CEL EPI-PLEX Promo

koi1214

koi1214

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CEL.Epi.Plex.Rendering.300dpi.jpg

CEL_Epi.Plex_Label_Supp_Facts_.jpg

We need 2 loggers to try our Epi-Plex.

Here's how it will work!!


1.Simply post any picture,video or photoshopped pic with you and ANYTHING CEL related(NO PH"S)
OR
2.Post a video of what motivates you to work harder or post a video to motivate others


**Get Creative! Include pics, vids, show your personality, share your workouts, etc!***



PRODUCT LOG REQUIREMENTS:
1. Must have a USA Mailing Address.
2. Must be 18+ years of age.
3. Must be in good health with no known medical conditions.
4. Must do a Full Log in the Supplements Log section.
5. Must update at least 3 times a week/post final review
6. Can you post before/After pics?


Winners to be announced Saturday 5/30/2015
 
koi1214

koi1214

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The Science Behind Epi-Plex

At Competitive Edge Labs, we don’t just selectively pick out information from research studies to just support the marketing and sales of our products. Our research is intensive and involves the meticulous scrutinizing of available data, including breakthrough landmark papers as well as potentially overlooked prior studies. We understand that there are many consumers that aren’t science minded and simply want to know what a product does and how it benefits them; however, we also understand that there are science minded consumers that wish to learn the pharmacology of supplements and may be frustrated at the strong emphasis on marketing and picking and choosing of research information hand-picked to support marketing efforts. It is easy to pull claims from studies and research papers but not so easy to delve further and identify the ‘how’s’ and ‘why’s’.

(-)-Epicatechin is a very popular ingredient but as of yet, there doesn’t appear to be very comprehensive elaboration as to the mechanisms of action of -(-) epicatechin which essentially limits the true exploitation of its benefits as a supplement. Yes, there are studies that show a decrease in Myostatin, an increase in Follistatin, and increase in NO and exercise performance, but how does it do these things?

Let Competitive Edge Labs be the first to provide you with this information and enlighten you.

Increased Muscle Endurance via Enhanced PGC-1alpha activity

Epicatechin holds demonstrated capability to stimulate the nuclear translocation and activation of known transcriptional modulators of super oxide dismutase-2 and catalase (1-7). Of particular interest is the capacity to increase activation and translocation of one these transcriptional modulators known as peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1 alpha) (3-7). This activity is seemingly a proven mechanistic role in the increased skeletal muscle endurance observed in research (8-10) and increasingly through anecdote. Experimental and animal research models testing the cellular activity of endurance exercise have identified PGC-1 alpha as the intracellular mediator of skeletal muscle fiber composition remodeling (11-13). It has been observed that increased PGC-1 alpha activation and translocation decreases the ratio of the type IIb fibers to the type I and type IIa fibers (14,15). This recomposition essentially mediates skeletal muscle adaptations to resistance and endurance exercise by reducing the rate of metabolic oxidation in the muscle cells which translates to increased resistance to fatigue (15-18).

Increased Muscle Endurance via Improved Calcium Tolerance of Mitochondria

Epicatechin is capable of increasing resistance to calcium-induced mitochondrial swelling in muscle (19,20). This activity appears to be mediated through increasing membrane rigidity and integrity through increasing expression of proteins mitofilin and porin (9,20). By increasing these, muscle cell resistance is augmented reducing vulnerability to acute and chronic exercise induced damage, metabolic stress and consequential impaired ATP synthesis (21,22). In fact new research suggests that not only does epicatechin protect the mitochondria through these mechanisms, it can directly influence mitochondrial function to stimulate and maintain cellular respiration and optimize ATP synthesis (23). These mechanisms, as well as the capacity enhance PGC1-alpha activity, may provide the mode of action for increased muscle endurance to exercise observed with (-)-epicatechin supplementation.

