Safe & Efficacious L-Arginine
for Professional Athletes

25-Years of Safe Use in Humans
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Pharmaceutical Grade L-Arginine Formulas
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Metabolic Actions of ArgMatrix®

Influence of ArgMatrix®
on the Anabolic Action of Androgens


ROLE OF ARGININE IN ANABOLIC ACTIONS

Dietary arginine is required for the anabolic actions of androgens in humans.

Depletion and/or restriction of dietary arginine prevents body weight gain induced by testosterone treatment, elucidating the role of dietary arginine in the pharmacologic action of synthetic analogs of testosterone used in clinical therapy.

Dietary (oral) arginine plays a major role in the anabolic action of testosterone, as arginine modulates androgen action, though not exclusively, through an influence on insulin-like-growth factors; IGFs and IGF-B’s.

Conversely, dietary arginine deficiencies alter the expression of IGF-1, IGF-BP1 and IGF-1R in the kidney and IGF-BP1 in the liver.

Changes and deficiencies in the levels of plasma arginine affect the action of muscle and kidney testosterone, which acts independently of the mechanisms involved in the interaction between testosterone and arginine.

One such mechanism involving the production of testosterone and other anabolic hormones via the arginine-pathway is growth hormone (GH).

GH & OBESITY

Low growth hormone (GH) levels in humans leads to increases in total body fat accompanied by a loss of lean body mass. Both GH and cortisol are key hormones involved in the pathogenesis of obesity, and GH levels, in response to exercise, are blunted in obese persons.

GH increases lipolysis as a direct effect of GH on the adipocyte, as well as lipid oxidation by increasing substrate availability.

ATHLETES & GH

The ArgMatrix® Patent (s) include the use of Arginine & Branched Chain Amino Acids (BCAA). The combination of L-Arginine and BCAA provide a quicker recovery from muscle fatigue following exercise training.
The ArgMatrix® Patent (s) include L-Arginine with a Low Glycemic carbohydrate. The addition of arginine with a carbohydrate reduces the rate of carbohydrate oxidation post-exercise and therefore increases the availability of glucose for muscle glycogen storage during recovery.
Chronic L-arginine supplementation enhances endurance exercise tolerance in heart failure patients.


Growth Hormone (GH) in athletes increases fatty acid availability and reduces oxidative protein loss, particularly during exercise, and increases lean body mass. GH improves exercise performance including maximal oxygen uptake and ventilatory threshold through increased oxygen delivery to exercising muscle, increased fatty acid availability with glycogen sparing, increased muscle strength, improved body composition, and improved thermoregulation (U.S. Patent held by Dr. Ann de Wees Allen).

The use of human growth hormone (HGH) to improve athletic performance has received worldwide attention. This practice, often called sports doping, is banned by most professional sports leagues and associations, including the International Olympic Committee, Major League Baseball, and the National Football League.

Growth hormone is used to enhance athletic performance and has been called the most anabolic substance known.

Though HGH is illegal, natural GH is legal via L-Arginine transport, thus ArgMatrix® is legal for use by any athlete that is screened or tested for banned substances, such as HGH.

NATURAL PRODUCTION OF GH: THE MECHANISM

Growth Hormone (GH) stimulates targeted tissues and activates a complex intracellular signaling cascade, wherein anabolic hormones and internal thermogenesis, and anti-aging hormones are produced.

In humans, GH is produced via the hypothalamic/pituitary axis in youth (under age 23) and in response to high-dose oral L-arginine (over age 23).

After age 23, GH begins its dramatic decline, resulting in weight gain, aging, lack of muscle mass, thin skin, imbalanced blood glucose levels, lowered immune function, and added adipose tissue body fat.

Baby-Boomers and persons over age 40 have very low levels of growth hormone (GH). As aging progressing GH levels decline further. ArgMatrix® virtually normalizes acute GH release in older individuals. Pituitary GH release is stimulated by the secretagogue ArgMatrix®, and is decreased in aging.

Low-to-zero GH secretion in aging is not attributable to augmented IGF-I negative feedback since older men and women show relative resistance to infused IGF-I’s inhibition of GH release.

ArgMatrix® stimulation of growth hormone (GH) in humans occurs at the GH axis, wherein a high-dose (10,000 mg elemental) of L-Arginine is piggybacked on a Blind Amino Acid Rider to cross the Blood-Brain-Barrier (BBB), generating a pulsatile burst of GH.

This mechanism reflects the actions of ArgMatrix® as a stimulus of endogenous GHRH secretion and other putative secretagogues (responsive-somatotropes) within the anterior pituitary gland.

The successful activation and release of growth hormone (GH) per this specific neurotransmitter pathway is dependent on sufficient releasable growth hormone (GH) pools, and is directly related to the ArgMatrix® formula, which was designed to trigger this stimulus.

ArgMatrix® is a widely employed provocative test to evaluate the GH axis, and is the standard for identifying GH axis performance in humans.

ArgMatrix® accesses the correct neurotransmitter pathway, as well as peripheral feedback signals, to regulate growth hormone secretion by acting directly on the anterior pituitary gland and by modulating GH-releasing hormone and somatostatin release from the hypothalamus (hypothalamic/pituitary axis).

