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Core Nutritionals - Core FURY 28sv

Core Nutritionals - Core FURY 28sv


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Extreme Pre-Workout Performance Amplifier

When we first released Core FURY, we said a few things: we said that it was revolutionary, because it didn’t try to be. We said that it was formulated with clinically researched serving sizes, in a non-proprietary blend, that was made to be our most effective pre-workout supplement. We said it was amazing. We said that it couldn’t be topped. Well, we were wrong.

With Core FURY Extreme, we have somehow improved on our best, most-potent, most-concentrated pre-workout by including even more science-backed ingredients, in even bigger servings. Best of all? We have crammed every last milligram of PR-smashing Core FURY Extreme goodness into a single scoop.

No more debates about two scoops or three. Actually, no more debates period. Core FURY Extreme has every conceivable angle, mechanism, or benefit you’d want in a pre-workout covered, and we somehow managed to combine that with an amazing taste? An actual serving of creatine, one that would be enough for a creatine-only product? Yeah, we have that. One of the highest servings of citrulline, betaine, and agmatine out there? That too. What about an insane stimulant mixture, including a longer-lasting, more effective, clinically-studied form of caffeine in combination with pterostilbene? Of course.

What Core FURY Extreme doesn’t have is room for error, or a proprietary blend that masks the amount of every ingredient. This product was made by the best, for the best, to be used as a single scoop, single product arsenal against fatigue and excuses. You want the scoop? You can’t handle the scoop.

Scientific breakdown:

Creatine monohydrate:

Sometimes called the “grandfather” of dietary supplements, creatine is, along with caffeine, one of the most extensively studied dietary compounds. Certainly, it is the most well-studied ergogenic aid. Generally speaking, the extensive amount of data on creatine demonstrates that it positively contributes to dilation of the vasculature, plasma-nutrient mobilization, post-workout nitrogen retention and protein synthesis, along with dose-dependently increasing contractile force through ATP (adenosine triphosphate) provision (i.e., it helps support increased strength).*

If the human body could be considered a bank account, then ATP would be the currency, and every cellular process would be like spending a little money from that account. Without making a deposit, the account runs dry (fatigue). Unfortunately, making a direct deposit to that account in the form of exogenous adenosine triphosphate is impossible, given that ATP itself is incredibly unstable. The use of supplemental creatine, however, is analogous to making a deposit in the body’s energy bank, given that creatine is eventually metabolized to ATP via several steps. In skeletal muscle, creatine is first phosphorylated into its primary derivative, known as phosphocreatine (PCr), by the muscle-specific creatine kinase, creatine kinase-MB (muscle-brain). Following the phosphorylation of creatine, phosphocreatine may then anaerobically donate a phosphate molecule to adenosine diphosphate (ADP) to form the ATP required during the initial stages of intense muscular contraction. The result is not only an increase in contractile force, but also an increase in potential type IIx (‘fast-twitch’) muscle recruitment – the type of muscle fibers which are not only traditionally associated with speed, strength, and physique, but which are also unsurprisingly the most energy-demanding fiber types. Literally speaking, creatine contributes to the building of muscle.*

Both through the ATP provision just described, as well as effects on nutrient mobilization, protein-sparing, and fluid dynamics, creatine has been consistently suggested to support both lean and muscle mass in clinical data. In the short-term, these effects are most likely the result of extra-cellular fluid retention normally associated with exogenous creatine use. In the long term, these effects are likely attributable to creatine’s collective effect on muscle metabolism. The most recent research on creatine suggests it exerts direct effects on muscle metabolism, including altering the expression of genes responsible for ribosomal assembly, attenuating the breakdown of leucine, and most famously, by expanding cell volume. Cutting through the jargon, let us just say that the amount of creatine monohydrate contained in Core FURY Extreme simply works: these servings have been shown time and again to significantly increase lean body mass and muscle volume, lower fatigue, and support performance (measured in several ways).*

Skip the gimmick, alternative forms of creatine (creatine ethyl ester, “buffered” creatines, etc) and stick to the tried and true creatine monohydrate found in Core FURY Extreme! Unlike many of the preworkouts on the market that will “sprinkle” creatine monohydrate in their proprietary blend, at 5,000 mg per one scoop serving, Core FURY Extreme uses a clinically supported serving of creatine monohydrate.

L-Citrulline

Citrulline is a non-essential, non-protein amino acid that forms during the urea cycle and forms ornithine when combined with carbon dioxide. Citrulline is also a critical source of endogenous (natural) arginine, as it is rapidly and efficiently converted to arginine in the vascular endothelium and other tissues.

Like agmatine, the other arginine pre-cursor/byproduct featured in Core FURY Extreme, citrulline’s benefits have been shown to be greater than its parent compound. While arginine undergoes direct hepatic (liver) metabolism through the enzyme arginase, citrulline bypasses hepatic metabolism entirely and it is delivered straight to the bloodstream. The result is that gut absorption and plasma (blood) bioavailability studies comparing citrulline and arginine have shown two things. First, that citrulline is less readily destroyed and has greater absorption than arginine. Second, that citrulline supplementation increases arginine levels more effectively than arginine supplementation itself.

