4.3 Article

Molecular Regulation of Exercise Induced Muscle Fiber Hypertrophy

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COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a029751

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资金

  1. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [T32HD071866] Funding Source: NIH RePORTER
  2. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK079626] Funding Source: NIH RePORTER
  3. NATIONAL INSTITUTE ON AGING [F32AG058380] Funding Source: NIH RePORTER
  4. NCRR NIH HHS [M01 RR000032] Funding Source: Medline
  5. NIA NIH HHS [F32 AG058380, R01 AG046920] Funding Source: Medline
  6. NICHD NIH HHS [P2C HD086851, T32 HD071866] Funding Source: Medline
  7. NIDDK NIH HHS [P30 DK079626] Funding Source: Medline

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Skeletal muscle hypertrophy is a widely sought exercise adaptation to counteract the muscle atrophy of aging and disease, or to improve athletic performance. While this desired muscle enlargement is a well-known adaptation to resistance exercise training (RT), the mechanistic underpinnings are not fully understood. The purpose of this review is thus to provide the reader with a summary of recent advances in molecular mechanisms-based on the most current literature-that are thought to promote RT-induced muscle hypertrophy. We have therefore focused this discussion on the following areas of fertile investigation: ribosomal function and biogenesis, muscle stem (satellite) cell activity, transcriptional regulation, mechanotransduction, and myokine signaling.

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