While SAN’s Vault is promoted as a cell volumizer, its ingredients confer additional health and ergogenic benefits over and above what traditional volumizers such as Creatine Monohydrate provide. Let’s run through the list of ingredients in Vault and see how each contributes to an overall ergogenic effect. The proprietary formula consists of the following categories and respective weight proportions:


Vault’s formula:

Insulinotropic Osmolytes:

(L-Taurine, Betaine Anhydrous, L-Leucine, Glycocyamine, Guanidinopropionic Acid, Cinnamon Extract (Aqueous) 5.30 g

Nitro-Fuel-Fusion:

(Di-L-Arginine-L-Malate, Arginine-AKG, Phytic Acid, L-Citrulline-Malate, L-Norvaline) 4.05 g

Tricreatine-Fusion:

(Dicreatine-Malate, Monocreatine-Malate, Creatine Anhydrous) 4.00 g

Gluta-Sorp / NAGTM Matrix:

(N-Acetyl-L-Glutamine, Fermented L-Glutamine) 2.00 g


MyoTropic Phosphate & Orotate Fusion:

(Magnesium Orotate, Potassium Orotate, Calcium Phosphate, Sodium Bicarbonate, Sodium Citrate) 1.37 g


Neuro-FlowTM Substrates:

(Choline Bitartrate, Vinca Minor P., Huperzia Serrata P.) 720 mg



TRICREATINE-FUSION


Of all the ingredients seen above, creatine in its various forms is perhaps the most familiar to supplement users. Numerous studies have shown the creatine consumption leads to increased strength and athletic performance. There are several theories about how creatine works. The original theory, and perhaps still the most widely accepted, is that oral creatine supplementation increases total creatine and creatine phosphate (CrP) in human skeletal muscle. An increased muscle CrP concentration increases its availability for ATP synthesis. This additional ATP can be used by the muscle to perform work.


When malic acid and creatine monohydrate form the compound Dicreatine-Malate, the resulting product is more water-soluble than regular creatine monohydrate, and hence eliminates the possibility of gastric upset, and is more efficient at elevating ATP production. Furthermore, Dicreatine-Malate is believed to offer greater bioavailability over regular creatine monohydrate. Monocreatine-Malate shares the same ergogenic properties as dicreatine malate, but it simply contains one instead of two creatine molecules.


Studies have also shown that creatine supplementation increases the glycogen content of skeletal muscle along with an increase in myosin heavy chain synthesis (1,2). The increases in lean body mass associated with creatine use may be a result of creatine’s ability to elevate insulin like growth factor 1 (IGF-1) in muscle tissue (3).


Why do we see Malate combined with creatine in the formulation? Malate is an intermediate in the so-called Tricarboxylic Acid Cycle (TCA). While being processed in the TCA, each kind of major fuel is converted to acetyl groups, which are handled by attachment to a particular coenzyme known as coenzyme A. Ultimately ATP is produced from another compound, NADH, generated by the TCA.


Malate is dehydrogenated in the TCA cycle to oxaloacetate, the concentration of which is one of the most critical controls of the rate of aerobic ATP production. During prolonged aerobic activity, and in patients suffering from malate deficiency, malate becomes depleted and the TCA is unable to produce ATP fast enough to meet the demands of working muscle. One classic disease characterized by malate deficiency is fibromyalgia. When patients suffering with this disease are given malate, their energy levels improve dramatically (4).


Not only patients suffering from malate deficiency benefit from malate supplementation. As mentioned above, strenuous, prolonged aerobic activity depletes the body’s malate stores. One recent study looked at the effects of Citrulline Malate (CM) supplementation in 18 otherwise healthy men who complained of easy fatigability. (5) The subjects were administered 6 gm/day of CM for 15 days. To quote from the results of the study,


“CM ingestion resulted in a significant reduction in the sensation of fatigue, a 34% increase in the rate of oxidative ATP production during exercise, and a 20% increase in the rate of phosphocreatine recovery after exercise, indicating a larger contribution of oxidative ATP synthesis to energy production. The expansion of the TCA intermediate pool [through malate supplementation] can therefore be regarded as a means of attaining higher rates of aerobic energy production, in agreement with our results showing that malate supplementation promotes a greater contribution of aerobic ATP production to total energy production. These results suggest that this hyperactivation of aerobic ATP production coupled to a reduction in anaerobic energy supply may contribute to the reduction in fatigue sensation reported by the subjects.”