This translates to promising results. For example, animal studies show a significant increase in anaerobic performance at a 250mg/kg/day serving of citrulline, while studies in humans implicate citrulline in both aerobic and anaerobic performance increases. As a critical part of the urea cycle, citrulline’s performance benefits are thought to be a result of its role in ammonia clearance. Citrulline is implicated in reducing the oxygen cost of muscle processes, along with increasing the rate of post-exercise ATP and phosphocreatine replenishment. As ATP and phosphocreatine are the body’s ‘exercise fuel,’ this may result in citrulline delaying time to exhaustion in aerobic and anaerobic exercise.*

Trimethylglycine (Betaine):

Betaine (trimethylglycine) is found naturally in most living organisms. It is well known to protect non-mammalian animal life in conditions of osmotic stress (a rapid change in the amount of solute surrounding a cell), in addition to functioning as an osmolyte in mammalian (including human) tissues). Betaine is formed in cells as an oxidation product of choline and can be obtained in the diet from foods such as spinach and beets.

Though data on betaine is limited, and recent, the available literature suggests that this compound may have effects in a number of areas. Studies on betaine using servings as little as 1.25g/day and up to 5g/day for up to 14 days have shown promising results. In one study, a 2.5g/day serving was found to enhance endurance and total repetition volume for the squat, bench press, and jump squat in in healthy-exercised trained adults. A similar study using the same serving found that betaine use increased peak power and maximum peak power, along with force and the maintenance of both force and power in healthy, exercise-trained subjects.*

Perhaps more interesting, however, is a study which examined betaine’s effect on the endocrine system. This study revealed that betaine may exert an effect on several endocine processes given the proper conditions, causing the authors to hypothesize that long(er) term betaine supplementation may support the hypertrophic response to resistance training.*

Agmatine sulfate:

Agmatine is part of a group of compounds known as polyamines, alphatic amines which play multiple physiological roles in tissue growth and differentiation, body weight increment, brain organization, molecular mechanisms of hormonal action, intracellular signaling, and extracellular communication. Agmatine itself is naturally produced in the body by the breakdown of arginine. Paradoxically, the studied effects of agmatine not only appear to mimic those of its parent compound arginine, but in many cases, surpass it. These effects include an increase in localized bloodflow (better plasma delivery), dilation of the vasculature (expanding of blood vessels), increased nutrient delivery, and a hypothesized support for the health of the hypothalamic-pituitary axis.*

The literature suggests that agmatine sulfate’s positive regulation of NO (nitric oxide) levels occur within the classical NO-eNOS (endothelial nitric oxide synthase) pathway. Like arginine, agmatine appears to increase plasma nitric oxide via functioning as a competitive inhibitor of nitric oxide synthase. As a polyamine, agmatine may also play a role in the functioning of the hypothalamic-pituitary axis (HPTA). Data in mammals have shown that polyamines are related to gonadotropin release, and in particular, promote an increased luteinizing hormone (LH) production. This positive regulation of gonadotropin is suggested to be the result of increased γ-aminobutyric acid (GABA) synthesis, a neurotransmitter critically involved in the regulation of gonadotropin secretion.*

N-acetyl-tyrosine

Tyrosine is amongst a class of amino acids known as ‘non-essential’ amino acids, so called because the body can produce them endogenously, and it is therefore not essential to consume dietary tyrosine. That said, tyrosine is also what is known as a conditionally-essential amino acid; conditionally-essential because, along with glucose and ammonia, the synthesis of tyrosine additionally requires adequate levels of phenylalanine. Once synthesized, tyrosine is one of the most critical amino acids, given its prominent role as a substrate in the synthesis of the catecholamines dopamine, norepinephrine, and epinephrine, in addition to both T3 (triiodothyronine) and T4 (thyroxine) thyroid hormones.*

In studies on stress modulation, tyrosine has been suggested to reduce norepinephrine depletion and the depressant-behavioral effects normally associated with heavy physical training.* In simpler terms, tyrosine may, in certain conditions, dampen the extent to which norepinephrine is removed from the bloodstream during workouts.* In simpler terms still, tyrosine may help to mitigate the sense of depletion and fatigue felt at the end of a workout.*

Tyrosine may also play important metabolic functions, mostly related to its role in synthesizing compounds which stimulate the nervous system. While not traditionally considered a sympathomimetic amine, studies which have coadministered tyrosine and stimulants demonstrate a synergistic effect. These studies suggest that tyrosine may potentiate the effects of both endogenous and supplemental norepinephrine and its mimetics (in the case of exogenous use) with respect to lipolysis, thermogenesis, and energy expenditure. Meaning that tyrosine may play a role in assisting norepinephrine to break up triglycerides and increase body heat transiently.*

N-acetyl L-tyrosine, the form used in Core FURY Extreme, is widely believed to be a more bioavailable form of tyrosine. And, not surprisingly, the serving size contained in just a single scoop of Core FURY Extreme lines up with the provided servings in man studies on tyrosine.