Increase Follistatin via Inhibition of DNA Methylation

There is evidence that indicates that epicatechin can indirectly inhibit DNA methylation through its COMT metabolism that increases formation of potent non-competitive inhibitor of DNA methylation enzymes (24-26). DNA methylation decreases gene transcriptional activation by physically impeding the transcriptional proteins binding to the gene loci (27-29). It can also do this through the formation of methyl-CpG-binding domain proteins which bind DNA and inactivate gene promoter regions (28-31). Follistatin promoter regions are particularly sensitive to DNA methylation enzymes which can restrict expression of the peptide and ultimately can potentially attenuate follistatin secretion (32). Evidence suggests that inhibiting enzymes that mediate DNA methylation can potentially increase follistatin expression up to 17 fold after one week (32).Biochemical studies on muscles during acute exercise have associated DNA hypo methylation with increased expression of PGC-1 alpha (33,34) which, as previously mentioned, can also be increased by epicatechin. Other research has identified that long term exercise induced adaptations are associated with expression of polymorphic enzymes that result in DNA hypo methylation and ultimately promote myogenesis (35-37). Therefore, it would certainly seem viable that inhibiting DNA methylation could serve as a potential target for increasing muscle mass and athletic performance. Although this has not been specifically tested, this activity may impart mechanistic explanation for the decrease in myostatin and increase in follistatin observed with epicatechin supplementation.

Increase Follistatin via Augmenting Nitric Oxide Signalling
(-)-Epicatechin is capable of augmenting nitric oxide via activating the skeletal muscle expressed neuronal nitric oxide synthase (nNOS) (9,38) and also through inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) by its O-methyl metabolites (39). It has been proposed that former is directly activated via a novel cell surface receptor in skeletal muscle which mediates an intracellular cascade that results in increased NO production (40). Together these mechanisms are active both with and without exercise and are associated with the acute augmentation of NO observed with (-)-epicatechin supplementation (41,42). Although this activity does not appear to be largely active for increasing muscular endurance observed with (-)-epicatechin, it may play an indirect role in the myogenic potential(9). This may occur by compensating NO scavenged by myoglobin (41,44) and preserving Dynamin type-1 protein (DRP-1) (45) as well as promoting S-nitrosylation and inactivation of class II histone deacetylases (38,46-47). Hypothetically these effects may promote the prior mentioned skeletal muscle remodeling and the increased expression of follistatin (46,47).
 
Last edited:
fightbackhxc

fightbackhxc

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Ah yea. Nice to see this added to the portfolio!
 
N

NewAgeMayan

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Is there still a bit more to come of the write-up? Not talking about the references, but the end of koi's 2nd post appears to be incomplete (was there a section on NO signaling intended?)
 
furion

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...the rest (and references)

(-)-Epicatechin is capable of augmenting nitric oxide via activating the skeletal muscle expressed neuronal nitric oxide synthase (nNOS) (9,38) and also through inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) by its O-methyl metabolites (39). It has been proposed that former is directly activated via a novel cell surface receptor in skeletal muscle which mediates an intracellular cascade that results in increased NO production (40). Together these mechanisms are active both with and without exercise and are associated with the acute augmentation of NO observed with (-)-epicatechin supplementation (41,42). Although this activity does not appear to be largely active for increasing muscular endurance observed with (-)-epicatechin, it may play an indirect role in the myogenic potential(9). This may occur by compensating NO scavenged by myoglobin (41,44) and preserving Dynamin type-1 protein (DRP-1) (45) as well as promoting S-nitrosylation and inactivation of class II histone deacetylases (38,46-47). Hypothetically these effects may promote the prior mentioned skeletal muscle remodelling and the increased expression of follistatin (46,47).