So not only were objective measures of energy production increased, but the study participants felt a subjective improvement in energy levels as well.


Creatine Anhydrous is the form of creatine most readily dissolved in water. When stirred into water it dissolves instantly and remains perfectly and unnoticeably dispersed. No clumping or and like residue (meaning wasted creatine) in the bottom of the glass.


NITRO-FUEL-FUSION


One of the major controlling factors in the expansion and contraction of blood vessels is nitric oxide (NO). In the body NO is produced from the amino acid arginine. When exposed to NO, blood vessels dilate, allowing for increased blood flow due to the vessel’s increased crossectional area. Working muscles require a copious blood supply to deliver nutrients and carry away waste products. Since arginine is the direct precursor to NO, Bodybuilders have taken to supplementing with arginine based compounds to increase NO production. This leads to the sought-after “pump” associated with muscle blood vessels engorged with blood.


Arginine alpha-ketoglutarate (AKG) reportedly is better absorbed into tissues once it has entered the bloodstream than arginine, and has a more sustained effect on NO production. AKG itself has been used extensively for nutritional support in various illnesses and in the post surgery setting. Supplementing with AKG helps replenish this vital tricarboxylic acid intermediary. As mentioned above, the TCA or Krebs cycle creates the fuel that runs every cell of your body. AKG is involved in one of the critical step in this multi-part cycle and therefore a vital part of the energy-creating mechanism for every cell. While AKG supplementation can certainly increase ATP production, just as Malate, another TCA intermediate was shown to above, it is not clearly understood how AKG increases nitric oxide production. One popular theory is that AKG inhibits the arginase pathway so more arginine is routed to the nitric oxide synthase pathway instead of being transformed into urea.



Di-arginine malate consists of 2 arginine molecules bonded to a malic acid molecule. Many anecdotal reports by users claim a more sustained effect from Di-arginine than from other NO precursors, although there are no experimental data to support these claims.

.


Citrulline can be converted to arginine, so besides providing malate, L-Citrulline-Malate donates citrulline as an arginine precursor. Citrulline is also involved in the so-called urea cycle, which is responsible for the removal of excess nitrogen from the breakdown of amino acids. Were excessive levels of nitrogen to accumulate in the body, ammonia toxicity would develop. Besides stimulating hepatic ureogenesis , citrulline also promotes the renal reabsorption of bicarbonates. The latter acts as a buffer against lactic acidosis, which also helps to stave off fatigue. In fact there has been some debate over the years whether citrulline or malate is primarily responsible of prolonging endurance (6). The consensus now seems to be that the two compounds work in concert, with malate maintaining TCA intermediates and allowing for increased ATP production, and citrulline buffering against lactic acid and ammonia buildup.


L-arginine is used as a substrate by both nitric oxide synthase (NOS) and arginase to produce nitric oxide (NO) and urea, respectively. Clearly one way to do maximize NO production is to shunt more arginine toward NOS and away from arginase. L-Norvaline is a compound that is an arginase inhibitor; hence the rationale for its inclusion in Vault.


GLUTASORP


This component of Vault contains two highly bioavailable forms of glutamine. Glutamine, being the most abundant amino acid in the circulation should be expected to play roles in a number of metabolic process. As an osmolyte, glutamine causes cellular swelling of hepatic cells (7) leading to anabolic processes such as protein synthesis and glycogen storage (7). Cell shrinkage from glutamine depletion has the opposite effect.


Animal studies have demonstrated the same anabolic effect of glutamine on skeletal muscle (8). The authors of (8) concluded that:


“Control of the size of the intramuscular free pool of glutamine may be important in determining the muscle protein mass”.