Choline Bitartrate:

Choline is an essential nutrient involved in numerous metabolic pathways, including DNA regulation and repair, protein function, and metabolism. Perhaps most importantly, the critical neurotransmitter acetylcholine is produced directly from free choline via cholinergic neurons. Acetylcholine is then responsible for a number of functions itself, most crucially as the compound which induces muscular contraction, and as the neuromodulator partially responsible for modulating risk/reward, arousal, and supporting memory.*

Choline’s essential role as a substrate for acetylcholine, and therefore brain development, is well documented in animal models. Choline’s supporting effect is particularly prominent in the hippocampus. In humans, the hippocampus is primarily involved in the consolidation of memory (taking short, episodic memory and translating it into long-term memory) and the learning of new information. Acetylcholine is a critical component in these processes, as mentioned above, and choline may therefore play a potential role in these processes as well by providing the substrate for acetylcholine synthesis.

Tartaric acid occurs naturally in the food source, while its salt derivatives (tartrate, for example) have been used as acidulants, antioxidant synergists, buffers and sequestrants. As free base choline is rapidly destroyed in metabolism, attaching a salt to enhance absorption is necessary. The bitartrate salt addition preserves choline from being destroyed during metabolism.

1,3,7-trimethylxanthine (Caffeine) and Theobromine (3,7-dimethyl-1H-purine-2,6-dione) 99%

Caffeine and its fellow xanthine and metabolite, theobromine, are some of the most widely consumed, and perhaps some of the most reviewed, psychoactive compounds. Their physiological effects in a range of areas have been well-documented, including exercise performance, information processing, alertness and mood enhancement, attention, and awareness, along with its anti-lipogenic and lipolytic abilities.

Most importantly to Core FURY Extreme, caffeine has been shown to have significant effects on exercise performance, even with ingestion in servings as small 3 to 9mg/kg/bw/day (the equivalent of 2 cups of standard coffee, for a 170lb male). In endurance training, possible explanations for caffeine’s performance-enhancing effects lie in its metabolic effects on both lean and fat tissue. It is suggested that caffeine’s potent lipolytic (the breakdown of fat tissue into fatty acids) and oxidative (the actual ‘burning’ of fat) action allow the body to utilize these sources during prolonged submaximal exercise. As a consequence, muscle glycogen is spared and available for use later in the training session. Practically speaking, this means caffeine is forcing your body to preferentially use fat tissue as a fuel source, while sparing the glycogen which gives you the full-bodied look!

In short-term exercise, both caffeine’s and theobromine’s demonstrated role in the inhibition of cyclic AMP- phosphodiesterases (PDE), adenosine receptor antagonism, and adrenoreceptor agonism come into play. These three pathways collectively stimulate lipolytic activity, boost fat metabolism, increase metabolic rate and energy expenditure, and regulate the body’s thermogenic activity. The practical results of activating these pathways are increases to the contractile force of both cardiac and skeletal muscle (harder flexion), an increase in energy expenditure (freeing up more caloric energy to be used in contraction), dilation of vasculature (better blood flow), and improvements to both nitrogen retention and skeletal muscle protein synthesis (key components to muscle building).

In Core FURY Extreme, we have included a per-serving amount of caffeine and theobromine that is neither excessive, nor arbitrary, but that instead reflects the servings used in clinical research.

Niacin, also commonly known as nicotinic acid, has been demonstrated to exert potent effects on lipid metabolism; and a significant body of literature exists, focusing on its role as a therapeutic target in that context. In addition to playing a role in supporting healthy HDL cholesterol levels, and rapidly and dose-dependently inducing a decrease in the concentrations of plasma triglycerides, niacin is a powerful vasodilator.

PURENERGY™ (Caffeine Pterostilbene Complex):

PURENERGY™ is a highly interesting, novel new dietary ingredient created by combining caffeine (at a 43% proportion) with pTeroPure, a 99% pure all-trans pterostilbene (at 53% proportion).

Pterostilbene is, in turn, itself a highly interesting compound, and the subject of considerable excitement and clinical research within the sports community. Found in small concentrations in blueberries and grapes, pterostilbene is a dimethylated version of the well-known compound resveratrol, and as a consequence, appears to share many of its beneficial physiological effects. Pterostilbene in addition has been hypothesized to exert unique effects in the human body through both genomic and enzymatic pathways, including functioning as a potent antioxidant, as well as playing a role in the regulation of glycolytic/gluconeogenic enzymes such as hexokinase, glucose-6-phosphatase, and fructose-1,6-bisphosphatase.

In combination as PURENERGY™, caffeine and pterostilbene have been the subject of a single, but promising, human trial. The results from this trial demonstrated:

  • PURENERGY™ delivers almost 30% more caffeine into the blood than ordinary caffeine.

