The latest on arachidonic acid, translated by ergogenics.org

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    Thumbs up The latest on arachidonic acid, translated by ergogenics.org


    William Llewellyn was right. About ten years ago Llewellyn invented the theory that the fatty acid arachidonic acid be a key factor in muscle growth could be. Llewellyn took a supplement containing arachidonic acid in the market, and funded a study that although no anabolic effect discovered, but ergogenic effects demonstrated. Yet this anabolic effect is probably, according to researchers at the University of Auckland in New Zealand.The body converts the n-6 fatty acid linoleic acid to gamma-linolenic acid or GLA , GLA and then to arachidonic acid. Arachidonic acid is another precursor of hormone-like signal substances such as PGE2 and PGF2a. How exactly, that you see below.Arachidonic acid has a bad reputation. The fatty acid, or rather its metabolites, could boost inflammation, and thus responsible for the negative effects of a diet with excess n-6 fatty acids. Llewellyn has always stressed that it is not so simple. Some metabolites of arachidonic acid inhibit inflammation correct. [vpxsports.com January 4, 2013]Llewellyns business Molecular Nutrition sponsored seven years ago a study in which young bodybuilders arachidonic acid were administered. Their anaerobic capacity increased substantially, but the subjects were not muscular. Published in January 2013 the New Zealand researcher James Mark Worth a test tube study showing the Llewellyns theory indeed makes sense.Mark Worth suggested C2C12 muscle cells exposed to different concentrations of arachidonic acid. The higher the concentration, the thicker, the muscle fibers that the cells formed, and the more protein laid them down.Exposure to arachidonic acid inhibited the increase in the total number of muscle fibers, says the figure left. Click on it for a bigger version. Dark bars = muscle cells exposed to arachidonic acid.Right, you see that arachidonic acid resulted in an increase in the number of muscle fibers bigger - with more than five nuclei. This means that arachidonic muscle fibers bigger late.The researchers repeated their experiments with compounds containing the COX-2 enzyme. COX-2 converts arachidonic acid into PGE2 . By blocking these remained almost nothing about the anabolic effect of arachidonic acid. Experiments with a non-metabolizable version of arachidonic acid also yielded nothing." The Findings of the present study show That an Increased availability of free arachidonic acid and Subsequent metabolism by the COX-2 pathway just have a stimulatory effect on in vitro skeletal muscle cell growth , "the researchers conclude.Source: Am J Physiol Cell Physiol. 2013 Jan 1, 304 (1): C56-67.Celstudie: meer arachidonzuur, meer spiergroei
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    What was used to translate this? - The OG content was in Dutch, the translation is very hard to read and incoherent.

    Here's the pertinent study's abstract in it's original English:

    Am J Physiol Cell Physiol. 2013 Jan 1;304(1):C56-67. doi: 10.1152/ajpcell.00038.2012. Epub 2012 Oct 17.
    Arachidonic acid supplementation enhances in vitro skeletal muscle cell growth via a COX-2-dependent pathway.

    Markworth JF, Cameron-Smith D.
    Source

    School of Exercise and Nutrition Science, Deakin University, Melbourne, Australia.

    Abstract

    Arachidonic acid (AA) is the metabolic precursor to a diverse range of downstream bioactive lipid mediators. A positive or negative influence of individual eicosanoid species [e.g., prostaglandins (PGs), leukotrienes, and hydroxyeicosatetraenoic acids] has been implicated in skeletal muscle cell growth and development. The collective role of AA-derived metabolites in physiological states of skeletal muscle growth/atrophy remains unclear. The present study aimed to determine the direct effect of free AA supplementation and subsequent eicosanoid biosynthesis on skeletal myocyte growth in vitro. C2C12 (mouse) skeletal myocytes induced to differentiate with supplemental AA exhibited dose-dependent increases in the size, myonuclear content, and protein accretion of developing myotubes, independent of changes in cell density or the rate/extent of myogenic differentiation. Nonselective (indomethacin) or cyclooxygenase 2 (COX-2)-selective (NS-398) nonsteroidal anti-inflammatory drugs blunted basal myogenesis, an effect that was amplified in the presence of supplemental free AA substrate. The stimulatory effects of AA persisted in preexisting myotubes via a COX-2-dependent (NS-389-sensitive) pathway, specifically implying dependency on downstream PG biosynthesis. AA-stimulated growth was associated with markedly increased secretion of PGF(2α) and PGE(2); however, incubation of myocytes with PG-rich conditioned medium failed to mimic the effects of direct AA supplementation. In vitro AA supplementation stimulates PG release and skeletal muscle cell hypertrophy via a COX-2-dependent pathway.

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    Quote Originally Posted by Resolve View Post
    What was used to translate this? - The OG content was in Dutch, the translation is very hard to read and incoherent.

    Here's the pertinent study's abstract in it's original English:

    Am J Physiol Cell Physiol. 2013 Jan 1;304(1):C56-67. doi: 10.1152/ajpcell.00038.2012. Epub 2012 Oct 17.
    Arachidonic acid supplementation enhances in vitro skeletal muscle cell growth via a COX-2-dependent pathway.

    Markworth JF, Cameron-Smith D.
    Source

    School of Exercise and Nutrition Science, Deakin University, Melbourne, Australia.

    Abstract

    Arachidonic acid (AA) is the metabolic precursor to a diverse range of downstream bioactive lipid mediators. A positive or negative influence of individual eicosanoid species [e.g., prostaglandins (PGs), leukotrienes, and hydroxyeicosatetraenoic acids] has been implicated in skeletal muscle cell growth and development. The collective role of AA-derived metabolites in physiological states of skeletal muscle growth/atrophy remains unclear. The present study aimed to determine the direct effect of free AA supplementation and subsequent eicosanoid biosynthesis on skeletal myocyte growth in vitro. C2C12 (mouse) skeletal myocytes induced to differentiate with supplemental AA exhibited dose-dependent increases in the size, myonuclear content, and protein accretion of developing myotubes, independent of changes in cell density or the rate/extent of myogenic differentiation. Nonselective (indomethacin) or cyclooxygenase 2 (COX-2)-selective (NS-398) nonsteroidal anti-inflammatory drugs blunted basal myogenesis, an effect that was amplified in the presence of supplemental free AA substrate. The stimulatory effects of AA persisted in preexisting myotubes via a COX-2-dependent (NS-389-sensitive) pathway, specifically implying dependency on downstream PG biosynthesis. AA-stimulated growth was associated with markedly increased secretion of PGF(2α) and PGE(2); however, incubation of myocytes with PG-rich conditioned medium failed to mimic the effects of direct AA supplementation. In vitro AA supplementation stimulates PG release and skeletal muscle cell hypertrophy via a COX-2-dependent pathway.

    Hey Resolve, long time no see we are just now back at AM!

    We simply used Google Chrome's translate feature.

    Typically, ergolog translates everything from ergogenics... for reasons unknown to us, this article was never published on the english site only the Dutch site.
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    Good to have ya back. It's a promising study. Always been a fan of X-Factor.
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    Quote Originally Posted by Resolve View Post
    Good to have ya back. It's a promising study. Always been a fan of X-Factor.
    Thanks for your support of XF, and congrats on being w BPS. Matt is great people!
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