deserusan 
"To help set a new standard and level of trust in the supplement industry through innovation, stringent quality control, and better results experienced by all."
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Archive for the 'Advanced Supplement Discussion' Category
Monday, June 2nd, 2008
If you have been following the mainstream supplement market I’m fairly certain you are no stranger to coenzyme Q10 aka ubiquinone, CoQ10. This powerhouse of a molecule plays a major role in mitochondrial energy metabolism and its reduced metabolite ubiquinol is responsible for antioxidant capability. Fortunately, clinical research is beginning to uncover the benefits of CoQ10 supplementation in the arena of athletic performance.
A recent study from the Graduate School or Comprehensive Human Sciences at the University of Tsukuba uncovered some beneficial properties of CoQ10 with relation to recovery. Eighteen elite Japanese kendo athletes participated in a single-blinded placebo controlled clinical study to determine whether or not supplementing with 300mg CoQ10 per day would reduce exercise induced muscular damage and oxidative stress.
As expected, skeletal muscle damage indicators increased greatly in the placebo group. Quite simply, creatine kinase levels increased 5 times and serum myoglobin increased upwards of 7.7 times during the five day training camp. The CoQ10 supplemented group showed significant attenuation of the same clinical markers which proved indeed that CoQ10 supplementation can quite possibly reduce exercise induced skeletal muscle damage. It should be noted also that in both groups both clinical markers returned to base line and changes in leukocytes, neutrophils, and monocytes were unaffected by CoQ10.
In closing, CoQ10 supplementation is beginning to prove itself as a potential aide to athletic recovery. Kendo training is no walk in the park and this clinical study put CoQ10 to the test through 5.5 hours of high impact physical training per day. The results of this study conclude that CoQ10 can be implemented into an athlete’s supplement protocol to assist in reducing exercise induced muscle injury.
Reference.
Kon M, Tanabe K, Akimoto T, Kimura F, Tanimura Y, Shimizu K, Okamoto T, Kono I. Reducing exercise-induced muscular injury in kendo athletes with supplementation of coenzyme Q10. The British Journal of Nutrition. 2008 Feb 20:1-7.
Posted in Advanced Supplement Discussion
Friday, May 23rd, 2008
Whitt KN, Ward SC, Deniz K, Liu L, Odin JA, Qin L Seminars in Liver Disease. 2008 May;28(2):226-31.Cholestatic liver injury associated with whey protein and creatine supplements. Semin Liver Dis. 2008 May;28(2):226-31
We present a case of acute cholestatic liver injury associated with the combination of whey protein and creatine supplements. The difficulty of diagnosing drug-induced liver injury is emphasized. The patient is a healthy, 27-year-old man who presented with painless jaundice. He had no occupational exposures to solvents, was not taking prescription medications, and did not use recreational drugs or alcohol. He was an enthusiastic weight-lifter and had been taking creatine for 8 to 9 months and whey protein supplements for 4 weeks prior to the development of symptoms. Laboratory tests revealed elevated total bilirubin (54.7 mg/dL) and alkaline phosphatase (436 U/L), minimally elevated transaminases, and a creatinine of 3.1 mg/dL. Serologic work-up was negative for viral hepatitis and autoimmune liver disease, and Wilson’s disease was ruled out. Magnetic resonance cholangiopancreatogram was unremarkable, but a liver biopsy showed marked cholestasis with ductular proliferation. He had dramatic clinical improvement with intravenous fluids and discontinuation of the nutritional supplements. In patients with acute liver injury, clinicians should inquire about dietary supplement usage and consider immediate discontinuation of all unnecessary products. We describe a case of profound jaundice related to a commonly used and reportedly safe combination of such supplements”
As many of you may or may not know, there are relatively new adverse reaction reporting protocols in place for dietary supplements which began December 2006. Essentially, this serves as a collection house for healthcare professionals and consumers to report negative experiences with dietary supplements. Politics aside, this has been put in place to protect consumers and to hopefully root out dangerous or mislabeled dietary supplements.
Now if you read the abstract above, you are probably wondering how could creatine or whey protein cause cholestatic liver injury? The fact of the matter is, supplemental creatine would only raise creatinine to a significant degree and not the other clinical markers (1,2). So should we point the finger at whey protein for elevating the questionable clinical markers since creatine most likely did not?
In reality, whey protein has actually proven to have a positive impact on the liver in many clinical studies (3-5) often lowering the same parameters including bile duct proliferation (3). The same can be said for casein protein and whey hydrolysates (3,5) but that is a moot point. Regardless, we are still left with the question of what could have potentially caused this man’s cholestatic liver injury?
One use of terminology that I found rather intriguing in this citation was the term “enthusiastic weight lifter” and also the time frame in which he began using “whey supplements.” Now I may be going out on a limb here, but perhaps instead of starting whey protein four weeks prior to his ailment, could there be a possibility he was taking some form of oral steroid? It’s not like anyone hasn’t done a four week cycle of oral steroids before and had elevated liver values right? Either way, it is a definite possibility that an “enthusiastic weightlifter” might turn to steroids to increase their strength and muscle mass. There is no doubt about that.
