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Thread: DNP information

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    Andy13's Avatar
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    DNP information

    Hopefully this will clear up some misinformatio on DNP .


    Even on high dose of DNP, the majority of ATP is STILL made via oxidative phosphorilation. A lot of people think that DNP completely eliminates oxidative phosphorilation and that cellular ATP synthesis relies exclusively on substrate level phosphorilation. Actually though, DNP just makes oxidative phosphorilation a LITTLE less efficient. ATP levels in cells really don't change that much. Previously in many biochemistry books, ATP is listed as an important metabolic regulator. In reality, ATP isn't an important regulator since the energy charge of a cell doesn't change all that much. What IS an important metabolic regulator is AMP. And what DNP does do is keep AMP levels high enough to keep green lights going on all glycolytic and TCA enzymes.

    Incedentally, the high AMP levels inhibit glycogen synthesis in liver as well as muscle. This means that glucagon and epinephrine dominate over insulin . While this is great for fat loss, it isn't so great for muscle preservation since glucagon also stimulates the liver to make glucose out of amino acids (gluconeogenesis) derived from muscle tissue. Hence DNP being "anti-proteolytic" isn't a great assumption.

    DNP does not directly stimulate muscle breakdown however the effects that it causes in the body certainly promote muscle breakdown. This can somewhat be reduced if dietary carbohydrate and protein intake is kept high. I might also add that the causes of death from DNP is not a result of low ATP but, rather, from the extreme heat that DNP causes.

    As far as limiting factors with DNP and fat loss, well, there aren't any. In a test tube with mitochondria, oxygen becomes the limiting factor. However this is not the case in vivo since the levels of DNP used for the in vitro tests are far beyond what would be lethal in a human body.


    Andy

  2. #2
    CYCLEON Guest
    Good stuff Andy - some questions for you - especially since im on crystal right now

    1) If o2 is a limiting factor then presumably bronchial dilation, enhancing o2 uptake would be beneficial while on DNP , besides its effects on thermogenesis and beta2&3 agonism

    2) If ATP isn’t the primary regulator then at what point does the AMP levels increase enough to send inhibitory signals to the thyroid?

    3) Would pyruvate supplementation (as well as proper carbs or fructose) - so as to have some sort of bypass - be of any assistance in keeping up levels so as help prevent muscle catabolism?

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    Andy13's Avatar
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    Originally posted by CYCLEON
    Good stuff Andy - some questions for you - especially since im on crystal right now

    1) If o2 is a limiting factor then presumably bronchial dilation, enhancing o2 uptake would be beneficial while on DNP , besides its effects on thermogenesis and beta2&3 agonism

    2) If ATP isn’t the primary regulator then at what point does the AMP levels increase enough to send inhibitory signals to the thyroid?

    3) Would pyruvate supplementation (as well as proper carbs or fructose) - so as to have some sort of bypass - be of any assistance in keeping up levels so as help prevent muscle catabolism?
    Did you get that pm I sent you a while ago here?

    O2 is only the limiting factor in a TEST TUBE. There's no limiting factor in a human, unless, of course that human is doing some kind of moderate to high intensity cardio which he shouldn't be!!

    Pyruvate supplementation as well as carbs will help SOME with muscle catabolism but, ultimatly, it's inevitable when the liver cannot store glycogen.

    Andy

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