Muscle Chemistry Archive
2020 – NPC Ronnie Coleman Classic
2020 – NPC Ronnie Coleman Classic Sat Apr 4th Dallas Market Hall, 2200 N Stemmons Fwy, Dallas, TX 75207, USA map #metroflexevents#metroflexevents-#ronniecolemanclassic-#ronniecoleman-#bodybuilding-#strongman-#powerlifting-#NPC-#IFBB-#Bikini-#physique-#fitness-#grappling-#jiujitsu-#armwrestling-#figure-#fortworthconventioncenter-#fitnessexpo#strongman-#stongwoman-#metroflexplano-#metroflexnorthdallas-#metroflexevents#texasbodybuilding-#npctexas-#texasbodybuildingcontest 2020 NPC Ronnie Coleman Classic NATIONAL QUALIFIER- Sanction# 3293 – April 4th – Dallas Market Hall 2200 N Stemmons Fwy, Dallas, TX 75207
NPC Texas Legends Championships
NPC Texas Legends Championships Sat Feb 22nd Round Up Inn, 3400 Burnett Tandy Dr, Fort Worth, TX 76107, USA map 2020 NPC Texas Legends Championships metroflexevents.com NATIONAL QUALIFIER- Sanction # 3863 February 22nd, Round Up Inn-3400 Burnett Tandy Dr. Fort Worth Texas 76017
2020 NPC Worldwide Olympia Amateur South America
2020 NPC Worldwide Olympia Amateur South America
Road to IFBB Professional League Pro Card
Road to IFBB Professional League Pro Card Men’s Physique Pro Derrick Stevenson Filmed & Interviewed By J.M. Manion at the NPC Photo Gym in Pittsburgh,PA for npcnewsonline.com Men’s Physique Pro Derrick Stevenson
The Most Effective GH Dose For Fat Loss Per Administration
[embedded content]Contrary to popular belief, more is not better when it comes to exogenous GH use for fat loss.There is a ceiling on lipolysis, and the highest GH dose for maximizing fat loss per administration is much lower than most people think. As you can see here in the following study assessing the pharmacokinetics and acute lipolytic actions of GH, there were significant dose-response effects when comparing the incremental area under the curve of both free fatty acids and blood 3-hydroxy-butyrate following 0, 1, and 3 mcg/kg GH, whereas there were no differences between the responses following 3 and 6 mcg/kg GH [R].These dosages were administered intravenously. 1 mg of Somatropin corresponds to 3 IU (International Units) of Somatropin [R].So, this means that for someone who weighs 100 kg, lipolysis is maxed out at about 300 mcg of Somatropin, which is 0.9 IU’s of pharma grade GH IV. We need to math out the corresponding subcutaneous dose based on the bioavailability and bioactivity comparison data we have on humans administered HGH. Obviously IV dosages are not representative of what dosages would be via the far more realistic and tolerable method of administration (subcutaneous). In one study, the mean estimated availability of subcutaneous injected HGH was shown to be 63% of that of HGH administered I.V. after correcting for differences in the GH dose [R].Another study found the availability of subcutaneous injected HGH to be about 70% of that of HGH administered I.V. [R].So, for a 100 kg man, fat loss benefits would be maxed out around 1.35 IU of GH per administration subcutaneously. There is a refractory period cells need before another pulse of exogenous GH can even be useful in a lipolysis context, which I will delve into further in a future article. Related
IGF-1 lr3 Permanent muscle gains, healing, and anti-aging benefits
IGF-1 lr3 Permanent muscle gains, healing, and anti-aging benefits Gym-Rats Before and After IGF-1 lr3 Administration IGF-1 LR3, Long R3 IGF-1, IGF-1- Insulin-like Growth Factor ? is an experimental drug that represents the next generation in performance enhancing in bodybuilding athletes. This peptide hormone also has the promise of becoming the ultimate fountain of…
Insulin-like growth factor 1 lr3 – IGF-1 lr3 Users Guide
IGF-1 was originally developed in 1993 by Groprep in Australia. IGF-1 is a 70 amino acid sequence similar to the size and structure of Insulin. IGF-LR3 belongs to the peptide family of substances identified as growth factors. It is a highly anabolic hormone released in the liver as well as in peripheral tissues such as skeletal…
Will Taking GH Before Going To Sleep Suppress Your Natural Production Of GH?