Let’s think about this for second. Have oral steroids over cause cholestatic liver injury? Have oral steroids ever been attributed to elevated bilirubin that can cause Jaundice? Have they been attributed to raising liver enzymes such as the ones noted in the case study? The answer quite succinctly is yes (7-13). For detailed description of how this occurs please read A Closer Look at Steroid Liver Toxicity by M. Fischer. Now what is absolutely disturbing regarding our case study is that they did not even think or have the wherewithal to investigate this possibility. Instead, they based their conclusions on the patient’s testimonial regarding creatine and whey protein instead checking for an elevated T/E ratio or serum testosterone levels.
Now what is more alarming? The fact that these hepatologists do not even know how some of the most widely consumed dietary sport supplements effect the organ which they specialize in? On the flipside, is it even worse the board of reviewers who accepted this case study for publication didn’t think to question their results either? Perhaps the stark possibility this case study might be presented one day as justification to remove access to proven ergogenic aides? We could speculate all day what a travesty this is, but the fact remains this misinformation is still out there. Even the safest of supplements are sure to be scrutinized under false pretenses.
The reason why I brought your attention to this particular case study is that it really illustrates just how ill-informed and prejudiced the established medical community can be against dietary supplements like creatine and whey protein. It is my hope that many of the myths regarding supplementation are dispelled so the tide of ignorance that is quite prevalent among some medical researchers doesn’t catch the watchful eye of Uncle Sam anymore then they already have. It’s up to every one of you to help secure your rights to freedom of choice before those choices are taken away from you.
1. Robinson TM, Sewell DA, Casey A, Steenge G, Greenhaff PL. Dietary creatine supplementation does not affect some haematological indices, or indices of muscle damage and hepatic and renal function. Br J Sports Med. 2000 Aug;34(4):284-8.
2. Bizzarini E, De Angelis L.Is the use of oral creatine supplementation safe? J Sports Med Phys Fitness. 2004 Dec;44(4):411-6.
3. Morifuji M, Sakai K, Sugiura K.Dietary whey protein modulates liver glycogen level and glycoregulatory enzyme activities in exercise-trained rats. Exp Biol Med (Maywood). 2005 Jan;230(1):23-30.
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4. Belobrajdic D, McIntosh G, Owens J.The effects of dietary protein on rat growth, body composition and insulin sensitivity. Asia Pac J Clin Nutr. 2003;12 Suppl:S42.
5. Pacheco MT, Sgarbieri VC.Effect of different hydrolysates of whey protein on hepatic glutathione content in mice. J Med Food. 2005 Fall;8(3):337-42.
6. Kume H, Okazaki K, Sasaki H. Hepatoprotective effects of whey protein on D-galactosamine-induced hepatitis and liver fibrosis in rats. Biosci Biotechnol Biochem. 2006 May;70(5):1281-5.
7. Giannattasio A, D’Ambrosi M, Volpicelli M, Iorio R. Steroid therapy for a case of severe drug-induced cholestasis. Ann Pharmacother. 2006 Jun;40(6):1196-9.
8. Habscheid W, Abele U, Dahm HH.Severe cholestasis with kidney failure from anabolic steroids in a body builder Dtsch Med Wochenschr. 1999 Sep 10;124(36):1029-32
9. Stang-Voss C, Appell HJ.Structural alterations of liver parenchyma induced by anabolic steroids. Int J Sports Med. 1981 May;2(2):101-5.
10. Hartleb M, Nowak A.Severe jaundice with destructive cholangitis after administration of methyltestosterone. Am J Gastroenterol. 1990 Jun;85(6):766-7.
11. Lucey MR, Moseley RH.Severe cholestasis associated with methyltestosterone: a case report. Am J Gastroenterol. 1987 May;82(5):461-2.
12. Shah NL, Zacharias I, Khettry U, Afdhal N, Gordon FD. Methasteron-associated cholestatic liver injury: clinicopathologic findings in 5 cases. Clin Gastroenterol Hepatol. 2008 Feb;6(2):255-8.
13. Jasiurkowski B, Raj J, Wisinger D, Carlson R, Zou L, Nadir A. Cholestatic jaundice and IgA nephropathy induced by OTC muscle building agent superdrol. Am J Gastroenterol. 2006 Nov;101(11):2659-62.
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Posted in Advanced Supplement Discussion
Tuesday, May 6th, 2008
Here is a candid interview conducted on another site with 3-AD formulator, Matt Cahill. I’m featuring this in my blog because this is one of the few effective supplements I’ve seen released in quite a while with regards to putting on true mass. Matt is also good friend and one of the truly brightest minds in the industry with regards to raw formulation whom I owe many thanks. Enjoy!

“3-AD: Revamped, Reloaded, Released!
An Interview with Matt Cahill
In this issue of our Industry Spotlight Interview, we are honored to have the opportunity to speak with industry guru, Matt Cahill, CEO and founder of Designer Supplements. Matt Cahill is renowned for his innovation and unique design of cutting edge supplements based on science, not marketing hype. Many are aware of Designer Supplements cutting edge compounds such as Superdrol, Lean Xtreme, and ActivaTe (just to name a few). In this sit down interview, we will be discussing in detail the revolutionary new product, 3-AD by Anabolic Xtreme; another innovative formula uniquely designed by Cahill himself to further push the envelope in achieving breakthrough results in physiological metamorphosis!