  • The rate of caffeine absorption is significantly slower with PURENERGY™, by about 30% as compared to ordinary caffeine

  • The half-life of caffeine from PURENERGY™ is extended significantly by about 25% over that of ordinary caffeine.

  • At 4 hours, there was 45% more caffeine from PURENERGY™ compared to ordinary caffeine alone

  • At 6 hours, there was 51% more caffeine from PURENERGY™ compared to ordinary caffeine alone.

  • At 6 hours, subjects taking PURENERGY™ supportted significantly less fatigue and greater concentration compared to baseline.* Ordinary caffeine did not.

  • At 6 hours, subjects taking PURENERGY™ supported improved energy, alertness and focus compared to baseline.* Ordinary caffeine did not.

  • Coupled with a lack of adverse events seen in the trial, PURENERGY™ may represent a significant leap forward in the dietary supplement field.

Hordenine (N,N-dimethyltyramine) HCl:

Hordenine is one of the most favored stimulant ingredients in bodybuilding circles, and has been for some time. Users rave about hordenine, due to its structural similarity with several potent nootropics and stimulants.*

Though limited, some animal research suggest that hordenine may modulate certain brain and nervous system processes, and perhaps regulating the body’s release of and response to noradrenaline.

Synephrine HCL:

Synephrine is a naturally-occurring alkaloid with adrenergic agonist activity, structurally related to epinephrine, norepinephrine, ephedrine, and other compounds with a phenethylamine base structure. Despite its chemical similarity to these compounds, synephrine in its various isomers exerts unique effects on adrenergic receptors, in particular, and the human body, in general.

Synephrine exists in three isomer forms: para-, meta- and ortho-synephrine. The molecular changes between the three isoforms are minute, but even this small change results in significant alterations to each isomer’s physiological and pharmacokinetic profile. Two of synephrine’s isomers, both p- and m-synephrine, have been shown to naturally occur in mammals (in low concentrations).

As a sympathomimetic, synephrine has been the subject of numerous trials, assessing its effects on weight management, thermogenesis, metabolic rate, and caloric expenditure. In a double-blind, randomized, and placebo-controlled trial involving 10 healthy individuals, the p-synephrine isomer was administered at a 50mg serving, both alone, and in combination with hesperidin and naringin. The authors measured resting metabolic rate (RMR), blood pressure, and heart rate, along with subjective feelings of mood and energy, at baseline, and at 45-mintues and 75-minutes after ingestion. The authors reported a significant increase in RMR in each of the supplement groups, relative to placebo.*

In combination with caffeine, synephrine’s metabolic effects appear to be potentiated – with rates of fatty acid liberation, heart rate, metabolic rate, and fatty acid oxidation increased.

 

References:

Tipton KD, Cocke TL, Wolf SE, Wolfe RR. Response of muscle protein metabolism to resistance training and acute resistance exercise during hyperaminoacidemia. Am J Physiol, 2006.

Borsheim E, Tipton KD, Wolf SE, Wolfe RR. Essential amino acids and muscle protein recovery from resistance exercise. Am J Physiol Endocrinol Metab. 2002;283.

Rudman D, Kutner M, Ansley J, et al. Hypotyrosinemia, hypocystinemia and failure to retain nitrogen during total parenteral nutrition of cirrhotic patients. Gastroenterology 1981; 81: 1025-35.

Rasmussen D. Effects of tyrosine and tryptophan ingestion on plasma catechloamine concentrations. J Clin Endo Metab 1983; 57(4):760-763.

Agharanya JC, Alonso R, Wurtman RJ. Changes in catecholamine excretion after short-term tyrosine ingestion in normally fed human subjects. Am J Clin Nutr 1981 Jan;34(1):82-7.

Shurtleff D, Thomas JR, Shlers ST, et al. Tyrosine ameliorates a cold-induced delayed matching-to sample performance decrements in rats. Psychopharmacology 1993; 112:228-232, .

Owasoyo JO, Neri DF, Lamberth JG. Tyrosine and its potential use as a countermeasure to performance decrement in military sustained operations. Aviation Space and Enviromental Medicine 1992; 63:364-369.

Lehnert H, Reinstein DK, Strowbridge BW et al. Neurochemical and behavioral consequences of acute, uncontrollable stress: effects of dietary tyrosine. Brain Res 1984 Jun 15;303(2):215-23

Shurtleff D, Thomas JR, Schrot J, et al. Tyrosine reverses a cold-induced working memory deficit in humans. Pharmacol Biochem Behav 1994 Apr;47(4):935-41.

Deijen JB, Wientjes CJ, Vullinghs HF et al. Tyrosine improves cognitive performance and reduces blood pressure in cadets after one week of a combat training course. Brain Res Bull 1999 Jan 15;48(2):203-9.

Thomas JR, Lockwood PA, Singh A, et al. Tyrosine improves working memory in a multitasking environment. Pharmacol Biochem Behav 1999 Nov;64(3):495-500.