Li, Y. M., Chan, H. Y. E., Huang, Y., & Chen, Z. Y. (2007). Green tea catechins upregulate superoxide dismutase and catalase in fruit flies. Molecular nutrition & food research, 51(5), 546-554.
Charles, A. L., Meyer, A., Dal‐Ros, S., Auger, C., Keller, N., Ramamoorthy, T. G., & ...Geny, B. (2013). Polyphenols prevent ageing‐related impairment in skeletal muscle mitochondrial function through decreased reactive oxygen species production. Experimental physiology, 98(2), 536-545.
Moreno-Ulloa, A., Nogueira, L., Rodriguez, A., Barboza, J., Hogan, M. C., Ceballos, G.,... & Ramirez-Sanchez, I. (2014). Recovery of Indicators of Mitochondrial Biogenesis, Oxidative Stress, and Aging With (−)-Epicatechin in Senile Mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, glu131.
Ramirez‐Sanchez, I., De los Santos, S., Gonzalez‐Basurto, S., Canto, P., Mendoza‐Lorenzo, P., Palma‐Flores, C., ... & Coral‐Vazquez, R. (2014). (–)‐Epicatechin improves mitochondrial‐related protein levels and ameliorates oxidative stress in dystrophic δ‐sarcoglycan null mouse striated muscle. FEBS Journal, 281(24), 5567-5580.
Shay, J., Elbaz, H. A., Lee, I., Zielske, S. P., Malek, M. H., & Hüttemann, M. (2015). Molecular Mechanisms and Therapeutic Effects of (−)-Epicatechin and Other Polyphenols in Cancer, Inflammation, Diabetes, and Neurodegeneration. Oxidative Medicine and Cellular Longevity, 2015.
Hüttemann, M., Lee, I., Perkins, G. A., Britton, S. L., Koch, L. G., & Malek, M. H. (2013). (−)-EPICATECHIN IS ASSOCIATED WITH INCREASED ANGIOGENIC AND MITOCHONDRIAL SIGNALING IN THE HINDLIMB OF RATS SELECTIVELY BRED FOR INNATE LOW RUNNING CAPACITY. Clinical science (London, England: 1979), 124(11), 663.
Gutierrez-Salmean, G., Ciaraldi, T. P., Nogueira, L., Barboza, J., Taub, P. R., Hogan, & Ramirez-Sanchez, I. (2014). Effects of (−)-epicatechin on molecular modulators of skeletal muscle growth and differentiation. The Journal of nutritional biochemistry, 25(1), 91-94.
Hüttemann, M., Lee, I., & Malek, M. H. (2012). (−)-Epicatechin maintains endurance training adaptation in mice after 14 days of detraining. The FASEB Journal, 26(4), 1413-1422.
Nogueira, L., Ramirez‐Sanchez, I., Perkins, G. A., Murphy, A., Taub, P. R., Ceballos, G., & Malek, M. H. (2011). (–)‐Epicatechin enhances fatigue resistance and oxidative capacity in mouse muscle. The Journal of physiology, 589(18), 4615-4631.
Barnett, C. F., Moreno-Ulloa, A., Shiva, S., Ramirez-Sanchez, I., Taub, P. R., Su, Y., ... & Villarreal, F. (2015). Pharmacokinetic, partial pharmacodynamic and initial safety analysis of (−)-epicatechin in healthy volunteers. Food & function.
Baar, K., Wende, A. R., Jones, T. E., Marison, M., Nolte, L. A., Chen, M. A. Y., ... & Holloszy, J. O. (2002). Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC-1. The FASEB Journal, 16(14), 187
Pérez-Schindler, J., Svensson, K., Vargas-Fernández, E., Santos, G., Wahli, W., & Handschin, C. (2014). The coactivator PGC-1α regulates skeletal muscle oxidative metabolism independently of the nuclear receptor PPARβ/δ in sedentary mice fed a regular chow diet. Diabetologia, 57(11), 2405-2412.
Pilegaard, H., Saltin, B., & Neufer, P. D. (2003). Exercise induces transient transcriptional activation of the PGC‐1α gene in human skeletal muscle. The Journal of physiology, 546(3), 851-858.
Lin, J., Wu, H., Tarr, P. T., Zhang, C. Y., Wu, Z., Boss, O., ... & Spiegelman, B. M. (2002). Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres. Nature, 418(6899), 797-801.
Liang, H., & Ward, W. F. (2006). PGC-1α: a key regulator of energy metabolism. Advances in physiology education, 30(4), 145-151.
Holloszy, J. O., & Coyle, E. F. (1984). Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. Journal of applied physiology, 56(4), 831-838.
Ruas, J. L., White, J. P., Rao, R. R., Kleiner, S., Brannan, K. T., Harrison, B. C., ... & Spiegelman, B. M. (2012). A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy. Cell, 151(6), 1319-1331.
Burd, N. A., Andrews, R. J., West, D. W., Little, J. P., Cochran, A. J., Hector, A. J., ... & Phillips, S. M. (2012). Muscle time under tension during resistance exercise stimulates differential muscle protein sub‐fractional synthetic responses in men. The Journal of physiology, 590(2), 351-362.
Kopustinskiene, D. M., Savickas, A., Vetchý, D., Masteikova, R., Kasauskas, A., & Bernatoniene, J. (2015). Direct Effects of (−)-Epicatechin and Procyanidin B2 on the Respiration of Rat Heart Mitochondria. BioMed research international, 2015.
Ramirez‐Sanchez, I., De los Santos, S., Gonzalez‐Basurto, S., Canto, P., Mendoza‐Lorenzo, P., Palma‐Flores, C., ... & Coral‐Vazquez, R. (2014). (–)‐Epicatechin improves mitochondrial‐related protein levels and ameliorates oxidative stress in dystrophic δ‐sarcoglycan null mouse striated muscle. FEBS Journal, 281(24), 5567-5580.
Fernström, M., Tonkonogi, M., & Sahlin, K. (2004). Effects of acute and chronic endurance exercise on mitochondrial uncoupling in human skeletal muscle. The Journal of physiology, 554(3), 755-763.
Baird, M. F., Graham, S. M., Baker, J. S., & Bickerstaff, G. F. (2012). Creatine-kinase-and exercise-related muscle damage implications for muscle performance and recovery. Journal of nutrition and metabolism, 2012.