NP: Matt, thank you for taking the time out of your busy schedule to sit down with us today. We are excited to discuss with you the long awaited release of 3-AD. Many of us are aware of the compound Adrenosterone, but 3-AD contains Androsterone. For those who are not familiar with Androsterone, can you give us some information about this compound?
MC: I’d just like to say thank you for having me, it is my pleasure to be talking with you. Androsterone is a pro-hormone which converts to the powerful hormone Stanolone through the 3aHSD, 3bHSD, and 17bHSD enzymes. Stanolone is 400% more anabolic then Testoterone which is considered the King of Mass. Most companies would stop there but not AX. They wanted a complete formula that blows away everything else out there which is why I added 11-alpha and 2-androstenol acetate. Both of which dramatically increase nitrogen retention which promotes anabolism and intense pumps.
NP: Androsterone sounds like an extremely potent hormone as a standalone. How did you raise the bar with 3-AD, and can you explain why you included some of the other ingredients in your formulation?
MC: The bigger picture. Androsterone is a good compound but the entire 3-AD formula combines to provide the best legal anabolic available. 3-AD also addresses the shortcomings of all other products in this category, the androgen receptor. The more androgen receptors you have the better the anabolic effect will be. PLCAR increases the amount of androgen receptors, which is why it’s included in 3-AD.
NP: We noticed one of the ingredients in 3-AD is considered a “pheromone”. Can you further explain to our readers the actions and roles of pheromones and how it relates to muscle? Obviously we’re not talking about a “sex in a bottle” scent that will have women fighting over you (sorry guys).
MC: Of course not, and don’t be fooled into thinking that pheromones are exclusive to sexual attraction. Some creatures use them to let others know where food is, where home is, whether a predator is coming and quite a few more. The sexual pheromones are typically released in relation to a female’s monthly cycle (i.e. if she’s ripe for breeding), and from men in order to persuade the female that they’re worthy enough of procreating with. With these being tied tightly to the reproductive system and sexual characteristics, it is no surprise that the structure of pheromones typically reflect that of androgens. The only real requirement from that is, and which is applicable in the case of 2-androstenol, to ensure it’s orally bioavailable, and that’s been accomplished with the acetate ester.
NP: Wow, this truly sounds like a potent lineup of formidable ingredients! So are there any side effects associated with 3-AD such as hepatoxicity, hypertension, adverse estrogenic effects, etc??
MC: There is no risk of hepatoxicity because neither androsterone nor 2-androstenol are methylated. Hypertension shouldn’t be a cause for concern, although hormonals in general can increase red blood cell count or lead to slight water retention. Neither compound aromatizes, so there is no direct conversion to estrogen and therefore no anticipation of estrogenic-related side effects. I have however, seen some compounds that alter mineral levels which can cause slight water retention. The obvious side effects are all possible though, which is to be expected: acne, slight aggression and maybe mild shedding, suppression of natural testosterone production. Each user is different, but these are all possible. Some steroid users use Finasteride to overcome the shedding issues, but in this case 5AR inhibitors will not have any effect on either compound as they are already 5-alpha reduced.
NP: Is post cycle therapy (PCT) required for 3-AD?
MC: Absolutely. 3-AD is hormonal so I highly recommend everyone that uses it has adequate post-cycle therapy on hand from the get-go. I used and would recommend AX’s Advanced PCT, along with Activate Xtreme.
NP: How should one cycle 3-AD for optimal results?
MC: The dosing listed on the bottle is what will work best. Some users depending on bodyweight (220+lbs) may need a slightly higher dose but no one should assume they need it. Users should start at 2 caps twice a day for at least 7 days before increasing the dose to 2 caps- 3 times per day.
NP: How would you cycle 3-AD for maximum growth with minimal side effects?
MC: I think beginners should follow the dosing I’ve recommended until they know how they will respond to 3-AD. For experienced users I’ve always preferred high dosing for short periods of time. I feel this best mimics the way people grow, in short bursts. With 3-AD I would expect great results with 6-8 caps per day for no more then 24-28 days, followed by a 3 week PCT off period.
NP: So what’s the overall consensus on this revolutionary product? What types of gains should one expect to see with 3-AD?
MC: The feedback has been unbelievable! We’ve been seeing gains of anything from 3-18lbs over a four week cycle, with the average being around 12lbs. Side effects have been pretty much non-existent. So obviously I?m very excited about 3-AD and can’t wait to see how everyone else responds to it.
NP: So obviously 3-AD is great for packing on slabs of quality muscle, but is it also beneficial for recompositioning?
MC: Of course! The formula combines a very strong anabolic blend that is ideal for preserving muscle mass while trying to reduce fat stores and PLCAR. PLCAR is clinically proven to enhance the shuttling of fatty acids into muscle cellular mitochondria to be burned as a fuel source for greater energy production and is one of the reasons people feel warm when they take 3-AD.
NP: So what?s next on the horizon for you, Matt? Any other new compounds in the works? any sneak peaks for our subscribed readers?
MC: Yes, actually. We’re working on a follow-up to the hugely successful Glucophase XR product, only we’re taking it up a few notches. Of course it will cover insulin control for near-perfect calorie partitioning like its predecessor but finally we will introduce an actual IGF-1 promoting component that I’m sure will catch everyone’s interest.
NP: Sounds Great! We’re looking forward to the release of the new GXR! Matt, it was great talking to you my friend! NP wishes both Designer Supplements and Anabolic Xtreme continued growth and success, and we are proud to partner with these great companies!