Shukitt-Hale B, Stillman MJ, Lieberman HR. Tyrosine administration prevents hypoxia-induced decrements in learning and memory. Physiol Behav 1996 Apr-May;59(4-5):867-71.

Lehnert H, Wurtman RJ. Amino acid control of neurotransmitter synthesis and release: physiological and clinical implications. Psychotherapy and Psychosomatics 1993, 60:18-32.

Hull KM, Maher TJ. L-Tyrosine in rats. J Pharm Exp Ther 1990, 255:403-409.

Hull KM, Maher TJ. L-Tyrosine fails to potentiate several peripheral actions of the sympathomimetics. Pharm Biochem Behav 1991, 39:755-759.

Alonso R, Gibson CJ, Wurtman RJ, et al. Elevation of urinary catecholamines and their metabolites following tyrosine administration in humans. Biol Psychiatry 1982, 17:781-790.

Lever M, Sizeland PC, Bason LM, Hayman CM, Chambers ST. Glycine betaine and proline betaine in human blood and urine. Biochim Biophys Acta1994;1200:259–64.

Sakura N, Ono H, Nomura S, Ueda H, Fujita N. Betaine dose and treatment intervals in therapy for homocystinuria due to 5, 10-methylenetetrahydrofolate reductase deficiency. J Inherit Metab Dis1998;21:84–5.

Virtanen E, Junnila M, Soivio A. Effects of food containing betaine/amino acid additive on the osmotic adaptation of young Atlantic salmon, Salmo salar L. Aquaculture 1989;83:109–22.

Virtanen E, Cambell R. Reduction of backfat thickness through supplementation of diets for fattening pigs. In: Verlag H, ed. Handbuch der tierischen Veredlung. Oesnabruek, Germany: Kamlage, 1994:145–50.

McCully KS. Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am J Pathol 1969;56:111–28.

Eikelboom JW, Lonn E, Genest J Jr, Hankey G, Yusuf S. Homocyst(e)ine: a critical review of the epidemiologic evidence. Ann Intern Med 1999;131:363–75.

Li YF, Gong ZH, Cao JB, Wang HL, Luo ZP, & Li J. (2003). Effect of agmatine and its possible mechanism. European Journal of Pharmacology. 469(1-3), 81-8.

Zhu MY, Wang WP, Cai ZW, Regunathan S, & Ordway G. (2008). Exogenous agmatine has neuroprotective effects against restraint-induced structural changes in the rat brain. The European Journal of Neuroscience. 27(6), 1320-32.

Demady DR, Jianmongkol S, Vuletich JL, Bender AT, & Osawa Y. (2001). Agmatine enhances the NADPH oxidase activity of neuronal NO synthase and leads to oxidative inactivation of the enzyme. Molecular Pharmacology. 59(1), 24-9.

Zarandi M, Serfozo P, Zsigo J, Bokser L, Janaky T, Olsen DB, Bajusz S, & Schally AV. (1992). Potent agonists of growth hormone-releasing hormone. Part I. International Journal of Peptide and Protein Research. 39(3), 211-7. Kalra SP, Pearson E, Sahu A, & Kalra PS. (1995). Agmatine, a novel hypothalamic amine, stimulates pituitary luteinizing hormone release in vivo and hypothalamic luteinizing hormone-releasing hormone release in vitro. Neuroscience Letters. 194(3), 165-8.

Arndt MA, Battaglia V, Parisi E, Lortie MJ, Isome M, Baskerville C, Pizzo DP, Ientile R, Colombatto S, Toninello A, & Satriano J. (2009). The arginine metabolite agmatine protects mitochondrial function and confers resistance to cellular apoptosis. American Journal of Physiology. Cell Physiology. 296(6), C1411-9.

Bemben MG, Lamont HS Creatine supplementation and exercise performance: recent findings. Sports Med. (2005) 35(2):107-25.

van Loon LJ et. al. Effects of creatine loading and prolonged creatine supplementation on body composition, fuel selection, sprint and endurance performance in humans. Clin Sci (Lond). (2003) 104(2):153-62.

Rawson ES, Volek JS. Effects of creatine supplementation and resistance training on muscle strength and weightlifting performance. J Strength Cond Res. (2003) 17(4):822-31.

Kreider RB. Effects of creatine supplementation on performance and training adaptations. Mol Cell Biochem. (2003) 244(1-2):89-94.

Willoughby DS and J. Rosene. Effects of oral creatine and resistance training on myosin heavy chain expression. Med Sci Sports Exerc. (2001) 33(10):1674-81.

Willoughby DS and JM Rosene. Effects of oral creatine and resistance training on myogenic regulatory factor expression. Med Sci Sports Exerc. (2003) 35(6):923-9.

Mihic S et. al. Acute creatine loading increases fat-free mass, but does not affect blood pressure, plasma creatinine, or CK activity in men and women. Med Sci Sports Exerc. (2000) 32(2):291-6.

