Regulatory mechanisms of skeletal muscle protein turnover during exercise

Adam John Rose, Erik A. Richter

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

    48 Citationer (Scopus)

    Abstract

    Skeletal muscle protein turnover is a relatively slow metabolic process that is altered by various physiological stimuli such as feeding/fasting and exercise. During exercise, catabolism of amino acids contributes very little to ATP turnover in working muscle. With regards to protein turnover, there is now consistent data from tracer studies in rodents and humans showing that global protein synthesis is blunted in working skeletal muscle. Whether there is altered skeletal muscle protein breakdown during exercise remains unclear. The blunting of protein synthesis is believed to be mediated by suppressed mRNA translation initiation and elongation steps involving, but not limited to, changes in eIF4E-binding protein 1 (4EBP1) and eukaryotic elongation factor-2 phosphorylation (eEF2), respectively. Evidence is provided that upstream signaling to translation factors is mediated by signaling downstream of changes in intracellular Ca(2+) and energy turnover. In particular, a signaling cascade involving Ca(2+)-calmodulin-eEF2 kinase-eEF2 is implicated. The possible functional significance of altered protein turnover in working skeletal muscle during exercise is discussed. Further work with available and new techniques will undoubtedly reveal the functional significance and signaling mechanisms behind changes in skeletal muscle protein turnover during exercise. Key words: Exercise, skeletal muscle, protein metabolism, translation.
    OriginalsprogEngelsk
    TidsskriftJournal of Applied Physiology
    Vol/bind106
    Udgave nummer5
    Sider (fra-til)1702-1711
    Antal sider10
    ISSN8750-7587
    DOI
    StatusUdgivet - 2009

    Bibliografisk note

    CURIS 2009 5200 035

    Citationsformater