MC: Thank you for having me, it has been my pleasure.”
More info on 3-AD can be found here: http://www.bodybuilding.com/store/ax/3ad.html
Posted in Training, Advanced Supplement Discussion
Wednesday, March 19th, 2008
There was a recent meta-study which showed a potential for the glycerol as a potential ergogenic aide but drew attention to the fact more studies need to be carried out. A few studies have been positive in the cyclists and a few haven’t in terms of performance. However, we have seen the rise of this compound in a few forum popular supplements like Glycergrow, SizeON, and PlasmaJet.
From my own use, it does seem to have some merit for hyperhydrating before weight training. It’s possible the this could help with force generation a bit but still needs to be observed in a clinical setting. Have you noticed any immediate “strength” increases while using it? I’d personally recommend 1-3 grams of GMS preworkout and intraworkout total if you want to experiment with it.
Here’s the meta-study I referenced above.
” Sports Med. 2007;37(11):981-1000. Links
Exploring the potential ergogenic effects of glycerol hyperhydration.
Nelson JL, Robergs RA.
Exercise Physiology Laboratories, University of New Mexico, Albuquerque, New Mexico 87131-1258, USA.
During athletic competition or recreational pursuits, a body’s hydration level can become compromised, resulting in a decrement in performance. Glycerol (1,2,3-propanetriol) has been used to induce hyperhydration in an attempt to offset the deleterious effects of dehydration. When glycerol is consumed orally, it is rapidly absorbed primarily in the small intestine. It is reported to be evenly distributed among all fluid compartments, with the exception of the cerebral spinal fluid and aqueous humour, and promotes hyperhydration by inducing an osmotic gradient. Through an increase in the kidney’s medullary concentration gradient, water absorption in the nephron is enhanced. When glycerol is consumed, the plasma glycerol concentration increases in proportion to the dose ingested, which easily exceeds the glycerol saturation point resulting in urinary glycerol excretion. Thus, without supplemental glycerol ingestion, there will be a decrease in the osmotic gradient resulting in a loss of hyperhydration. The ergogenic nature of glycerol has been investigated as to its effect on fluid retention, thermoregulation, cardiovascular responses and performance. While many studies provide evidence of hyperhydration, others do not. Only two studies reviewed showed a thermoregulatory advantage. Furthermore, the preponderance of evidence neither weighed for or against cardiovascular or performance advantages. What makes one study provide favourable results while another study does not is unclear. Possible explanations may include subject characteristics, environmental factors, research design, whether fluids with or without glycerol were given during exercise, the rate at which fluids are initially given to induce hyperhydration, the time between peak hyperhydration/peak plasma glycerol concentration and the trial (i.e. exercise), the glycerol dose (i.e. 1.0 g/kg body mass) and what it is based upon, the percentage glycerol solution (i.e. 5%, 20%), the variation of time between the end of the hydration protocol and the beginning of exercise, or perhaps the intensity of exercise (fixed, variable, percentage maximum oxygen uptake). What is clear is that glycerol has the capacity to enhance fluid retention. In so doing, glycerol hyperhydration may be a logistically preferred method due to concomitant decrease in urine output and free-water clearance, which may give a performance advantage by offsetting dehydration. Future research should focus on maintaining plasma glycerol concentrations at levels necessary to maintain osmotic forces required to support continued hyperhydration. Potential benefits of glycerol should be further explored to identify the circumstances or factors that may contribute to an ergogenic effect."
Posted in Advanced Supplement Discussion
Monday, February 18th, 2008
For the record pork, chicken, and red meat do contain carnosine and you can effect your intramuscular carnosine levels by eating a "bodybuilding" diet. Most people aren’t aware of this and no supplement company will market their product with this information.
For example I’m eating about 3 lbs of chicken and 1 pound of red meat a day. The typical carnosine content for chicken breasts is about 400mg/100g and beef is about 333mg/100g that would mean I getting in about 3.4 grams of carnosine from chicken and about 5.4 grams of carnosine from chicken and 1.51 grams from beef which is about 6.9 grams of carnosine total from my diet per day.
The reason I bring this up is two fold. One, the benefits of wholefood almost always trump that of supplements and animal meats certainly help provide a suitable source of carnosine albeit the not the most efficient mode due to the fact it’s broken down into beta alanine and histidine by carnosinase. Second, it also provides other benefits like protein, gluthionine, vitamin E, etc in their natural forms.This in part why protein powders are vastly inferior to animal meats except for the fact they are convenient.
Regardless, I don’t feel high dosed beta alanine is necessary if your diet is "good" like it should be. In the case of vegans this would be different story. However, there is no doubt that some supplementation is VERY beneficial as well from a wellness perspective as well as a proven physical performance enhancer.
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Originally Posted by LakunaKoil 
Excellent feedback , looks like BA is a staple for a lot of people
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I’ve made it a staple because it appears to fight glycation which is the cause for many age and diabetes related illnesse. It sucks that supplement companies can’t mention this because their is very strong evidence to suggest higher carnosine concentrations fights advanced glycation end products (AGEs). Here’s a good article by the Life Extension.