Kopustinskiene, D. M., Savickas, A., Vetchý, D., Masteikova, R., Kasauskas, A., & Bernatoniene, J. (2015). Direct Effects of (−)-Epicatechin and Procyanidin B2 on the Respiration of Rat Heart Mitochondria. BioMed research international, 2015.
Lee, W. J., Shim, J. Y., & Zhu, B. T. (2005). Mechanisms for the inhibition of DNA methyltransferases by tea catechins and bioflavonoids. Molecular pharmacology, 68(4), 1018-1030.
Fang, M., Chen, D., & Yang, C. S. (2007). Dietary polyphenols may affect DNA methylation. The Journal of nutrition, 137(1), 223S-228S.
Crescenti, A., Sola, R., Valls, R. M., Caimari, A., del Bas, J. M., Anguera, A., ... & Arola, L. (2013). Cocoa consumption alters the global DNA methylation of peripheral leukocytes in humans with cardiovascular disease risk factors: a randomized controlled trial. PloS one, 8(6), e65744.
Phillips, T. (2008). The role of methylation in gene expression. Nature Education, 1(1), 116.
Heyn, H., & Esteller, M. (2012). DNA methylation profiling in the clinic: applications and challenges. Nature Reviews Genetics, 13(10), 679-692.
Jones, P. A., & Takai, D. (2001). The role of DNA methylation in mammalian epigenetics. Science, 293(5532), 1068-1070.
Barrès, R., Osler, M. E., Yan, J., Rune, A., Fritz, T., Caidahl, K., ... & Zierath, J. R. (2009). Non-CpG methylation of the PGC-1α promoter through DNMT3B controls mitochondrial density. Cell metabolism, 10(3), 189-198.
Liu, C., & Lin, J. D. (2011). PGC-1 coactivators in the control of energy metabolism. Acta biochimica et biophysica Sinica, 43(4), 248-257.
Utriainen, P., Liu, J., Kuulasmaa, T., & Voutilainen, R. (2006). Inhibition of DNA methylation increases follistatin expression and secretion in the human adrenocortical cell line NCI-H295R. Journal of endocrinology, 188(2), 305-310.
Barres, R., Yan, J., Egan, B., Treebak, J. T., Rasmussen, M., Fritz, T., ... & Zierath, J. R. (2012). Acute exercise remodels promoter methylation in human skeletal muscle. Cell metabolism, 15(3), 405-411.
Baar, K. (2004). Involvement of PPARγ co-activator-1, nuclear respiratory factors 1 and 2, and PPARα in the adaptive response to endurance exercise. Proceedings of the nutrition society, 63(02), 269-273.
Terruzzi, I., Senesi, P., Montesano, A., La Torre, A., Alberti, G., Benedini, S., ... & Luzi, L. (2011). Genetic polymorphisms of the enzymes involved in DNA methylation and synthesis in elite athletes. Physiological genomics, 43(16), 965-973.
Ahmetov, I. I., Williams, A. G., Popov, D. V., Lyubaeva, E. V., Hakimullina, A. M., Fedotovskaya, O. N., ... & Rogozkin, V. A. (2009). The combined impact of metabolic gene polymorphisms on elite endurance athlete status and related phenotypes. Human genetics, 126(6), 751-761.
Koulmann, N., & Bigard, A. X. (2006). Interaction between signalling pathways involved in skeletal muscle responses to endurance exercise. Pflügers Archiv, 452(2), 125-139.
Loke, W. M., Hodgson, J. M., Proudfoot, J. M., McKinley, A. J., Puddey, I. B., & Croft, K. D. (2008). Pure dietary flavonoids quercetin and (−)-epicatechin augment nitric oxide products and reduce endothelin-1 acutely in healthy men. The American journal of clinical nutrition, 88(4), 1018-1025.
Steffen, Y., Schewe, T., & Sies, H. (2007). (–)-Epicatechin elevates nitric oxide in endothelial cells via inhibition of NADPH oxidase. Biochemical and biophysical research communications, 359(3), 828-833.
Ramirez-Sanchez, I., Maya, L., Ceballos, G., & Villarreal, F. (2010). (−)-Epicatechin activation of endothelial cell endothelial nitric oxide synthase, nitric oxide, and related signaling pathways. Hypertension, 55(6), 1398-1405.
Percival, J. M., Anderson, K. N., Huang, P., Adams, M. E., & Froehner, S. C. (2010). Golgi and sarcolemmal neuronal NOS differentially regulate contraction-induced fatigue and vasoconstriction in exercising mouse skeletal muscle. The Journal of clinical investigation, 120(3), 816.
Heiss, C., Schroeter, H., Balzer, J., Kleinbongard, P., Matern, S., Sies, H., & Kelm, M. (2006). Endothelial function, nitric oxide, and cocoa flavanols. Journal of cardiovascular pharmacology, 47, S128-S135.
Pisconti, A., Brunelli, S., Di Padova, M., De Palma, C., Deponti, D., Baesso, S., ... & Clementi, E. (2006). Follistatin induction by nitric oxide through cyclic GMP: a tightly regulated signaling pathway that controls myoblast fusion. The Journal of cell biology, 172(2), 233-244.
De Palma, C., & Clementi, E. (2012). Nitric oxide in myogenesis and therapeutic muscle repair. Molecular neurobiology, 46(3), 682-692.
Tanabe, K., Tamura, Y., Lanaspa, M. A., Miyazaki, M., Suzuki, N., Sato, W., ... & Nakagawa, T. (2012). Epicatechin limits renal injury by mitochondrial protection in cisplatin nephropathy. American Journal of Physiology-Renal Physiology, 303(9), F1264-F1274.
Nott, A., Watson, P. M., Robinson, J. D., Crepaldi, L., & Riccio, A. (2008). S-Nitrosylation of histone deacetylase 2 induces chromatin remodelling in neurons. Nature, 455(7211), 411-415.
Colussi, C., Mozzetta, C., Gurtner, A., Illi, B., Rosati, J., Straino, S., ... & Gaetano, C. (2008). HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment. Proceedings of the National Academy of Sciences, 105(49), 19183-19187.
 