At supraphysiological dosages, taking GH before going to sleep makes sense because there is a negative feedback loop on the growth hormone (GH)/insulin-like growth factor I (IGF-1) axis.In this study, IGF-1 was constantly infused, and the effect on endogenous GH secretion was assessed [R].Overall, GH concentrations were suppressed during the rhIGF-I infusion by 85±3%, mainly by attenuating spontaneous GH pulse amplitude (77±4% suppression).The apparent GH pulse frequency was attenuated from 7.8±0.9 to 4.7±0.6 pulses/24h (P= 0.006).IGF-1 is the primary feedback, and the mechanism is similar to what you see with the HPTA axis.When there is enough Testosterone and Estrogen, your body has this mechanism in place to prevent you from making more.The same thing happens with exogenous GH use.When you administer exogenous GH, IGF-1 elevates.When your body recognizes that IGF-1 is elevated, it starts to suppress GH pulse amplitude in a dose dependent manner.If you are using supraphysiological amounts of GH for bodybuilding purposes, you can assume that your natural secretion is greatly inhibited during sleep as this negative feedback loop will prevent your body from secreting GH in your sleep like it normally would.When endogenous GH production is suppressed, administering exogenous GH at times that lipolysis or muscle growth can be optimized is the most logical approach to injection timing.[embedded content]If fat loss is the goal, then taking GH in a fasted state prior to fasted cardio would be ideal.There is a ceiling on how much GH is needed to maximize lipolysis, so if your dosage exceeds 2 IU per day, then I would advise splitting up that dose into two (or more if needed) different periods of the day with as much time between them as possible.If muscle growth is the goal, GH should still be administered in a pulsatile fashion to mimic endogenous secretions.Topped out stimulation of autocrine IGF-1 in skeletal muscle can be achieved with fairly low dosages of exogenous GH, and administering a higher dose above and beyond that may just be a waste.This is why it would be wise to split up your daily GH dose into multiple administrations if you are using supraphysiological dosages.Related
RU58841 Vs. Finasteride For Hair Loss Prevention – Which Is Better?
RU58841 vs. Finasteride.As of now RU58841 is the most commonly used topical anti-androgen used for hair loss prevention, and Finasteride is the most commonly used 5α-Reductase inhibitor for hair loss prevention.Which is better for hair loss prevention?This is a common question I get asked and a dedicated post is long overdue.[embedded content]Table of ContentsStudy Comparing RU58841 Vs. Finasteride Head To HeadWhile there are tons of anecdotal reviews comparing Finasteride to RU58841, there is very little scientific data for us to refer to.There is some though that is worth delving into.In this study, Finasteride was stacked up against RU58841 to see which would be more effective for hair loss prevention, and how much each would impact systemic hormone levels [R].RU58841 was applied either in a 5% solution, a 0.5% solution, or just a vehicle with no RU58841 in it for 6 months to the bald scalp of 10 stump-tailed macaques.The 5% solution was applied to 4 of the 10 bald stump-tailed macaques, the 0.5% solution was applied to 3 of the 10 bald stump-tailed macaques, and the vehicle with no RU58841 was applied to the last 3 of the 10 bald stump-tailed macaques.The common dosing protocol for RU58841 is typically a 5% solution applied to androgenic alopecia affected areas, so this study was right in line with what we would want to see.Oral Finasteride was given in a dose of 1 mg/kg/day for 6 months to 10 bald stump-tailed macaques.An oral placebo was also given to 10 bald stump-tailed macaques.Male stump-tailed macaques weigh on average between 9.7–10.2 kg, so that would equate to a Finasteride dosage of roughly 10 mg orally per day.This dosage greatly exceeds the point of diminishing returns with Finasteride use, so this is also a great way for us to compare the efficacy of a standard dose of RU58841 to a maxed out dose of Finasteride.The stump-tailed macaque has shown to be a suitable biological model for human androgenetic alopecia as it possesses hereditary balding characteristics similar in many respects to that of androgenetic alopecia in humans [R].ResultsSkin biopsies for micromorphometric analysis (folliculogram) were taken at 0 and 6 months for Finasteride treated macaques and at 0 and 4 months for RU58841 treated macaques.The amount of anagen follicles (hairs in the active growth phase) and vellus follicles (short, thin, and barely noticeable hairs) enlarged to terminal size were compared to those in pre-treatment stages.Anagen follicles increased an average of 88% with Finasteride.Anagen follicles increased an average of 103% with 5% strength RU58841.The growth of vellus follicles to terminal size (thick, strong, pigmented hairs that have fully matured) was 12% with Finasteride.The growth of vellus follicles to terminal size was 26% with 5% strength RU58841.The 0.5% strength RU58841 solution induced almost no effect.Expectedly, the Finasteride placebo induced no effect.The 5% strength RU58841 solution induced the most hair growth after only 2 months of treatment.RU58841 