Glutamine has shown great promise in the treatment of the critically ill, since it is an immune stimulant. But it has other effects as well. Multiple meta-analyses have found that glutamine has many beneficial effects in critically ill patients, and glutamine may reduce mortality rates in Intensive Care Unit patients by as much as 20% Glutamine functions through multiple mechanisms of action, such as improving gastrointestinal tract health and immune health, acting as a precursor to glutathione, and decreasing ammonia buildup in the liver. Along with HMB and arginine, glutamine helps decrease lean tissue wasting in cancer and AIDS patients, and glutamine prevents muscle protein breakdown from synthetic glucocortcoids, analogs of our own body’s catabolic hormone cortisol. It is because of these benefits in catabolic states that it is postulated that glutamine supplementation would be beneficial for those engaged in intense exercise, Overtraining may lead to immune depression and it has been proposed, that glutamine could speed recovery in overworked athletes.


N-Acetyl-L-Glutamine or NAG more easily enters tissues once in the bloodstream compared to simple Glutamine. Besides being a simple glutamine donor, NAG has shown promise in a diverse array of experiments. In animals fed NAG, cognition improved over that seen in controls. NAG may enhance the effects of pyrimidines in the synthesis of ribonucleic acid, which is indispensable for learning and memory processes. It has the additional interesting property of being an antiulcer agent



NEUROFLOW SUBSTRATES


The rationale for employing choline bitartrate in Vault is based on the positive effects of choline supplementation on neurodegenerative diseases (9). As we age, or are subjected to high levels of free radicals, choline may confer some protective benefit. In accord with this notion, one study showed that choline administration lowers lipid peroxidation, and promotes conservation of retinol and alpha-tocopherol in free-living women. As we know lipid peroxidation is the first stage of the development of atherosclerosis.

Huperzine A (HupA), extracted from a club moss (Huperzia serrata), is a sesquiterpene alkaloid and a powerful and reversible inhibitor of acetylcholinesterase (AChE). It has been used in China for centuries for the treatment of swelling, fever and blood disorders. It has demonstrated both memory enhancement in animal and clinical trials and neuroprotective effects. Recently it has undergone double-blind, placebo-controlled clinical trials in patients with Alzheimer's disease (AD), with significant improvements both to cognitive function and the quality of life

Acetylcholine is a primary neurotransmitter in the brain. Low levels of acetylcholine are associated with cognitive impairment. AchE is the enzyme that breaks down acetylcholine, so by blocking the action of AchE with Huperzine, we can maintain higher levels of acetlycholine.


Vinpocetine, beside its therapeutical utilization, has become a reference compound in the pharmacological research of cognitive deficits caused by hypoxia and ischaemia as well as in the cellular and biochemical investigations related to cyclic nucleotides. Early experiments with vinpocetine indicated five main pharmacological and biochemical actions: (1) selective enhancement of the brain circulation with an increase in glucose and oxygen utilization without significant alteration in parameters of systemic circulation, (2) increased tolerance of the brain toward hypoxia and ischemia, (3) anticonvulsant activity, (4) inhibitory effect on phosphodiesterase (PDE) enzyme and (5) improvement of rheological properties of the blood and inhibition of aggregation of thrombocytes. Later studies in various laboratories confirmed the above effects and clearly demonstrated that vinpocetine offers significant and direct neuroprotection both under in vitro and in vivo conditions. Evidence has been obtained that neuroprotective action vinpocetine is related to the inhibition of operation of voltage dependent neuronal Na(+)-channels, indirect inhibition of some molecular cascades initiated by the rise of intracellular Ca(2+)-levels and, to a lesser extent, inhibition of adenosine reuptake. Vinpocetine has been shown to be selective inhibitor of Ca(2+)-calmodulin dependent cGMP-PDE. It is assumed that this inhibition enhances intracellular a GMP levels in the vascular smooth muscle leading to reduced resistance of cerebral vessels and increase of cerebral flow. This effect might also beneficially contribute to the neuroprotective action (10). Vinpocetine has been shown to increase neuronal ATP bio-energy production, even under hypoxic (low oxygen) conditions. Recent studies concluded that vinpocetine enhances both glycolytic and oxidative reactions of glucose breakdown in the central nervous system (“CNS”). Additional studies further indicated that changes in the concentration of K [potassium] and Mg [magnesium] may be considered a sign of recovery of the energy metabolism of the nerve cells and therefore essential to the dieting individual.