How Carnosine Protects Against Age-Related Disease By Edward R. Rosick, DO, MPH, MS
When I reviewed Octane I brought all of this up just because I felt it opened up a new perspective to the forum on this great supplement. This could apply to any BA product and is why I have my father taking it. He could care less about greater endurance, but does care about atherosclerosis and Alzheimer’s disease.
Posted in Advanced Supplement Discussion
Friday, February 8th, 2008
Curr Opin Clin Nutr Metab Care. 2008 Jan;11(1):50-4.
Growth hormone, arginine and exercise
Kanaley JA.
Department of Exercise Science, Syracuse University, Syracuse, New York, USA. jakanale@syr.edu
“PURPOSE OF REVIEW: To describe the effect of an acute bout of exercise on growth hormone responses and to discuss the effect of L-arginine supplementation on growth hormone responses. RECENT FINDINGS: Recent studies have shown that resting growth hormone responses increase with oral ingestion of L-arginine and the dose range is 5-9 g of arginine. Within this range there is a dose-dependent increase and higher doses are not well tolerated. Most studies using oral arginine have shown that arginine alone increases the resting growth hormone levels at least 100%, while exercise can increase growth hormone levels by 300-500%. The combination of oral arginine plus exercise attenuates the growth hormone response, however, and only increases growth hormone levels by around 200% compared to resting levels. SUMMARY: Exercise is a very potent stimulator of growth hormone release and there is considerable research documenting the dramatic growth hormone rise. At rest oral L-arginine ingestion will enhance the growth hormone response and the combination of arginine plus exercise increases growth hormone, but this increase may be less than seen with exercise alone. This diminished response is seen in both in both younger and older individuals.”
This study caused quite an stir on the forums because most preworkout nitric oxide formulas contain a hefty dose of arginine. What upset is the fact this study overlooked a lot of research which CLEARLY shows that when arginine is combined with certain amino acids or in the presence of carbs a conclusion like this is unfounded. Here is why.
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Originally Posted by Elliptical Envy
VS, I believe there are 2 or 3 studies posted in the supp science section. I haven’t came across any other studies regarding arginine and GH release. I was ready to jump to conclusions about the whole GH issue until I found other factors that could blunt or lower GH release as well.
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That’s the issue here few are taking into account. GH release is very sensitive to many stimuli which is why the construct of the arginine based studies is extremely flawed in the context of a normal athlete, bodybuilder, etc. No one is fasting for 12 hours before and arginine based supplement which is the point conveniently overlooked.
When combined with other aminos the effect of free form arginine is greatly diminished and is why in this study had to use a 12 hour fast to buffer the effect. I posted a link to the 1987 Ho study (that sounds funny) because it discusses the problems between elliciting and measuring enhanced GH secretion in the fed vs. fasted state. When you think about it, how many of us are ever in a fasted state let alone the fact numerous arginine based products contain carbs, BCAA (Superpump), etc which completely take you out of the fed state and blunt GH secretion at the time of injestion do to an insulin response. Pure arginine doesn’t do this and can clearly cause a autonegative feedback as seen in the Kanely 2006 study in which all subject were fasted.
That is the key here, when you have an insulin response you don’t have a GH response. When you don’t kick the GH negative feedback loop into effect which can attenuate its release while sleeping in theory GH response will still be high. Again, optimal GH secretion calls for exercising above the lactate threshold for a certain amount of time which few rarely do either as well. It also calls for an uninterrupted circadian rhythm too and healthy diet which fasting for 12 hours doesn’t seem to fit into. None of these factors were addressed Kanaley 2008 study and her generalizations without taking into the difference between the fasted and fed states is a bit disturbing to say the least.
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Originally Posted by Elliptical Envy
You really do make some awesome points there, Mr. Deserusan. I was reading chapter 21 in Natural Hormone Enhancement book and it touches on GH release and exercise.
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I really don’t want to come off like an ******* with my responses (it’s hard for me and we all know that) but a fundamental knowledge of GH secretion and insulin can answer many of these questions. It really gets on my nerves when abstract get presented in such a manner because had it been read it’s entirety you could easily see the problem of the construct which is why assertions should never be made on one to three line abstract conclusion. I’ve always had a problem with this regardless of the ingredient.
Here’s an except from the conclusion of the Kanaley 2008 study which would certainly afford a mode for the further discussion as opposed to just saying preworkout arginine blunts GH response during sleep implying it’s “bad. ”
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Originally Posted by Kanaley 2008
Studies have also examined the effect of short-term supplementation on the GH responses. Using a double-blind crossover protocol, Fogelhom et al. [41] studied the effects of a 4-day combined L-arginine, L-ornithine and L-lysine supplementation (2 g/day in two doses) on 24-h GH levels in weight lifters. Supplementation did not affect the physiological variation of serum GH or insulin concentrations. The ergogenic value of low-dose oral arginine ingestion for amino acid supplementation is questionable in healthy young individuals. Likewise, Abel et al. [42] questioned whether arginine effects would be apparent in healthy individuals. They investigated whether the daily intake of two different doses of arginine aspartate for 4 weeks affected parameters of overtraining syndrome in 30 male endurance trained athletes. These athletes either ingested arginine aspartate in a high dose (5.7 g arginine/8.7 g aspartate) or low dose (2.8 g arginine/2.2 g aspartate), or a placebo. Compared to placebo, no differences in maximal oxygen consumption, time to exhaustion, GH, glucagon, cortisol or testosterone concentrations were observed, and there was no difference between groups for dosage. Again this infers that arginine supplementation is not an effective ergogenic aid in healthy individuals.