was given less time to work and still significantly outperformed Finasteride in this study.Although Finasteride significantly reduced DHT levels, DHT remaining and produced by Type I 5α-reductase isoenzyme still contributed to hair follicle miniaturization.Because Testosterone and DHT both bind to the androgen receptor, a locally sufficient dose of an “AR blocker” (topical anti-androgen) appears to suppress Testosterone and DHT induced follicular regression more effectively than 5α-reductase inhibition.Systemic EffectsPlasma RU58841 and metabolites (10-20 ng/ml) were detected in 2 of the stump-tailed macaques that were applied the 5% strength RU58841 solution at the 3 month mark of treatment.Only 1 of the stump-tailed macaques had detectable plasma RU58841 and metabolites at at the 6 month mark of treatment.RU58841 had no significant impact on serum DHT or Testosterone levels at any point.Finasteride decreased serum DHT levels by about 70%, and Testosterone levels increased as a result of the 5α-reductase blockade.If Estrogen levels were assessed in the Finasteride treated group, their Estrogen levels would have showed significant elevation as well as a result of increased aromatization.My Concluding Thoughts On This StudyThis study shows that RU58841 can go systemic when topically applied, although there is no effect on endogenous androgen levels.First of all, I do believe that RU58841 can go systemic, in fact, I think it is an inevitable outcome.However, the degree to which it goes systemic and if the amount that goes systemic will cause anti-androgenic side effects will be based on several factors.These factors include but are not limited to endogenous androgen production, sex hormone metabolism, androgen receptor density and expression, scalp skin porosity, the dosage used, if there are open wounds on the scalp or not, the vehicle used, frequency of administration, and more.Does this ensure side effects? No.However, applying anything to your skin with a low enough molecular weight to be absorbed and not expecting it to go systemic at all is wishful thinking.The molecular weight of RU58841 is 369.34 g/mol [R].1 Da (dalton) = 1 g/mol.The molecular weight of a compound must be under 500 Dalton to allow skin absorption (which RU58841 is) [R].With that being said, RU58841 is well tolerated by the majority of users for a reason.In the study, at the 3 month mark 2 of the stump-tailed macaques had detectable plasma RU58841 and metabolites.By the 6 month mark, only 1 of the stump-tailed macaques had detectable plasma RU58841 and metabolites.If there was a cumulative drug effect we would have seen more animals with detectable metabolites after an additional 3 months of dosing, not less.What most fail to consider is that RU58841 is non-steroidal and acts as a competitive silent antagonist of the androgen receptor.This means that even if RU58841 goes systemic, by creating a blockade of the androgen receptor, RU58841 prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men.By binding to androgen receptors, RU58841 will induce anti-androgen effects without reducing serum androgen levels in the body.Finasteride on the other hand works by directly crushing DHT levels rather than by occupying androgen receptors.The ideal treatment would be a topical non-steroidal anti-androgen or SARM with a high binding affinity, and harmless metabolites void of anti-androgenic activity upon systemic absorption.Achieving Complete Hair Loss Protection By Addressing The Androgen Receptor, Not Just 5α-ReductaseWhen you inhibit 5α-Reductase with Finasteride or Dutasteride, serum Testosterone and Estrogen levels increase will increase.A common mistake is to ignore the fact that scalp Testosterone levels rise dramatically after inhibiting 5α-Reductase.This occurs to an even greater degree with Dutasteride use, and I believe is the reason why some men experience accelerated hair loss after switching from Finasteride to Dutasteride.Typically, most men will see better results with Dutasteride as scalp DHT is almost always going to be more of a problem than scalp Testosterone.However, the consequent spike in scalp Testosterone levels with Dutasteride use is significant, and Testosterone will bind to androgen receptors and induce miniaturization just the same.5 mg of Finasteride resulted in a 23% increase in scalp Testosterone levels with a concurrent 41% suppression of scalp DHT levels.0.5 mg Dutasteride resulted in a 99% increase in scalp Testosterone levels with a concurrent 51% suppression of scalp DHT levels.This is why the androgen receptor needs to be addressed, not just nuking 5α-reductase with Dutasteride.Scalp Testosterone will still slowly chip away at your hair, regardless if DHT is there or not.In addition, Finasteride is insufficient to completely eliminate scalp DHT, which also needs to be taken into account and addressed.When you inhibit 5α-reductase, that Testosterone that would have otherwise converted to DHT doesn’t just disappear, it remains as the parent hormone, thus raising total Testosterone levels in the body.Dutasteride doesn’t just randomly stop working one day, Testosterone and other endogenous androgens are still eating away at your hair, just at a much slower pace than DHT would.The only way to prevent other androgens