N

NewAgeMayan

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Awesome.

furion, dont suppose you have any similiar info as far as piperine is concerned; or if not, a source elsewhere youd consider legit/reliable?
 
furion

furion

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Awesome.

furion, dont suppose you have any similiar info as far as piperine is concerned; or if not, a source elsewhere youd consider legit/reliable?
The write up is more focussed on the actual potential pharmacological activity of epicatechin. Not necessarily specifically to the CEL product.

Piperine- as far as the inclusion in the formula?
I was not intimately involved in the formulation- but I can tell you that it it was included for purposes of inhibiting enterocyte glucoronidation in attempt to direct pre-hepatic conjugation and maximise specific metabolites- not specifically for the bioavailability of the parent compound itself- as it has been established that the oral bioavailability is sufficient to produce the intended activity.
 
Afi140

Afi140

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Been waiting for this bad boy. Well done CEL. Non prop blend, enhanced absorption, getting exactly what is on the label=success in my book.
 
D

De__eB

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The write up is more focussed on the actual potential pharmacological activity of epicatechin. Not necessarily specifically to the CEL product.

Piperine- as far as the inclusion in the formula?
I was not intimately involved in the formulation- but I can tell you that it it was included for purposes of inhibiting enterocyte glucoronidation in attempt to direct pre-hepatic conjugation and maximise specific metabolites- not specifically for the bioavailability of the parent compound itself- as it has been established that the oral bioavailability is sufficient to produce the intended activity.
Really glad to have you on board Furion :D
 
bswanny

bswanny

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When is this guy coming out?
 