The mechanism for the increase in GH with arginine is suspected to be by inhibition of endogenous somatostatin release [43]. Although the mechanism has not been specifically outlined, it is speculated that if arginine induces GH release via somatostatin and if the exercise-induced GH release is preferentially mediated by somatostatin withdrawal then potentially these two methods should be additive. Oral arginine taken about 30 min prior to exercise may cause an autonegative feedback on the somatotrope; thus it does not respond as efficiently as it would to just the exercise alone. The somatotrope is also known to have a refractory period when subjected to repeated GHRH stimulation due the autonegative feedback [44?47] and possibly the 30-min time period falls within that refractory period, and this becomes an issue of appropriate timing between the arginine ingestion and the exercise.
In contrast to the above findings, however, there is one study that coupled intravenous arginine with aerobic, constant load exercise. In this study, 30 g of intravenous arginine was administered immediately prior to exercise. GH area under the curve was slightly larger with arginine plus exercise than exercise alone and Wideman et al. [48] reported a doubling of GH secretory burst mass by arginine plus exercise vs. exercise alone. They concluded that exercise releases both GHRH and somatostatin, and L-arginine may limit somatostatin release. The dose of the arginine infusion used in the Wideman study (30 g of intravenous arginine) may, however, have overwhelmed the system, resulting in the higher GH response with arginine plus exercise than exercise alone. Studies using smaller doses (1500 mg to 9 g) taken orally 30 min prior to exercise may be reflecting the autonegative feedback from the arginine ingestion.
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Had this been read you could easily conclude that certain dietary elements will cause someone to avoid the pure arginine based autonegative feedback loop. It seems Ms. Jill Kanaley conveniently avoided a whole body of research to support her conclusion. Keep in mind this is her interpretation of her bibliography and not based on new clinical evidence which she participated in.
Quote:
Originally Posted by NO HYPE
So it is common knowledge that when arginine is combined with other amino’s and/or glucose, that the observed 50% decrease in GH during the fasted-state, is no longer an issue?
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Pretty much if you follow all the research. I also think it’s reaching to discuss anything in the fasted state to be honest because none of us who are following a typical bodybuilder or even “healthy” diet are never truly fasted.
Quote:
Originally Posted by NO HYPE
So if it’s already known that no “significant” inhibition will ocurr…. how much do the values actually change in a non-fasted state?
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Greatly especially if there is circulating glucose, insulin, etc. You have to understand that these fasted studies also shock the system and disrupt secretory patterns. Let’s say I eat certain meals at the same time practically everyday. My body can adjust it’s own GH secretory pattern around the insulin response from my meals.
My suggestion is that if you want to truly maximize GH output the best course of action is just following some of the basic fundamentals of a bodybuilding diet. Eating around every 3 hours, avoiding late night high GL carbs around bed time, etc. GH release just doesn’t happen while you sleep but rather in a pulsatile manner throughout the day. If you cause an extreme pulse at point X it could diminish the effect at point Y, thus decreasing the NET EFFECT of growth hormone secretion.
In all fairness, the Kanaley 2008 does have merit IF you are fasted and injesting pure l-arginine preworkout. However, if you take a look at most preworkout products they do contain carbohydrates and some even contain BCAA’s which are also insulinotropic. This outcome of this study would be much different in a real world application and thus I firmly believe both the title and conclusion are misleading.
Posted in Advanced Supplement Discussion
Friday, February 1st, 2008
I don’t use my blog as a platform for direct marketing of Gaspari Nutrition for numerous reasons. To me, this is an area for to express your thoughts, rant if need be, or share something with the rest of Bodybuilding.com community which you believe could be of interest of others. This is why I haven’t loaded this blog with affiliate links or tried to promote personal training or dieting services here to profit from. However, sometimes my role with Gaspari Nutrition does indeed give me cause to share something with you guys as it relates to my employment with them and so today’s story goes.

On the forums, our new NO2 product called PlasmaJet has been receiving a lot of attention which has mostly been positive. It is not yet sold on Bodybuilding.com but we have had a few members reviewing it and the results have been absolutely stellar. The majority of them has been reporting personal records on many lifts and truly been enjoying the effects. They are finding out while it is technically a NO2 product, it is the first one to actually improve physical performance in the gym in a significant manner.
Of course with the good comes the bad and we have been addressing some fairly poignant attacks regarding the inclusion of Peak ATP which we license from TSI Health Sciences. Despite my best efforts to break down some pretty dense research, the explanations would not appease those claiming to seek answers. Fortunately, since Gaspari Nutrition does respect intellectual property rights and understands the importance of utilizing the best compounds for our products we have access to some of the brightest minds in sport’s supplementation.

Adenosine 5′-triphosphate disodium salt
I’m not talking about people who lurk on forums or even authors who write for magazines. I’m talking about world renowned researchers with more published research and approved patents then you can shake a stick at. One of these great minds is Dr. Eliezer Rapaport who is the inventor of Peak ATP. Being able to interact with such an individual was an experience I will certainly not take for granted.