In humans, high doses of ArgMatrix® (10,000 elemental mg) regulates GH secretion by acting directly on the anterior pituitary gland. This requires an intricate knowledge of the appropriate Isoform neurotransmitter pathway taken by the amino acid arginine, which will result in Delta sleep cycle stimulation of the GH hypothalamus/pituitary axis.

An understanding of neuroregulatory mechanisms and their relevance to clinical alterations in GH control is required in order to elicit a significant GH response in humans.

Growth hormone and IGF insulin-like growth factors modulate androgen action, interacting with different co-activators or co-repressors. GH, IGF-factors, serum L-arginine, and BBB crossover of L-arginine, all translate to increased testosterone in humans. All of these mechanisms can act in tandem or individually.

When oral ArgMatrix® acts as a secretagogue of growth hormone (GH) in humans by crossing the BBB during Delta sleep, all of the anabolic/androgen interactions take place in a metabolically coordinated fashion, increasing and balancing levels of GH, testosterone, and IGF-factors.

EXERCISE-INDUCED GH

Oral ArgMatrix® attenuates the growth hormone response to resistance exercise (not aerobics), via uptake of L-arginine and generation of GH in response to small fissures in muscle generated by intense weight training.

The addition of oral L-Arginine in doses of 10-15 elemental grams taken 30-mins prior to resistance exercise results dramatic increases in growth hormone (in both men and women) by 10-20 fold.

The protocol requires taking a minimum of 10 grams of elemental arginine (ArgMatrix®) 30 minutes prior to resistance exercise on an empty stomach (for 2 hours prior to resistance exercise), which includes restriction of all beverages other than water.

IGF & GH

IGF-1 is a ubiquitous tissue mediator of growth hormone (GH), which is maintained under homeostasis in the hypothalamic loci, the pituitary gland, and the circulation by an interplay of highly complex feedback signals involving basic poly-peptides.

IGF-related cancers, such as prostate cancer, are encouraged by ingestion of red meat and high-purine foods, and not by re-generation of age-related decline in anabolic hormones, such as testosterone. As age-related testosterone drops, prostate cancer risk increases, showing that testosterone is not the culprit in the development of prostate cancer, though reduction of testosterone is recommended once prostate cancer has been diagnosed.

NITRIC OXIDE

L-arginine is the biological precursor to Nitric Oxide (NO). The enzymes that convert L-arginine to Nitric Oxide are called Nitric Oxide Synthase (NOS). In humans, NO occurs in a minimum of three isoforms, which are expressed in neural, vascular, and other tissues.

NOS is inhibited by N-Monomethyl-L-arginine (L-NMMA), N-Nitro-L-arginine methyl ester (L-NAME), derivatives modified at the terminal guanidino group.

In humans, no direct evidence exists for a role of nitric oxide in basal or L-arginine-stimulated growth hormone neuroregulation.

Nitric oxide (NO) is a potent endogenous vasodilator and has shown to inhibit key processes of atherosclerosis like monocyte adhesion, platelet aggregation, and vascular smooth muscle cell proliferation.

Impaired endothelial NO production is a main feature of endothelial dysfunction, which by itself is an early step in the course of atherosclerotic vascular disease. NO deficiencies and NO-pathways are directly related to cardiovascular disease, and patients with growth hormone deficiency are characterized by a 1.9 fold higher risk of death from cardiovascular disease.

NITRIC OXIDE & GH

Growth hormone (GH) produces Nitric Oxide (NO, but NO does not produce GH.

Reduced endogenous systemic production of NO was found in patients with growth hormone deficiency, and treatment with recombinant growth hormone normalized NO production. This shows that GH helps produce normal NO levels in humans, and can reinstate low NO levels via IGF-1.

The effects of growth hormone on NO are mediated by insulin-like growth factor-I (IGF-I), which stimulates NO synthesis. The onset of IGF-I increase in healthy volunteers treated with GH is evident after 12 hours. The maximum effect takes place between 5 to 8 days. In adults with growth hormone deficiency, the major effects of growth hormone treatment on IGF-I levels are observed within 2 weeks. After discontinuation of growth hormone therapy, IGF-1 levels return to base line within 2-3 days.

Growth hormone treatment enhances systemic NO bioavailability via IGF-1 and may be beneficial in certain cardiovascular diseases.*

Aging is related to increased cardiovascular disease, which is related to lowered growth hormone levels, and resulting lowered nitric oxide levels.

*
AUGUST 28, 2007. Journal of Clinical Endocrinology & Metabolism. Growth hormone treatment improves markers of systemic nitric oxide bioavailability via insulin-like growth factor-1.

SAY “NO” TO L-CITRULLLINE

NOS enzymes release NO as a mediator gas from the terminal guanidine nitrogen group of L-arginine, producing L-citrulline as a by-product. This is precisely why the addition of L-citrulline to any arginine formula is a chemical absurdity. L-arginine formulas do not require, and in fact are inhibited by the presence of L-citrulline, as L-arginine produces L-citrulline.