Branch JD. Effect of creatine supplementation on body composition and performance: a meta-analysis. Int J Sport Nutr Exerc Metab. (2003) 13(2):198-226.

Louis M et. al. No effect of creatine supplementation on human myofibrillar and protein synthesis after resistance exercise. Am J Physiol Endocrinol Metab. (2003) 285(5):E1089-94.

Louis M et. al. Creatine supplementation has no effect on human muscle protein turnover at rest in the postabsorptive or fed states. Am J Physiol Endocrinol Metab. (2003) 284(4):E764-70.

Juhn MS, Oral creatine supplementation and athletic performance: a critical review. Clin J Sport Med. (1998) 8(4):286-97.

Chwalbinska-Moneta J. Effect of creatine supplementation on aerobic performance and anaerobic capacity in elite rowers in the course of endurance training. Int J Sport Nutr Exerc Metab. (2003) 13(2):173-83.

Engelhardt M et. al. Creatine supplementation in endurance sports. Med Sci Sports Exerc. (1998) 30(7):1123-9. Santos RV et. al. The effect of creatine supplementation er a 30km race. Life Sci. (2004) 75(16):1917-24.

van Loon LJ et. al. Creatine supplementation increases glycogen storage but not GLUT-4 expression in human skeletal muscle. Clin Sci (Lond). (2004) 106(1):99-106.

Syrotuik DG, Bell GJ.Acute creatine monohydrate supplementation: a descriptive physiological profile of responders vs. nonresponders. J Strength Cond Res. (2004) 18(3):610-7.

Hespel P et. al. Opposite actions of caffeine and creatine on muscle relaxation time in humans. J Appl Physiol. (2002) 92(2):513-8.

Vandenberghe K, et. al.Caffeine counteracts the ergogenic action of muscle creatine loading. J Appl Physiol. (1996) 80(2):452-7.

van Leemputte M et. al. Shortening of muscle relaxation time after creatine loading. J Appl Physiol. (1999) 86(3):840-4.

Bizzarini E et. al. Is the use of oral creatine supplementation safe? J Sports Med Phys Fitness. (2004) 44(4):411-6.

Greenwood M, et. al. Creatine supplementation during college football training does not increase the incidence of cramping or injury. Mol Cell Biochem. (2003) 244(1-2):83-8.

Casey A and PL Greenhaff PL. Does dietary creatine supplementation play a role in skeletal muscle metabolism and performance? Am J Clin Nutr. (2000) 72(2 Suppl):607S-17S.

Steenge GR et. al. Protein- and carbohydrate-induced augmentation of whole body creatine retention in humans. J Appl Physiol. (2000) 89(3):1165-71.

Burke DG et. al. Effect of alpha-lipoic acid combined with creatine monohydrate on human skeletal muscle creatine and phosphagen concentration. Int J Sport Nutr Exerc Metab. (2003) 13(3):294-302.

Preen D et. al. Int J Sport Nutr Exerc Metab. Creatine supplementation: a comparison of loading and maintenance protocols on creatine uptake by human skeletal muscle. (2003) 13(1):97-111.

Burke DG et. al. Effect of creatine and weight training on muscle creatine and performance in vegetarians. Med Sci Sports Exerc. (2003) 35(11):1946-55.

Tarnopolsky, M. et. al. Acute and moderate-term creatine monohydrate supplementation does not affect creatine transporter mRNA or protein content in either young or elderly humans. Mol Cell Biochem. (2003) 244(1-2):159-66.

Alfieri RR, Bonelli MA, Cavazzoni A et al (2006) Creatine as a compatible osmolyte in muscle cells exposed to hypertonic stress. J Physiol 576:391–401.

Bloomer RJ, Farney TM, Trepanowski JF, McCarthy CG, Canale RE. Effect of betaine supplementation on plasma nitrate/nitrite in exercise-trained men. J Int Soc Sports Nutr. 2011 Mar 18;8:5.

Craig SA. Betaine in human nutrition. Am J Clin Nutr. 2004; 80: 539–549.

del Favero S, Roschel H, Artioli G, Ugrinowitsch C, Tricoli V, Costa A, Barroso R, Negrelli AL, Otaduy MC, da Costa Leite C, Lancha-Junior AH, Gualano B. Creatine but not betaine supplementation increases muscle phosphorylcreatine content and strength performance. Amino Acids. 2012 Jun;42(6):2299-305.

Hoffman JR, Ratamess NA, Kang J, Rashti SL, Faigenbaum AD. Effect of betaine supplementation on power performance and fatigue. J Int Soc Sports Nutr. 2009 Feb 27;6:7.

Hoffman JR, Ratamess NA, Kang J, Gonzalez AM, Beller NA, Craig SA. Effect of 15 days of betaine ingestion on concentric and eccentric force outputs during isokinetic exercise. J Strength Cond Res. 2011 Aug;25(8):2235-41.