In today’s conference call involving Dr. Rapaport, Rich Gaspari, our COO, a representative of TSI, and myself, we were truly given an insight into PlasmaJet I never thought possible. I have to tell you it was pretty cool listening to Rich and Dr. Rapaport discuss the intricacies of the product and at times I was a bit too humbled to speak up and participate. However, I held my own and gained a much better perspective on how Peak ATP works in the context of PlasmaJet and truly improves performance to agree never seen before in any product in the nitric oxide class.
After lengthy discussion Dr. Rapaport also provided us with a nice position paper as well which you can read here.
Mr. Richard Gaspari
President and CEO
Gaspari Nutrition
501 Prospect St. Suite 107
Lakewood, NJ 08701 USA
Dear Rich,
Thank you for your time today on the conference call. Pursuant to your request, I wish to address some the questions you referenced today with respect to PEAK ATP?, and its ability to be absorbed by the body effectively when delivered in a liquid capsule formulation.
PlasmaJet is a glycerol based product containing PEAK ATP (disodium salt of adenosine 5?-triphosphate (ATP)). ATP, which is highly soluble in water, is not soluble in glycerol, we feel this benefits its stability this liquid capsule delivery vehicle in general.
Further, it is our position that ATP is stable in liquid capsules that contain the L-Arginine proprietary mixture developed by Gaspari Nutrition. After swallowing the capsules, they disintegrate in the stomach where ATP, along with the other ingredients, dissolve readily after the dilution of the glycerol (especially when athletes consume PlasmaJet with your recommended consumption of water). ATP, at a level of 200-250 mg/day, has its own buffering capacity in solution (pH 4-4.5), and it is completely stable in the gastric environment. Furthermore, it is now well established that absorption from a solution is much faster than absorption from a solid formulation, 20-30 minutes versus 30-120 minutes respectively. ATP is highly soluble in saliva or gastric juices and has its own buffering capacity, and it is completely protected from the gastric acidity of pH 1-2. The acidity of the stomach, over time at 370C, would cause a breakdown of the adenine-ribose bond in ATP. This is, however, not the case in PlasmeJet or any solid dose of ATP.
Scientific evidence suggests the disodium salt of ATP does not need to be enteric coated in order to be protected to produce significant biological effects. However, it remains my position that the optimal delivery of ATP in solid dosage form is through enteric means, the exceptions are liquid capsules as well as effervescent tablets, quick dissolve tablets and drink mixes delivered through aqueous means.
Additionally, disodium-ATP is now an approved drug in France under the brand name ATEPADENE? marketed by Laboratoires Mavoly-Spindler. ATEPADENE was approved for the treatment of subacute low back pain, which is muscular in origin. Namely, patients whereby the low back pain is a result of trauma, cancer or causes other than muscle pain were excluded. The effectiveness of ATP in this indication is attributed to the enhanced removal of lactic acid from low back skeletal muscle environment. ATP was shown effective in two large multi-sited trials, one of which was also double-blinded. Disodium-ATP was delivered orally as a solid powder in a two part hard shell capsule, which is not enteric coated. Patients took a dose of 90 milligrams disodium-ATP per day. These two clinical trials demonstrated that disodium-ATP is active without enteric coating at much lower levels than the doses recommended for PlasmaJet, for this specific indication. In addition, subacute low back pain (lumbago) is muscular in origin and the stimulation of blood flow, which is the biological basis for recovery, is a mechanism that operates after taking PlasmaJet. PlasmaJet is most likely more effective than disodium-ATP alone because of the presence of multiple mechanisms due to the action of ATP and L-Arginine in synergy. I enclose copies of the two published French papers, which clearly show that disodium-ATP need not be enterical coated to be effective in stimulation of blood flow along with the insert of ATEPADENE, the brand name of the product.
Once the L-Arginine and ATP are absorbed in the duodenum (the proximal part of the small intestine), and following established mechanisms, the increased level of blood plasma ATP and its degradation product adenosine stimulate both the uptake of L-Arginine by vascular endothelial cells and the synthesis of nitric oxide (NO), which is catalyzed by nitric oxide synthase (NOS).
The elevated NO produces an immediate vasorelaxation (vasodilation) increased blood flow to skeletal muscle resulting in enhanced disposal of oxygen, glucose and other nutrients to the working muscle, along with significant stimulation of removal of lactic acid and ammonia which are byproducts of the exercising muscle. Overall, the stimulated removal of lactic acid yields a decrease in muscle ache and enhanced recovery.
I hope this answers your questions. Please let me know if you are in need of further assistance.
Best regards,
Eliezer Rapaport, Ph.D. ”
When all is said and done, I said to myself, “You are one lucky mother****er Dan.” How many opportunities in life do you have to sit down and discuss your passions with PhD’s like Dr. Rapaport and an IFBB Hall of Famer like Rich Gaspari? Fortunately for me, occurrences like this are now a reality in my roll with Gaspari Nutrition. The future is certainly bright and it’s truly an honor to have opportunities to be in the presence of both physical and intellectual greatness.
-What a man can be, he must be. This need we call self-actualization.
Abraham Maslow
Posted in Advanced Supplement Discussion
Tuesday, January 22nd, 2008
Quote:
| Zhang G, Shirai N, Higuchi T, Suzuki H, Shimizu E. Effect of Erabu Sea Snake (Laticauda semifasciata) Lipids on the Swimming Endurance of Aged Mice.Nutr Sci Vitaminol (Tokyo). 2008 Dec;53(6):476-81.
