the atherosclerotic process and it is associated with several risk factors in adults and children<bold><sup>54,55</sup></bold>. In the presence of HF (ischemic or non-ischemic), endothelial dysfunction is associated with increased mortality<bold><sup>56</sup></bold>. On the other hand, some evident findings have helped to establish improved endothelial function and increased blood flow in HF patients after aerobic training<bold><sup>57,58</sup></bold>. This vascular adaptation seems to also occur after resistance exercise programs associated with aerobic stimuli. Maiorana et al<bold><sup>59</sup></bold> noted an increase in dependent and independent endothelial vasodilation in HF patients (EF: 26&#177;3%, VO<sub>2</sub><sup>peak</sup>: 19.5&#177;1.2ml.kg<sup>-1</sup>.min<sup>-1</sup>) after eight weeks of combined training<bold><sup>59</sup></bold>. In cardiac patients with coronary disease, combined training predominantly of the lower limbs increased flow- mediated dilation by the flow in the brachial artery, indicating systemic endothelial adaptation afforded by exercise<bold><sup>60</sup></bold>, whereas the response independent of the endothelium was unchanged. </p>
      <p>As to exclusive resistance training, there is evidence that clearly shows its effects primarily on the increase of basal blood flow. Initially, a pilot study showed that after 11 weeks of circuit training, patients with HF class II and III (EF: 26&#177;6 %) obtained an increase in resting blood flow (p&lt;0.01), albeit without changes in vasodilation responses (endothelial response)<bold><sup>61</sup></bold>. Nonetheless, another study evidenced results such as an increased basal blood flow besides an improvement in endothelial function<bold><sup>62</sup></bold>. In this randomized controlled clinical study, the HF patients submitted to three months of moderate-intensity resistance training showed an increase in blood flow, both at rest and in response to exercise stimuli or ischemia (greater hyperemia after occlusion, indicating an increase in vasodilation mediated by the endothelium). </p>
      <p>Resistance training also seems to elevate the basal blood flow of healthy individuals. In healthy young men who underwent three months of resistance training, an increase in resting blood flow was noted in addition to evidence of arterial remodeling, findings observed from the increased diameter of the brachial artery. However, this sample showed no changes in brachial endothelial function. The explanation for these findings may be related to the fact that participants had normal vascular function at the onset of the study, which would not provide a greater adaptation during the three months of training<bold><sup>63</sup></bold>. </p>
      <p>On the other hand, in aging, blood flow and vascular conductance diminish, and this can contribute to a reduction in muscle perfusion and functional capacity<bold><sup>64</sup></bold>. While aerobic exercise does not seem to attenuate the drop in blood flow that happens with aging, a cross-sectional study suggested that men submitted to strength training did not display a decrease in age-related peripheral blood flow<bold><sup>65,66</sup></bold>. Based on this, data from a recent prospective study indicated the apparent efficacy of resistance training on the maintenance of peripheral blood flow in individuals with advanced ages<bold><sup>67</sup></bold>. In this paper, elderly and middle-aged adults randomized to resistance training for 13 weeks showed an increase in blood flow and vascular conductance in the femoral artery. </p>
      <p>In summary, information available in medical literature indicates that resistance training, whether carried out exclusively or in combination with aerobic exercises, can improve endothelial function. Additionally, evidence also points to an important effect of resistance exercise on the increase of peripheral blood flow, which can contribute to minimizing the functional limitations present in aging or in different pathological conditions.</p>
      <p>
        <bold>Final considerations</bold>
      </p>
      <p>Resistance exercise has progressively gained importance in cardiovascular prevention and rehabilitation programs. The perspectives of possible studies with relevant validated outcomes may reinforce the current reliable information that allows safe prescriptions for the practice of this type of exercise by different populations. </p>
      <p>The proposal of this review was to update the evidence concerning cardiovascular responses to chronic and acute resistance exercise. The information found in literature demonstrates hemodynamic stability during exercise and potential effects that help in blood pressure control. In addition, this review presents important peculiarities of arterial distensibility adaptation, vascular function, and peripheral blood flow in face of resistance training. </p>
      <p>Finally, the body of evidence available on the applicability and safety of resistance training in cardiac patients is consistent with what is already established regarding aerobic exercise.</p>
      <p>
        <bold>Potential Conflict of Interest</bold>
      </p>
      <p>No potential conflict of interest relevant to this article was reported.</p>
      <p>
        <bold>Sources of Funding</bold>
      </p>
      <p>There were no external funding sources for this study.</p>
      <p>
        <bold>Study Association</bold>
      </p>
      <p>This article is part of the thesis of master submitted by Daniel Umpierre, from Universidade Federal do Rio Grande do Sul (UFRGS), Laborat&#243;rio de Fisiopatologia do Exerc&#237;cio (LasiEx), Servi&#231;o de Cardiologia.</p>
      <p>
        <bold>References</bold>
      </p>
      <p>
        <fn id="end-body2" fn-type="corresp">
          <label>
            <bold>Mailing address:</bold>
          </label>
          <p> Ricardo Stein</p>
          <p> Rua Jo&#227;o Caetano, 20/402 &#150; Tr&#234;s Figueiras</p>
          <p> 90460-270 - Porto Alegre, RS - Brazil</p>
          <p> E-mail: </p>
          <p><email xlink:href="kuqui2@terra.com.br">kuqui2@terra.com.br</email> / </p>
          <p>
            <email xlink:href="rstein@cardiol.br">rstein@cardiol.br</email>
          </p>
        </fn>
      </p>
      <p>Manuscript received March 24, 2007; revised manuscript received May 10, 2007; accepted May 10, 2007.</p>
    </body>
  </sub-article>
</article>
