NO-inducing component of Lit-Up?

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    NO-inducing component of Lit-Up?


    I'm curious to try this product and have read about it here and on the company site. It does mentions a nitric oxide part, but I am unclear what ingredient you are using to induce NO production and also why arginine wasn't used when it is used in another one of your products.
    Thank you!

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    I just ordered a bottle of Lit-Up but was wondering the same thing. I am planning to stack it with NO2 Black by MRI as a preworkout combination. Any problems or issues with this?
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    This product is more about test boosting, focus, and bigger/better reps IMO. Curious about the NO since it is mentioned though.

    Although I won't dispute arginine being good for pumps, it's NO producing qualities have been proven to be less than efficient.

    I logged this product, then ordered two tubs cuz I think it's that good. I did stack some creatine with it and did not miss a thing. Had pump, vascularity, etc. Even started feeling really full 24/7 in the pec and shoulder regions.
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    Quote Originally Posted by besherman View Post
    I just ordered a bottle of Lit-Up but was wondering the same thing. I am planning to stack it with NO2 Black by MRI as a preworkout combination. Any problems or issues with this?
    I don't see anything wrong with stacking it but also think it's a waste of money. For me, a good preworkout meal and some BCAA's during your workout accomplish the same thing.
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    Quote Originally Posted by ccnAbolic View Post
    Although I won't dispute arginine being good for pumps, it's NO producing qualities have been proven to be less than efficient.
    I should preface this by saying my entire PhD thesis was written on the role of nitric oxide in schizophrenia. And while nNOS is a different enzyme from eNOS, both isomers produce NO the same way. There are other cofactors involved, but the basic reaction is the conversion of arginine to nitric oxide and citrulline.

    As for the benefits of NO in pre-workout drinks, THAT I think can be debated, but I was just curious because they do mention nitric oxide in the description.
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    Quote Originally Posted by Aleksandar37 View Post
    I should preface this by saying my entire PhD thesis was written on the role of nitric oxide in schizophrenia. And while nNOS is a different enzyme from eNOS, both isomers produce NO the same way. There are other cofactors involved, but the basic reaction is the conversion of arginine to nitric oxide and citrulline.

    As for the benefits of NO in pre-workout drinks, THAT I think can be debated, but I was just curious because they do mention nitric oxide in the description.
    I will be getting back to you with a 100% accurate answer to it all shortly and possibly even have the product formulator himself come in the thread to talk with you about.
    - Join Me: Tex89 M-Sten RX Log... Dicing that iron -
    http://anabolicminds.com/forum/cycle-info/222790-tex89s-msten-rx.html
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    Quote Originally Posted by TexasLifter89 View Post
    I will be getting back to you with a 100% accurate answer to it all shortly and possibly even have the product formulator himself come in the thread to talk with you about.
    That would rock! Thank you! Also, sorry to ccnAbolic if my post seemed harsh. Looking at how I worded it, it makes me sound like an arrogant prick and that wasn't my intention..this time lol. Just after having spent my whole thesis on this stuff and about 4 hours of a defense on it, I'm still suffering from nitric oxide PTSD.
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    ive already sent the email out tex.
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    Quote Originally Posted by Aleksandar37 View Post
    That would rock! Thank you! Also, sorry to ccnAbolic if my post seemed harsh. Looking at how I worded it, it makes me sound like an arrogant prick and that wasn't my intention..this time lol. Just after having spent my whole thesis on this stuff and about 4 hours of a defense on it, I'm still suffering from nitric oxide PTSD.
    No worries. I didn't think you came off arrogant. A prick, maybe I keed, I keed. Plus, since you repped me, I figured it wasn't where you were coming from.

    Always good to have people on here who can speak to the science...
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    Quote Originally Posted by Aleksandar37 View Post
    That would rock! Thank you! Also, sorry to ccnAbolic if my post seemed harsh. Looking at how I worded it, it makes me sound like an arrogant prick and that wasn't my intention..this time lol. Just after having spent my whole thesis on this stuff and about 4 hours of a defense on it, I'm still suffering from nitric oxide PTSD.
    Here you go Alek, hope this helps!