Lee EC, Maresh CM, Kraemer WJ, Yamamoto LM, Hatfield DL, Bailey BL, Armstrong LE, Volek JS, McDermott BP, Craig SA. Ergogenic effects of betaine supplementation on strength and power performance. J Int Soc Sports Nutr. 2010 Jul 19;7:27.

Ortiz-Costa S, Sorenson MM, Sola-Penna M (2002) Counteracting effects of urea and methylamines in function and structure of skeletal muscle myosin. Arch Biochem Biophys 408:272–278

Pryor JL, Craig SA, Swensen T. Effect of betaine supplementation on cycling sprint performance. J Int Soc Sports Nutr. 2012 Apr 3;9(1):12.

Trepanowski JF, Farney TM, McCarthy CG, Schilling BK, Craig SA, Bloomer RJ. The effects of chronic betaine supplementation on exercise performance, skeletal muscle oxygen saturation and associated biochemical parameters in resistance trained men. J Strength Cond Res. 2011 Dec;25(12):3461-71.

Ueland PM. Choline and betaine in health. J Inherit Metab Dis. 2011;34:3–15.

Zeisel SH, Niculescu MD. Perinatal choline influences brain structure and function. Nutr Rev 2006;64:197–203.

Zeisel SH. The fetal origins of memory: the role of dietary choline in optimal brain development. J Pediatr 2006;149(suppl):S131–6.

Michel V, Yuan Z, Ramsubir S, Bakovic M. Choline transport for phospholipid synthesis. Exp Biol Med (Maywood) 2006;231:490–504.

Zeisel SH. Nutritional importance of choline for brain development. J Am Coll Nutr 2004;23(suppl):621S–6S.

Blusztajn JK. Choline, a vital amine. Science 1998;281:794–5.da Costa KA, Gaffney CE, Fischer LM, Zeisel SH. Choline deficiency in mice and humans is associated with increased plasma homocysteine concentration after a methionine load. Am J Clin Nutr 2005;81:440–4.

Zeisel SH. Gene response elements, genetic polymorphisms and epigenetics influence the human dietary requirement for choline. IUBMB Life 2007;59:380–7.

Zeisel SH. Choline: an essential nutrient for humans. Nutrition 2000;16:669–71.

Ulus IH, Wurtman RJ, Mauron C, Blusztajn JK. Choline increases acetylcholine release and protects against the stimulation-induced decrease in phosphatide levels within membranes of rat corpus striatum. Brain Res 1989;484:217–27.

Blusztajn JK, Wurtman RJ. Choline and cholinergic neurons. Science 1983;221:614–20.

Meck WH, Smith RA, Williams CL. Pre- and postnatal choline supplementation produces long-term facilitation of spatial memory. Dev Psychobiol 1988;21:339–53.

Buchman AL, Sohel M, Moukarzel A, et al. Plasma choline in normal newborns, infants, toddlers, and in very-low-birth-weight neonates requiring total parenteral nutrition. Nutrition 2001;17:18–21.

Meck WH, Williams CL. Simultaneous temporal processing is sensitive to prenatal choline availability in mature and aged rats. Neuroreport 1997;8:3045–51.

Mellott TJ, Williams CL, Meck WH, Blusztajn JK. Prenatal choline supplementation advances hippocampal development and enhances MAPK and CREB activation. FASEB J 2004;18:545–7

PNAS, Sep 20 2005, 102(38):13681-13686. L-citrulline and L-arginine supplementation.

Br J Clin Pharma, 2008, 65:51-59 Pharmacokinetic and pharmacodynamic properties of oral L-citrulline and L-arginine: impact on nitric oxide metabolism.

Urology, Jan 2011, 77(1):119-22.

Tangphao O, et al. Pharmacokinetics of intravenous and oral L-arginine in normal volunteers. Br J Clin Pharmacol. (1999).

Curis E, Crenn P, Cynober L. Citrulline and the gut. Curr Opin Clin Nutr Metab Care. (2007).

Bahri S, et al. Mechanisms and kinetics of citrulline uptake in a model of human intestinal epithelial cells. Clin Nutr. (2008).

Takeda K, et al. Effects of citrulline supplementation on fatigue and exercise performance in mice. J Nutr Sci Vitaminol (Tokyo). (2011)

Giannesini B, et al. Citrulline malate supplementation increases muscle efficiency in rat skeletal muscle. Eur J Pharmacol. (2011).

Bendahan D, et al. Citrulline/malate promotes aerobic energy production in human exercising muscle. Br J Sports Med. (2002).

Pérez-Guisado J, Jakeman PM. Citrulline malate enhances athletic anaerobic performance and relieves muscle soreness. J Strength Cond Res. (2010)

.Fitts RH, Balog EM. Effect of intracellular and extracellular ion changes on E-C coupling and skeletal muscle fatigue. Acta Physiol Scand. (1996)

Merry TL, Lynch GS, McConell GK. Downstream mechanisms of nitric oxide-mediated skeletal muscle glucose uptake during contraction. Am J Physiol Regul Integr Comp Physiol. (2010)

Álvares TS, et al. L-Arginine as a potential ergogenic aid in healthy subjects. Sports Med. (2011)

Bailey SJ, et al. Acute L-arginine supplementation reduces the O2 cost of moderate-intensity exercise and enhances high-intensity exercise tolerance. J Appl Physiol. (2010).