from binding to androgen receptors and miniaturizing hair follicles is by competing with them for androgen receptor binding.That’s where the therapeutic promise of topical anti-androgens, anti-androgens in general, selective androgen receptor modulators, and other similar compounds that bind to androgen receptors can come into play and provide a compounding level of protection when needed, or as a form of monotherapy on their own if sufficient.If you only inhibit 5α-reductase with Finasteride, not only will you have residual amounts of DHT, but you will also have a spike in scalp Testosterone that is totally unaccounted for.Unfortunately, you can’t just partially inhibit 5α-reductase and expect complete protection for life unless you have very mild hair loss to begin with.Permanent prevention can only be achieved by addressing the androgen receptor itself.For some individuals, Finasteride monotherapy will be sufficient to stave off hair loss for a couple decades, but that residual DHT and spike in Testosterone will continue to chip away and eventually win in the end.For some with aggressive hair loss, Finasteride monotherapy isn’t even sufficient in the short-term.At the end of the day, regardless of how aggressive your hair loss is, prevention is mediated via the androgen receptor.Other treatment options may be implemented that interact with different downstream mechanisms in the cascade of events that lead to hair loss, but they will unlikely prove sufficient to completely mitigate androgenic alopecia on their own, and will be best utilized as an adjunct treatment to achieve a compounding level of protection with other compounds.Which Is Better For Hair Loss Prevention?RU58841 and Finasteride work via different mechanisms of action.They shouldn’t be pitted against one another as neither are likely to prove sufficient to completely prevent hair loss on their own.DHT has a much higher binding affinity than RU58841, but Testosterone doesn’t.Those with very aggressive hair loss would likely need to use a massive dose of RU58841 to compete with all of their scalp DHT and Testosterone.On the other hand, Finasteride can significantly decrease DHT levels, but causes a subsequent spike in scalp Testosterone that goes completely unaccounted for that will still work in tandem with the residual DHT to miniaturize hair follicles.A more complete level of protection would be achieved by using both Finasteride and RU58841, not one or the other.Finasteride will significantly reduce the amount of scalp DHT, and leave a hormonal environment that RU58841 is more capable of dealing with.RU58841’s binding affinity is at least as high as Testosterone, so if most of the DHT is cleared out of the way, RU58841 only has to compete with Testosterone and a much lower amount of DHT.Expecting RU58841 to out-compete all endogenous DHT and Testosterone without any assistance when its binding affinity is several times lower than DHT is a strategy that would likely only work long-term for someone with mild hair loss.The dose and frequency of administration relative to the half-life needs to be kept in mind as well.There’s a dose-dependent response with all drugs, including anti-androgens.Just because a 5% RU58841 solution applied once per day proves sufficient for one guy, that doesn’t mean that dosage will be sufficient for you too.Hair loss is basically just a giant chess match where the most efficacious treatments will either knock out the opponent (decrease endogenous androgen levels), or occupy a more advantageous position on the chess board (binding to androgen receptors).The more chess pieces you have, the better your chance of winning against the finite number of opponent chess pieces.This is why certain anti-androgens with very poor binding affinity can still be effective in a clinical setting.An anti-androgen dosed very aggressively will eventually overpower Testosterone and DHT just by sheer volume (e.g. Bicalutamide).The same applies for RU58841, assuming it gets absorbed, which will boil down to scalp skin porosity, vehicle, and so on.If you opted for CB-03-01 instead of RU58841, the same concept would apply, it would just need to be dosed even more aggressively until sufficient AR binding is achieved.For those prone to side effects, that strategy may be the better alternative with CB-03-01 rather than RU58841 as it seems that the metabolites of CB-03-01 may be better tolerated at higher dosages than those of RU58841.The binding affinity of CB-03-01 is much lower than RU58841 though and it is very cost prohibitive, so for the time being, that strategy is likely not viable for most.Where To Buy RU58841Most RU58841 sources do not third party test their products, nor do they have any satisfactory level of quality control whatsoever.I strongly advise that before you buy RU58841 from a company online you thoroughly evaluate their track record, their third party test results, and how they are marketing their products in general.These are the only companies I currently use for my own personal research:(Greater Than 99% Purity: FTIR, HPLC, GC-MS, LC-MS & NMR Tested)Anageninc – 10% off coupon code “DC10”Science.bio – 10% off coupon code “DC10”Chemyo – 10% off coupon code “DC10”Related
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