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Intermittent Reloading Attenuates Muscle Atrophy through Modulating Akt/mTOR Pathway

  • Autores: Mitsunori Miyazaki, Miho Noguchi, Tohru Takemasa
  • Localización: Medicine & Science in Sports & exercise: Official Journal of the American College of Sports Medicine, ISSN 0195-9131, Vol. 40, Nº. 5, 2008, págs. 848-855
  • Idioma: inglés
  • Texto completo no disponible (Saber más ...)
  • Resumen
    • Purpose: The aim of this study is to investigate the effects of intermittent reloading during hindlimb unloading (HU) on the changes in intracellular signaling pathways in skeletal muscle.

      Methods: Male Wister rats were divided randomly into one of three experimental groups: 1) nonsuspended control, 2) HU for 7 d, and 3) HU with intermittent reloading (HU/IR) for 4 h[middle dot]d-1. After each experimental period, the antigravitational soleus muscle was analyzed.

      Results: After 7 d of HU treatment, muscle fiber atrophy (decrease in relative muscle mass: 0.28 mg[middle dot]g-1 in the HU group vs 0.36 mg[middle dot]g-1 in the control group, P < 0.05; decrease in fiber CSA: 1682.6 [mu]m2 in the HU group vs 2673.0 [mu]m2 in the control group, P < 0.05) and a decrease in phosphorylation levels of anabolic signaling pathway (Akt and mTOR) were observed. Additionally, expressions of two types of muscle-specific E3 ubiquitin ligase mRNA (muscle atrophy F-box (MAFbx), and muscle ring finger 1 (MuRF1)) were upregulated during muscle atrophy. Increases in binding activities of nuclear factor kappa B (NF[kappa]B) were also determined. In contrast, IR treatment attenuated the muscle fiber atrophy (0.33 mg[middle dot]g-1 and 2067.5 [mu]m2) and partially increased the phosphorylation levels of anabolic signaling molecules. Expression of MAFbx and MuRF1 mRNA were returned to the control level, and binding activities of nuclear NF[kappa]B was suppressed with the effects of IR.

      Conclusion: These results suggest that IR-induced attenuation of skeletal muscle atrophy is achieved by the synergy between increased anabolic and decreased catabolic signaling mechanisms.


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