Rocket3015

Rocket3015

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I would be in on this but I don't think I have the computer skills to complete the application.
 
Spaniard

Spaniard

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That is for sure!!
Awesome to see this out, my friend!
...the rest (and references)

(-)-Epicatechin is capable of augmenting nitric oxide via activating the skeletal muscle expressed neuronal nitric oxide synthase (nNOS) (9,38) and also through inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) by its O-methyl metabolites (39). It has been proposed that former is directly activated via a novel cell surface receptor in skeletal muscle which mediates an intracellular cascade that results in increased NO production (40). Together these mechanisms are active both with and without exercise and are associated with the acute augmentation of NO observed with (-)-epicatechin supplementation (41,42). Although this activity does not appear to be largely active for increasing muscular endurance observed with (-)-epicatechin, it may play an indirect role in the myogenic potential(9). This may occur by compensating NO scavenged by myoglobin (41,44) and preserving Dynamin type-1 protein (DRP-1) (45) as well as promoting S-nitrosylation and inactivation of class II histone deacetylases (38,46-47). Hypothetically these effects may promote the prior mentioned skeletal muscle remodelling and the increased expression of follistatin (46,47).


Li, Y. M., Chan, H. Y. E., Huang, Y., & Chen, Z. Y. (2007). Green tea catechins upregulate superoxide dismutase and catalase in fruit flies. Molecular nutrition & food research, 51(5), 546-554.
Charles, A. L., Meyer, A., Dal‐Ros, S., Auger, C., Keller, N., Ramamoorthy, T. G., & ...Geny, B. (2013). Polyphenols prevent ageing‐related impairment in skeletal muscle mitochondrial function through decreased reactive oxygen species production. Experimental physiology, 98(2), 536-545.
Moreno-Ulloa, A., Nogueira, L., Rodriguez, A., Barboza, J., Hogan, M. C., Ceballos, G.,... & Ramirez-Sanchez, I. (2014). Recovery of Indicators of Mitochondrial Biogenesis, Oxidative Stress, and Aging With (−)-Epicatechin in Senile Mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, glu131.
Ramirez‐Sanchez, I., De los Santos, S., Gonzalez‐Basurto, S., Canto, P., Mendoza‐Lorenzo, P., Palma‐Flores, C., ... & Coral‐Vazquez, R. (2014). (–)‐Epicatechin improves mitochondrial‐related protein levels and ameliorates oxidative stress in dystrophic δ‐sarcoglycan null mouse striated muscle. FEBS Journal, 281(24), 5567-5580.
Shay, J., Elbaz, H. A., Lee, I., Zielske, S. P., Malek, M. H., & Hüttemann, M. (2015). Molecular Mechanisms and Therapeutic Effects of (−)-Epicatechin and Other Polyphenols in Cancer, Inflammation, Diabetes, and Neurodegeneration. Oxidative Medicine and Cellular Longevity, 2015.
Hüttemann, M., Lee, I., Perkins, G. A., Britton, S. L., Koch, L. G., & Malek, M. H. (2013). (−)-EPICATECHIN IS ASSOCIATED WITH INCREASED ANGIOGENIC AND MITOCHONDRIAL SIGNALING IN THE HINDLIMB OF RATS SELECTIVELY BRED FOR INNATE LOW RUNNING CAPACITY. Clinical science (London, England: 1979), 124(11), 663.
Gutierrez-Salmean, G., Ciaraldi, T. P., Nogueira, L., Barboza, J., Taub, P. R., Hogan, & Ramirez-Sanchez, I. (2014). Effects of (−)-epicatechin on molecular modulators of skeletal muscle growth and differentiation. The Journal of nutritional biochemistry, 25(1), 91-94.
Hüttemann, M., Lee, I., & Malek, M. H. (2012). (−)-Epicatechin maintains endurance training adaptation in mice after 14 days of detraining. The FASEB Journal, 26(4), 1413-1422.
Nogueira, L., Ramirez‐Sanchez, I., Perkins, G. A., Murphy, A., Taub, P. R., Ceballos, G., & Malek, M. H. (2011). (–)‐Epicatechin enhances fatigue resistance and oxidative capacity in mouse muscle. The Journal of physiology, 589(18), 4615-4631.
Barnett, C. F., Moreno-Ulloa, A., Shiva, S., Ramirez-Sanchez, I., Taub, P. R., Su, Y., ... & Villarreal, F. (2015). Pharmacokinetic, partial pharmacodynamic and initial safety analysis of (−)-epicatechin in healthy volunteers. Food & function.