    Theriogenology. 2007 Jan 15;67(2):249-54. Epub 2006 Sep 22.

    D-Aspartic acid and nitric oxide as regulators of androgen production in boar testis.
    Lamanna C, Assisi L, Vittoria A, Botte V, Di Fiore MM.

    Department of Life Sciences, Second University of Naples, via Vivaldi 43, 81100 Caserta, Italy.

    Abstract

    D-Aspartic acid (D-Asp) and nitric oxide (NO) are two biologically active molecules playing important functions as neurotransmitters and neuromodulators of nerve impulse and as regulators of hormone production by endocrine organs. We studied the occurrence of D-Asp and NO as well as their effects on testosterone synthesis in the testis of boar. This model was chosen for our investigations because it contains more Leydig cells than other mammals. Indirect immunofluorescence applied to cryostat sections was used to evaluate the co-localization of D-Asp and of the enzyme nitric oxide synthase (NOS) in the same Leydig cells. D-Asp and NOS often co-existed in the same Leydig cells and were found, separately, in many other testicular cytotypes. D-Asp level was dosed by an enzymatic method performed on boar testis extracts and was 40+/-3.6 nmol/g of fresh tissue. NO measurement was carried out using a biochemical method by NOS activity determination and expressed as quantity of nitrites produced: it was 155.25+/-21.9 nmol/mg of tissue. The effects of the two molecules on steroid hormone production were evaluated by incubating testis homogenates, respectively with or without D-Asp and/or the NO-donor L-arginine (L-Arg). After incubation, the testosterone presence was measured by immunoenzymatic assay (EIA). These in vitro experiments showed that the addition of D-Asp to incubated testicular homogenates significantly increased testosterone concentration, whereas the addition of L-Arg decreased the hormone production. Moreover, the inclusion of L-Arg to an incubation medium of testicular homogenates with added D-Asp, completely inhibited the stimulating effects of this enantiomer. Our results suggest an autocrine action of both D-Asp and NO on the steroidogenetic activity of the Leydig cell.

    Reprod Biol Endocrinol. 2008 Jul 4;6:28.

    Opposing effects of D-aspartic acid and nitric oxide on tuning of testosterone production in mallard testis during the reproductive cycle.
    Di Fiore MM, Lamanna C, Assisi L, Botte V.

    Department of Life Sciences, Second University of Naples, via Vivaldi 43, 81100 Caserta, Italy. MariaM.difiore@unina2.it

    Abstract
    D-Aspartic acid (D-Asp) and nitric oxide (NO) play an important role in tuning testosterone production in the gonads of male vertebrates. In particular, D-Asp promotes either the synthesis or the release of testosterone, whereas NO inhibits it. In this study, we have investigated for the first time in birds the putative effects of D-Asp and NO on testicular testosterone production in relation to two phases of the reproductive cycle of the adult captive wild-strain mallard (Anas platyrhynchos) drake. It is a typical seasonal breeder and its cycle consists of a short reproductive period (RP) in the spring (April-May) and a non reproductive period (NRP) in the summer (July), a time when the gonads are quiescent. The presence and the localization of D-Asp and NO in the testis and the trends of D-Asp, NO and testosterone levels were assessed during the main phases of the bird's reproductive cycle. Furthermore, in vitro experiments revealed the direct effect of exogenously administered D-Asp and NO on testosterone steroidogenesis.
    METHODS: By using immunohistochemical (IHC) techniques, we studied the presence and the distributional pattern of D-Asp and NO in the testes of RP and NRP drakes. D-Asp levels were evaluated by an enzymatic method, whereas NO content, via nitrite, was assessed using biochemical measurements. Finally, immunoenzymatic techniques determined testicular testosterone levels.
    RESULTS: IHC analyses revealed the presence of D-Asp and NO in Leydig cells. The distributional pattern of both molecules was in some way correlated to the steroidogenic pathway, which is involved in autocrine testosterone production. Indeed, whereas NO was present only during the NRP, D-Asp was almost exclusively present during the RP. Consistently, the high testosterone testicular content occurring during RP was coupled to a high D-Asp level and a low NO content in the gonad. By contrast, in sexually inactive drakes (NRP), the low testosterone content in the gonad was coupled to a low D-Asp content and to a relatively high NO level. Consequently, to determine the exogenous effects of the two amino acids on testosterone synthesis, we carried out in vitro experiments using testis sections deriving from both the RP and NRP. When testis slices were incubated for 60 or 120 min with D-Asp, testosterone was enhanced, whereas in the presence of L-Arg, a precursor of NO, it was inhibited.
    CONCLUSION: Our results provide new insights into the involvement of D-Asp and NO in testicular testosterone production in the adult captive wild-strain mallard drake. The localization of these two molecules in the Leydig cells in different periods of the reproductive cycle demonstrates that they play a potential role in regulating local testosterone production.
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    I too got a chance to log LIT-UP and liked it so much that I ordered 2 more tubs also. I took it with creatine mono also. I had the best mind-muscle connection off of this product and great fucus and endurance while useing this product. I got stronger and leaner which is a winning combo in my book. About a week or so in, I noticed I was getting more vascular and it took off from there. I think you will enjoy it. I see no need to stack with other stims but if thats what you want to do then have at it.
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    Quote Originally Posted by chubbarock View Post
    Here you go Alek, hope this helps!