INSULINOTROPIC OSMOLYTES



These are agents that act to lower blood sugar either by increasing insulin secretion, or improving insulin sensitivity. Taurine has been the subject of several studies along these lines. In one study glucose was administered either alone or with taurine. The taurine group showed a greater drop in plasma glucose corresponding to increased insulin secretion. (11). In addition, the same study confirmed what numerous other studies had determined; namely that taurine possesses clinically significant antioxidant properties in addition to its insulin stimulating action.


The antioxidant feature of taurine may be responsible for the cytoprotective effect of taurine administration during exercise. Dawson et.al (12) subjected animals to 90 minutes of strenuous downhill running after which muscle tissue damage was assessed. The taurine supplemented group not only showed less extensive tissue damage, but running performance as assessed by a subjective rating scale was improved by taurine supplementation. Exercise has been shown to deplete the muscle content of taurine. In light of its ergogenic actions, this warrants taurine supplementation during exercise


A similar experiment in young men showed similar results: After exhaustive exercise, the taurine group exhibited less cellular damage and enhanced performance (13).Quoting from the study,


“Significant increases were also found in VO(2)max, exercise time to exhaustion and maximal workload in test with taurine supplementation ( p<0.05). After supplementation, the change in taurine concentration showed positive correlations with the changes in exercise time to exhaustion and maximal workload. The results suggest that taurine may attenuate exercise-induced DNA damage and enhance the capacity of exercise due to its cellular protective properties.”

The branch chain amino acid L-Leucine stimulates insulin production, as do all amino acids. However, leucine is partucularly anabolic among the amino acids. A number of studies have shown that branched chain amino acids exert both an anabolic and ergogenic effect.


For example, one study showed that BCAA administration post exercise resulted in an approximately 30% decrease amino acid efflux from skeletal muscle. The authors concluded that BCAAs exert a post training protein-sparing effect on muscle tissue (14). These results have been verified in numerous other studies. It is now believed that BCAAs act through a specific pathway, the so-called signal transduction p70(S6k) pathway in skeletal muscle (15). p70(S6k) is believed to control growth-related protein synthesis (15). There is also some evidence that branched chain amino acids are preferentially broken down for fuel during exercise, arguing for BCAA supplementation to offset this effect. If this is the case, this might be one mechanism where BCAA supplementation would hold off fatigue. Leucine seems particularly critical in stimulating overall protein synthesis. Leucine mediated signaling results in a stimulation of initiation of mRNA translation and involves increases in the phosphorylation status of the translational repressor 4E-BP1 and the ribosomal protein S6 kinase S6K1mentioned above. It also requires sustained activation of the mammalian target of rapamycin (mTOR) protein kinase, a field of active research. Leucine, however, also signals to stimulate protein synthesis in skeletal muscle by a mammalian target of rapamycin protein kinase independent (i.e. rapamycin insensitive) pathway, suggesting that the amino acid may signal for protein synthesis through multiple pathways.



Interestingly, insulin is believed to exert at least part of its anabolic effect by activating the same p70(Sk6) pathway as leucine, but via different upstream channels. This argues for an additive role between elevated insulin levels and elevated BCAA levels in the promotion of anabolism. This is depicted in the graphic below:

Figure 1. Putative signaling pathways for the activation of p70S6k in human skeletal muscle. Mammalian target of rapamycin (mTOR) is also known as FRAP. PHAS-I is also known as eukaryotic initiation factor 4E binding protein-1 (4EBP-1). Both p70S6k and PHAS-I are depicted as phosphorylated, a modification associated with increased translation. Adapted from Am J Physiol Endocrinol Metab 281: E466-E471, 2001


Just as glucose uptake into cells is dependent upon a family of so called GLUT (Glucose Transporters), amino acids are transported into cells by a distinct family of transporters. One main transport system is the so-called System A. In vitro studies have shown that leucine upregulates System A transporters, allowing for greater entry of a number of amino acids into muscle cells (16). It should be noted that one of the anabolic effects of IGF-1 is believed to be upregulation of this same transport system. So in this sense leucine may share at least one of the anabolic effects associated with insulin like growth factor.