Baar, K., Wende, A. R., Jones, T. E., Marison, M., Nolte, L. A., Chen, M. A. Y., ... & Holloszy, J. O. (2002). Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC-1. The FASEB Journal, 16(14), 187
Pérez-Schindler, J., Svensson, K., Vargas-Fernández, E., Santos, G., Wahli, W., & Handschin, C. (2014). The coactivator PGC-1α regulates skeletal muscle oxidative metabolism independently of the nuclear receptor PPARβ/δ in sedentary mice fed a regular chow diet. Diabetologia, 57(11), 2405-2412.
Pilegaard, H., Saltin, B., & Neufer, P. D. (2003). Exercise induces transient transcriptional activation of the PGC‐1α gene in human skeletal muscle. The Journal of physiology, 546(3), 851-858.
Lin, J., Wu, H., Tarr, P. T., Zhang, C. Y., Wu, Z., Boss, O., ... & Spiegelman, B. M. (2002). Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres. Nature, 418(6899), 797-801.
Liang, H., & Ward, W. F. (2006). PGC-1α: a key regulator of energy metabolism. Advances in physiology education, 30(4), 145-151.
Holloszy, J. O., & Coyle, E. F. (1984). Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. Journal of applied physiology, 56(4), 831-838.
Ruas, J. L., White, J. P., Rao, R. R., Kleiner, S., Brannan, K. T., Harrison, B. C., ... & Spiegelman, B. M. (2012). A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy. Cell, 151(6), 1319-1331.
Burd, N. A., Andrews, R. J., West, D. W., Little, J. P., Cochran, A. J., Hector, A. J., ... & Phillips, S. M. (2012). Muscle time under tension during resistance exercise stimulates differential muscle protein sub‐fractional synthetic responses in men. The Journal of physiology, 590(2), 351-362.
Kopustinskiene, D. M., Savickas, A., Vetchý, D., Masteikova, R., Kasauskas, A., & Bernatoniene, J. (2015). Direct Effects of (−)-Epicatechin and Procyanidin B2 on the Respiration of Rat Heart Mitochondria. BioMed research international, 2015.
Ramirez‐Sanchez, I., De los Santos, S., Gonzalez‐Basurto, S., Canto, P., Mendoza‐Lorenzo, P., Palma‐Flores, C., ... & Coral‐Vazquez, R. (2014). (–)‐Epicatechin improves mitochondrial‐related protein levels and ameliorates oxidative stress in dystrophic δ‐sarcoglycan null mouse striated muscle. FEBS Journal, 281(24), 5567-5580.
Fernström, M., Tonkonogi, M., & Sahlin, K. (2004). Effects of acute and chronic endurance exercise on mitochondrial uncoupling in human skeletal muscle. The Journal of physiology, 554(3), 755-763.
Baird, M. F., Graham, S. M., Baker, J. S., & Bickerstaff, G. F. (2012). Creatine-kinase-and exercise-related muscle damage implications for muscle performance and recovery. Journal of nutrition and metabolism, 2012.
Kopustinskiene, D. M., Savickas, A., Vetchý, D., Masteikova, R., Kasauskas, A., & Bernatoniene, J. (2015). Direct Effects of (−)-Epicatechin and Procyanidin B2 on the Respiration of Rat Heart Mitochondria. BioMed research international, 2015.
Lee, W. J., Shim, J. Y., & Zhu, B. T. (2005). Mechanisms for the inhibition of DNA methyltransferases by tea catechins and bioflavonoids. Molecular pharmacology, 68(4), 1018-1030.
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Crescenti, A., Sola, R., Valls, R. M., Caimari, A., del Bas, J. M., Anguera, A., ... & Arola, L. (2013). Cocoa consumption alters the global DNA methylation of peripheral leukocytes in humans with cardiovascular disease risk factors: a randomized controlled trial. PloS one, 8(6), e65744.
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Utriainen, P., Liu, J., Kuulasmaa, T., & Voutilainen, R. (2006). Inhibition of DNA methylation increases follistatin expression and secretion in the human adrenocortical cell line NCI-H295R. Journal of endocrinology, 188(2), 305-310.
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Holy write-up! Phenomenal job, really nice work.
Been waiting for this bad boy. Well done CEL. Non prop blend, enhanced absorption, getting exactly what is on the label=success in my book.
The no prop blend is my favorite part. No prop blends for the win!
Really glad to have you on board Furion :D
Who is this mystery man???
 
booneman77

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Sick promo... Let's get some apps in here and see what this bad boy can do!
 