    Thank you for the response, but I'm sorry as it doesn't answer my question.
    I'm referring to this from the writeup for Lit-up : "•NO/H²S Pathway: Lit-Up™ takes the latest scientific research available to a whole new level by utilizing the synergism of the Hydrogen Sulfide (H²S) Nitric Oxide (NO) pathways: allowing for a huge increase in nutrient flow to target muscle tissue. The product also uses a unique nootropic/stimulant blend that allows for more targeted enhancement of the mind-muscle connection and greater neuromuscular strength."

    This suggests activation of eNOS and that study you cited points to NO actually decreasing T levels. I'm asking what ingredient in Lit-up is driving the NOS enzyme? Thanks.
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    Quote Originally Posted by chubbarock View Post
    Here you go Alek, hope this helps!
    Just to clarify- this study helps explain the linkage between NO, DAA, and the NMDA receptor- I will elaborate at the bottom....

    Endocrinology. 2010 Jun;151(6):2723-35. Epub 2010 Apr 6.

    Phosphorylation of N-methyl-D-aspartic acid receptor-associated neuronal nitric oxide synthase depends on estrogens and modulates hypothalamic nitric oxide production during the ovarian cycle.
    Parkash J, d'Anglemont de Tassigny X, Bellefontaine N, Campagne C, Mazure D, Buée-Scherrer V, Prevot V.

    Institut National de la Santé et de la Recherche Médicale, Unité, Bâtiment Biserte, Place de Verdun, 59045 Lille cedex, France.

    Abstract
    Within the preoptic region, nitric oxide (NO) production varies during the ovarian cycle and has the ability to impact hypothalamic reproductive function. One mechanism for the regulation of NO release mediated by estrogens during the estrous cycle includes physical association of the calcium-activated neuronal NO synthase (nNOS) enzyme with the glutamate N-methyl-d-aspartate (NMDA) receptor channels via the postsynaptic density 95 scaffolding protein. Here we demonstrate that endogenous variations in estrogens levels during the estrous cycle also coincide with corresponding changes in the state of nNOS Ser1412 phosphorylation, the level of association of this isoform with the NMDA receptor/postsynaptic density 95 complex at the plasma membrane, and the activity of NO synthase (NOS). Neuronal NOS Ser1412 phosphorylation is maximal on the afternoon of proestrus when both the levels of estrogens and the physical association of nNOS with NMDA receptors are highest. Estradiol mimicked these effects in ovariectomized (OVX) rats. In addition, the catalytic activity of NOS in membrane protein extracts from the preoptic region, i.e. independent of any functional protein-protein interactions or cell-cell signaling, was significantly increased in estradiol-treated OVX rats compared with OVX rats. Finally, lambda phosphatase-mediated nNOS dephosphorylation dramatically impaired NOS activity in preoptic region protein extracts, thus demonstrating the important role of phosphorylation in the regulation of NO production in the preoptic region. Taken together, these results yield new insights into the regulation of neuron-derived NO production by gonadal steroids within the preoptic region and raise the possibility that changes in nNOS phosphorylation during fluctuating physiological conditions may be involved in the hypothalamic control of key neuroendocrine functions, such as reproduction.