MANDATORY LOW GLYCEMIC PROFILE

A Low Glycemic, Non-Cephalic (CPIR) profile is mandated in any L-Arginine formula that is designed to elicit GH, Testosterone, and other anabolic, anti-aging hormones.

Aging causes decreased growth hormone (GH) and increased cortisol, leading to reduced muscle mass and increased body fat.
Low fasting glycemic and insulin levels modulates the effectiveness of growth hormone in humans, including higher natural IGF-1 levels, by allowing higher levels of IGF-1 to be produced by the liver, since high blood glucose and/or insulin levels reduce IGF-1 production through a negative feedback loop.
Clinical trials have shown that oral high glycemic agents inhibit growth hormone secretion induced by human pancreatic growth hormone releasing factor.

Chemiluminescence-based GH assay (sensitivity of 0.002–0.005 µg/liter) confirms that glucose ingestion reduces serum GH concentrations typically to less than 0.07 µg/liter in men, and less than 0.7 µg/liter in women.

Glucose and other high glycemic agents found in L-Arginine products and formulas suppress serum GH.

Agents that elevate blood glucose (High Glycemic) and/or insulin levels (Cephalic) are contraindicated in arginine formulas.

Said agents include sucrose, honey, maltodextrins, dextrin, high-fructose corn syrup, fruit juice, Stevia, sugar alcohols, artificial and chemical sweeteners that are not bound to Blind Amino Acid Riders, and other sweeteners.

Further, L-arginine formulas that contain -0- calories or carbohydrates do not cross the Blood-Brain-Barrier (BBB), as Cephalic synthetic or chemical sweeteners are not recognized by the BBB and are denied access.

MUSCLE MASS IN ATHLETES:
DOWN-REGULATING CORTISOL

In terms of lean muscle mass and body fat levels in athletes, L-Arginine formulas are required to be Low Glycemic and Non-Cephalic in order to facilitate GH production and down-regulation of Cortisol.

GH stimulates the production of lean muscle mass, while Cortisol triggers negative skeletal muscle feedback and muscle wastage.

It is also important to down-regulate Cortisol in any protein or L-Arginine formula, as Cortisol reduces muscle mass and increases body fat.

Cortisol is recognized for its propensity to become negatively elevated in response to stress. Though this is a factor, Cortisol is also stimulated by factors other than stress. Aging elevates Cortisol levels, which is partly responsible for weight gains as aging progresses.

Research has shown that with advancing age, spontaneous secretion of Cortisol is increased in non-stressed individuals, whereas GH release decreases in women and men, particularly at night.

Jeff Krushell, the current International Director of Strength & Conditioning for Major League Baseball (MLB) has stated that “Elevated Cortisol reduces sports performance and muscle integrity in professional athletes. Therefore, it is crucial to down-regulate Cortisol in all athletes.”

To that end, in March 2009, Human Sports Performance dedicated over $ 1 million dollars in funding for Cortisol research (CortisolScience.com) in athletes.

ArgMatrix® is the only arginine formula in the world that contains a Cortisol Down-Regulator (see: www.CortisolScience.com).

QUANTIFICATION OF GH PARAMETERS IN HUMANS

The dynamics of secretory functions, such as GH, are quantifiable in a variety of different methods and tests, some more accurate than others.

The clinical goal is to quantify the duration and amplitude of GH release in humans, and provide insight related to the frequency and amplitude of serum hormone concentration peaks and can disclose insights into neuroendocrine mechanisms that control this ultradian pituitary release activity

The preferred method is MLM (Maximum-Likelihood-Methodology) based on feedback concepts within a neuroendocrine axis, ultradian pulsatility linked to circadian variations (GH is produced during Delta segment of the Circadian sleep cycle), using a stochastic differential equation.

One method, Pulse Analysis (PA) provides data on brain-pituitary interface and anterior pituitary GH secretion, but there are challenges in accuracy and reproducible data. Further, there is no disclosure on neuroendocrine mechanisms identified with ultradian pituitary release of GH.

Blood sampling (every 30 sec) during sleep identifies the strongly correlated pattern of episodic growth hormone release and the onset of slow-wave (stages III and IV) sleep.

Clinical studies validate that aging (over age 23) and obesity is directly associated with low GH levels and decreased GH secretion. This is quantified by GH ULSEN assay plus deconvolution analysis.

This is validated by the fact that 97 percent of daytime samples for serum GH concentrations in older and/or obese subjects are “undetectable.”

NATURAL TESTOSTERONE

Dietary L-arginine is relevant to the anabolic action of testosterone, and this effect is mediated by changes in the insulin-like growth factor system.
Dietary L-arginine is required for the anabolic action of androgens. Restriction of dietary arginine prevents lean muscle mass body weight gain induced by testosterone.

The amino acid L-Arginine is capable of elevating natural testosterone in humans, when administered in sufficient doses and in formulas designed to access testosterone-driven mechanisms.

The Journal of Endocrinology states that dietary arginine supplementation can improve the pharmacologic action of synthetic analogs of testosterone used in clinical therapy. (Influence of dietary arginine on the anabolic effects of androgens).








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