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Dont think Ive come across any feedback yet of a prewo stack along these lines:

ArA + soy granules + -epi + HV/Conquer

...GOAT prewo pump stack, or too much?
 
booneman77

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Dont think Ive come across any feedback yet of a prewo stack along these lines:

ArA + soy granules + -epi + HV/Conquer

...GOAT prewo pump stack, or too much?
Pumps could be inhibitive but it would be godly to try ;)
 
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Pumps could be inhibitive but it would be godly to try ;)
Yeah, cant imagine Id full dose/serving all those every time I ran the stack, but like you said once or twice could be an experience.
 
NoAddedHmones

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Dont think Ive come across any feedback yet of a prewo stack along these lines:

ArA + soy granules + -epi + HV/Conquer

...GOAT prewo pump stack, or too much?
Definitely wouldn't attempt that on my high volume leg days. No way I could get through it without pumps becoming unbearable.
 
booneman77

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Yeah, cant imagine Id full dose/serving all those every time I ran the stack, but like you said once or twice could be an experience.
I plan on trying at some point here soon. Could be perfect during a low carb phase
 
McCrew530

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Say Whaaat!?! Two luck computer savvy people are going to be stoked
 
koi1214

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I would be in on this but I don't think I have the computer skills to complete the application.
1.Simply post any picture,video or photoshopped pic with you and ANYTHING CEL related(NO PH"S)

pct.jpg
tudca.jpg
ca.jpg
CEL.Epi.Plex.Rendering.300dpi.jpg




2.Post a video of what motivates you to work harder or post a video to motivate others


[video=youtube;ZmAFMNmSKus]https://www.youtube.com/watch?v=ZmAFMNmSKus[/video]
 
Misfit28

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Dont think Ive come across any feedback yet of a prewo stack along these lines:

ArA + soy granules + -epi + HV/Conquer

...GOAT prewo pump stack, or too much?
I intend on trying that out very soon, hopefully :)
 
Abe Lincoln

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Looking good, this product has been on my radar for some time
 
fightbackhxc

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koi1214

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Rocket3015

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I will give it a try

PRODUCT LOG REQUIREMENTS:
1. Must have a USA Mailing Address. Yes Sir
2. Must be 18+ years of age. 57 Years Old
3. Must be in good health with no known medical conditions. I'm Still Alive
4. Must do a Full Log in the Supplements Log section. No Problem
5. Must update at least 3 times a week/post final review OK
6. Can you post before/After pics? Yes

I never tried to use Photoshop so had to do it the old fashion way !

CEL.JPG



Not sure how to post a video ??

[video=youtube;4NjROLRTQHA]https://www.youtube.com/watch?v=4NjROLRTQHA[/video]
 
bswanny

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Is threre word on the %of epicat as to my knowlege there isnt 100% extract. Just curious if know. Thank you. I will take pic in morning when my girlish figure comes in a def through my hat into here.
 
Last edited:
Danes

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Same here. I have used epicatachien as a staple ne since its come out. Is threre word on the %of epicat as to my knowlege there isnt 100% extract. Just curious if know. Thank you.
You mean there ia no 100% epicatechin?
 
bswanny

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You mean there ia no 100% epicatechin?
Not sure if serious but iv only seen 90% extract in most epi. I could be wrong, im not oppose to being wrong. If its 100% then great.
 
NoAddedHmones

NoAddedHmones

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Not sure if serious but iv only seen 90% extract in most epi. I could be wrong, im not oppose to being wrong. If its 100% then great.
Whats the difference between 100mg of -epi from a 90% extract or 100mg of pure unicorn -epi?
 
bswanny

bswanny

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Unicorns can fly so......
 
bswanny

bswanny

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Well no argument here. Awhile back there was a talk about most epi products being of low quality epi. Just wanted to check as i currently enjoy CEL peoducts and think a bit of them.
 

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