    Basically how this works- nNOS enzyme are cross-linked to channels on the NMDA receptor. When the NMDA receptor is activated by its co-ligands at NR-1 and NR-2 (glycine binding site and NMDA binding site, respectively), it is connected to the nNOS enzyme via the postsynaptic density 95 scaffolding protein. When NMDA receptor activity is increased due to binding, nNOS Ser1412 phosphorylation is upregulated, thus increasing NO production in the pre-optic region. The above example was in response to estrogen, but a variety of stimulii can cause this type of reaction in the NMDA receptor.....it more or less simply has to be bound at NR-2, or both NR-1 and NR-2
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
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    Quote Originally Posted by Aleksandar37 View Post
    Thank you for the response, but I'm sorry as it doesn't answer my question.
    I'm referring to this from the writeup for Lit-up : "•NO/H²S Pathway: Lit-Up™ takes the latest scientific research available to a whole new level by utilizing the synergism of the Hydrogen Sulfide (H²S) Nitric Oxide (NO) pathways: allowing for a huge increase in nutrient flow to target muscle tissue. The product also uses a unique nootropic/stimulant blend that allows for more targeted enhancement of the mind-muscle connection and greater neuromuscular strength."

    This suggests activation of eNOS and that study you cited points to NO actually decreasing T levels. I'm asking what ingredient in Lit-up is driving the NOS enzyme? Thanks.
    D-Aspartic Acid- and yes the above studies do reference NO actually decreasing test levels- the point I am trying to make-Lit-Up is more suitable as a product for muscle-building and strength enhancement vs. many other products that just enhance NO, simply because while it does increase the activity of both NO and Hydrogen sulfide, it also increases testosterone levels, while arginine and some other NO increasers have no effect on this parameter, or may actually have detrimental effects......

    I can see where there is confusion- I never mentioned which type of NOS is effected- you are assuming eNOS (endothelial), while DAA has an effect on nNOS (neural)
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
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    Quote Originally Posted by rms80 View Post
    I can see where there is confusion- I never mentioned which type of NOS is effected- you are assuming eNOS (endothelial), while DAA has an effect on nNOS (neural)
    Indeed. I was going off this from the write up: "allowing for a huge increase in nutrient flow to target muscle tissue." To me that suggests eNOS activation which is the selling point for others, although I don't really need or agree with the selling point of other products. That you so much for clearing that up for me.

    I'm currently running a Drive/RPM/Neovar/IGF2 stack (suggested by Rosie who rocks!!!) after having run an epistane cycle. It's only day one, so I'll let you know how it goes and if everything goes well will run it again, possible replacing RPM with Lit-up. Thank you again!
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    Quote Originally Posted by Aleksandar37 View Post
    Indeed. I was going off this from the write up: "allowing for a huge increase in nutrient flow to target muscle tissue." To me that suggests eNOS activation which is the selling point for others, although I don't really need or agree with the selling point of other products. That you so much for clearing that up for me.

    I'm currently running a Drive/RPM/Neovar/IGF2 stack (suggested by Rosie who rocks!!!) after having run an epistane cycle. It's only day one, so I'll let you know how it goes and if everything goes well will run it again, possible replacing RPM with Lit-up. Thank you again!
    And that is def. what it looks like in the write-up- I can see where it is confusing- most people don't understand the difference between eNOS and nNOS- so this is actually the first time it came up- my apologies and thx for pointing it out- there is a sizeable difference between the two
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
  

  
 

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