Gille A, Bodor ET, Ahmed K, Offermanns S (2008). "Nicotinic acid: pharmacological effects and mechanisms of action". Annu. Rev. Pharmacol. Toxicol. 48: 79–106.

Matsuyama K, Yamashita C, Noda A, Goto S, Noda H, Ichimaru Y, Gomita Y (October 1984). "Evaluation of isonicotinoyl-gamma-aminobutyric acid (GABA) and nicotinoyl-GABA as pro-drugs of GABA". Chem. Pharm. Bull. 32 (10): 4089–95. doi:10.1248/cpb.32.4089.

Shephard RA (June 1987). "Behavioral effects of GABA agonists”. Life Sci. 40 (25): 2429–36.

Arbo MD, Larentis ER, Linck VM, Aboy AL, Pimentel AL, Henriques AT, Dallegrave E, Garcia

SC, Leal MB, Limberger RP. 2008. Concentrations of p-synephrine in fruits and leaves of Citrus

species (Rutaceae) and the acute toxicity testing of Citrus aurantium extract and p-synephrine.

Food Chem. Toxicol. 46: 2770-2775.

Arbo MD, Schmitt GC, Limberger MF, Charão MF, Moro AM, Ribeiro GL, Dallegrave E, Garcia SC, Leal MB, Limberger RP. 2009. Subchronic toxicity of Citrus aurantium L. (Rutaceae) extract and p-synephrine in mice. Regulatory Toxicol. Pharmacol. 54: 114-117.

Synephrine Octopamine Caffeine HRA Page 37 of 49 File Number: 172091.

Astrup A, Breum L, Toubro S, Hein P, Quaade F. 1992. The effect and safety of an compound compared to ephedrine, caffeine and placebo in obese subjects on an energy restricted diet. A double blind trial. Int. J. Obes. Relat. Metab. Disord. 16(4): 269-277.

Astrup A, Toubro S. 1993. Thermogenic, metabolic, and cardiovascular responses to caffeine in man. Int. J. Obes. Relat. Metab. Disord. 17(Suppl. 1): S41-S43.

Astrup A, Breum L, Toubro S. 1995. Pharmacological and clinical studies. Obesity Res. 3(Suppl. 4): 537S-540S.

Avula B, Upparapalli SK, Navarette A, Khan IA. 2005. Simultaneous quantification of adrenergic amines and flavonoids in C. aurantium, various Citrus species, and dietary supplements by liquid chromatography. J. AOAC Int. 88(6): 1593-1606.

Benowitz NL. 1990. Clinical pharmacology of caffeine. Ann. Rev. Med. 41: 277-288.

Bray GA, Greenway FL. 1999. Current and potential. Endocrine Rev. 20(6): 805-875.

Bray GA, Greenway FL. 2007. Pharmacological. Pharmacol. Rev. 59: 151-184.

Brent J, Wallace K, Burkhart K. 2005. Theophylline and other methyl xanthines. In: Critical Care Toxicology: Diagnosis and Management. Elsevier Health Sciences.

Blumenthal M. 1998. The Complete German Commission E Monographs: Therapeutic guide to Herbal Medicines. Austin, TX: America Botanical Council.

Blumenthal M. 2004-2005. Bitter orange peel and synephrine. Whole Foods (March 2004) and (March 2005), reprinted with permission by HerbalGram. URL: http://abc.herbalgram.org/site/DocServer/Bitter_Orange_Peel_and_Synephrine.pdf?docID=221,accessed 2011-05-16.

Bouchard NC, Howland MA, Greller HA, Hoffman RS, Nelson LS. 2005. Ischemic stroke associated with use of dietary supplement containing synephrine. Mayo Clin. Proc. 80(4): 541-545.

Brown CM, McGrath JC, Midgley JM, Muir AG, O’Brien JW, Thonoor, CM, Williams CM, Wilson VG. 1988. Activities of octopamine and synephrine stereoisomers on alphaadrenoceptors.

Br. J. Pharmacol. 93:417-429. Bui LT, Nguyen DTT, Ambrose PJ. 2006. Blood pressure and heart rate effects following a single dose of bitter orange. Ann. Pharmacother. 40(1): 53-57.

 

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Warnings: Not intended for use by persons under age 18. Do not exceed recommended dose. Get the consent of a licensed physician before using this product, especially if you are taking medication, have a medical condition, you are pregnant, nursing or thinking about becoming pregnant. KEEP THIS PRODUCT AND ALL SUPPLEMENTS OUT OF THE REACH OF CHILDREN.

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