The effect of Erabu sea snake (Laticauda semifasciata) lipids on the swimming endurance was investigated in aged mice. Fifty three-week-old male Crlj:CD-1 (ICR) mice were fed one of three experimental diets containing either 6% lard, 6% fish oil, or 6% sea snake lipids for 16 wk. The swimming exercise was carried out in an acrylic plastic tank filled with 25 cm of water maintained at 23(o)C. Swimming times to exhaustion were measured with a load of 2% of their body weights attached to the tails of the mice. The swimming times to exhaustion of the group that were fed the sea snake lipid diet tended to be longer than those of the lard diet group, and were significantly improved compared with the fish oil diet group (p<0.05). The plasma and muscle lactate levels were significantly lower in the sea snake lipid diet group than in the lard and fish oil diet groups (p<0.05). The liver glycogen and plasma glucose levels of the sea snake lipid diet group did not differ markedly from those of the lard diet group (p>0.05), and were significantly higher than those of the fish oil diet group (p<0.05). These results suggest that an intake of sea snake lipids but not the fish oil, which is also rich in n-3 polyunsaturated fatty acids (n-3 PUFAs), is useful for improving the swimming endurance of aged mice by attenuating lactate production and/or enhancing lactate clearance during swimming exercise, and the n-3 PUFAs contained in the sea snake lipids did little or nothing for this improved endurance. |
Apparently the sea snake lipids have the ability to increase lactate clearance from plasma. Lactate is formed during anaerobic exercise such as weight lifting, sprinting, and in some endurance exercise depending on the individual lactate threshold. Anyway, it appears at least in mice that snake oil does have some efficacy in raising the lactate threshold.
It would be interesting to see the implications of supplemental snake oil deployed in humans using Fartlek or interval training as the exercise medium. Either way, it looks the snake oil salesman might be getting his fifteen minutes of fame with some righteous humor.
Posted in Advanced Supplement Discussion
Sunday, January 13th, 2008
It’s no doubt that in the supplement industry us manufacturers are vying for market presence by “one upping” the competition in terms of marketing and formulation. Pick up any bodybuilding magazine and you will see RIDICULOUS advertisement claims which are often not supported by any clinical research. Sometimes I wish I had gone into law just I could throw the Lanham Act at some of these purveyors of “broscience.”
Broscience - a term first used on the Bodybuilding.com forums to describe those most likely to pass on false information while using the term “bro”
Yes, I work for the company that came out with the infamous “box” ad and you are probably thinking, “Who the **** is this guy?” Beyond the obvious marketing genius which captured our target market we did not make up the statistics used in the ad and every single one of the ingredients has research supporting its efficacy.
As you most of you may or may not know beta-alanine (3-Aminopropanoic acid) is hottest new supplement on the market since creatine. From the hardest training athlete looking for increased muscular endurance to the most disgusting Big Mac eating slob who needs to fight off diabetes related advanced glycation end products, beta alanine can certainly be of great benefit. Even better, this compound is dirt cheap, not aromatic, and is extremely water soluble. Keep in mind what percentage of your body mass is actually water too!
Beta-Alanine
Despite its solubility being so high some have found it necessary to bastardize this intriguing compound through esterfication. I’m fairly certain many of you of became aware of the “ethyl ester” craze when during the CEE boom which has essentially been pissed on by recent research studies conducted by Dr. Marc Tallon et al.
You’d even be surprised at what popular CEE products apparently are actually creatine monohydrate and have been “called out” in a recent class action lawsuit which I’ll leave nameless because I don’t need to be named in another federal lawsuit for merely stating the truth about some the scum in the supplement industry. They should have just called their product NO-CEE.
*This is a repost because the original post was altered somehow and not by me.
Posted in Advanced Supplement Discussion
Tuesday, January 8th, 2008
It appears that ingesting carbohydrates along with electrolytes (sodium and potassium are also in SizeON) these negative physiological processes are attenuated (5). By drinking something like SizeON you most notably limit the effects of that 5-HT has on limiting dopamine production (6) by limiting tryptophan transport into the brain (7).
5. Winnick JJ, Davis JM, Welsh RS, Carmichael MD, Murphy EA, Blackmon JA.Carbohydrate feedings during team sport exercise preserve physical and CNS function. Med Sci Sports Exerc. 2005 Feb;37(2):306-15.
6. Fernstrom JD, Fernstrom MH. Exercise, serum free tryptophan, and central fatigue. J Nutr. 2006Feb;136(2):553S-559S.
7. Davis JM, Bailey SP, Woods JA, Galiano FJ, Hamilton MT, Bartoli WP. Effects of carbohydrate feedings on plasma free tryptophan and branched-chain amino acids during prolonged cycling. Eur J Appl Physiol Occup Physiol. 1992;65(6):513-9.
Originally Posted by Peter LeDrew 
I thought carbs increased Tryptophan availablility in the brain?
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Not during exercise, but in a resting state yes. Here is a great paper on the matter. I suggest anyone who considers dosages of intraworkout BCAA’s over 7 grams highly effective in improving performance versus carbs read this. I’m still playing devil’s advocate on the matter for what it’s worth.
Follow the debate on intra-workout nutrition here:
Posted in Advanced Supplement Discussion
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