So we have seen that amino acids, and leucine in particular are capable of activating signal transduction pathways in an almost hormone like manner. They are much more than simple nutrients in this regard. To quote from one recent review,

"The protein kinase mTOR is a common intermediate in both nutrient and hormone signal transduction pathways. Signaling through mTOR is enhanced by nutrients and anabolic hormones, such as insulin or IGF-I and repressed by elevation of cAMP or activation of AMPK suggesting that one function of mTOR is to integrate the anabolic response to nutrients and insulin and the catabolic response to counter-regulatory hormones, such as glucagon...Although other amino acids have been shown to increase signaling through mTOR, leucine is arguably the most potent of the amino acids in activating the pathway." (17)


The importance of leucine to post resistance exercise recovery is highlighted in another recently published study where participants undertook a bout of resistance exercise and were fed either carbohydrates alone, carbohydrates plus whey protein, or a combination of carbs, whey and leucine (18). Subjects received a beverage volume of 3 ml.kg-1 every 30 minutes to ensure a given dose of 0.3 g carbohydrate.kg-1 (50% as glucose and 50% as maltodextrin) and 0.2 g.kg-1 of a protein hydrolysate [whey] every h, with or without the addition of 0.1 g.kg-1.h-1 leucine. To quote from the report,


"Mixed muscle [protein synthesis rate], measured over a 6h period of post-exercise recovery, was significantly greater in the CHO+PRO+leu trial compared to the CHO, with intermediate values observed in the CHO+PRO trial . We conclude that the co-ingestion of protein and leucine stimulates muscle protein synthesis and optimizes whole-body protein balance when compared to the intake of carbohydrate only."


Betaine has been well characterized as an agent capable of lowering levels of homocysteine in the body. High plasma concentrations of homocysteine may increase risk of cardiovascular disease. Betaine lowers plasma homocysteine up to 20% in normal humans (19). One interesting study looked at the effects of betaine on both trained and untrained animals. In the untrained group betaine lowered plasma lactate levels post-exercise significantly, implying that betaine should allow for a faster recovery from exercise. (Muscle fatigue is believed to be due to, at least in part, lactate buildup.)


In other animal studies, betaine increased muscle area and decreased fat thickness (20).


Betaine is capable of donating a methyl group to glycocyamine via methionine to produce creatine de novo (in the body). In human poliomyelitis ingestion of a betaine-guanidinoacetate combination leads to an improved sense of well-being, less fatigue, and greater general strength and endurance during recovery. Whenever motor unit activity or residual power remained in a muscle, betaine-guanidinoacetate led to a substantial increase. Betaine may improve athletic performance, because its addition to a carbohydrate-electrolyte fluid-replacement beverage results in improved mean sprint time to exhaustion and evidence of enhanced anaerobic and aerobic metabolism (27,28). Rehydration with betaine also results in differential plasma volume changes and reduced LDL and homocysteine.


Glycocyamine (GAA) and Guanidinopropionic Acid (GPA) mimic the actions of insulin in that they lower blood glucose in animal studies (21). This appears to be the result of increased expression of GLUT-4, a major glucose transporter (22). GAA is also converted in the liver into creatine, adding to plasma creatine levels. Because of the insulinomimetic effect of glycocyamine and GPA, taking these along with creatine is superior to simply taking more creatine.


It has been claimed that glycocyamine and GPA downregulate the creatine transporter and thus actually counter the effects of creatine. Research shows however that this effect occurs only at unrealisticaly high levels of glycocyamine and GPA, levels approaching 1% of bodyweight (2 lbs in a 200 lb individual).



Water-soluble polyphenol polymers found in Cinnamon extract have been shown to improve insulin action via increasing glucose uptake in vivo, at least in part through enhancing the insulin-signaling pathway in skeletal muscle (23).


Phytic Acid has been considered as an anti-nutritional component in cereals, seeds and beans. Research has traditionally focused on its structure that gives it the ability to bind minerals, proteins and starch, and the resulting lower absorption of these elements. However, recent research has shown that phytic acid has many health promoting effects. Phytic acid has antioxidant, anticarcinogenic, hypocholesterolemic and hypolipidemic effects (29). In animal studies phytic acid showed a protective action in carcinogenesis. This action could be explained by its mineral chelating potential. Phytic acid lowers blood glucose response by reducing the rate of starch digestion and slowing the gastric emptying. Some industry experts believe that Phytic acid elevates leptin even though we could not locate anything to support these claims. Phytic acid releases inositol that during digestion. Although inositol is not an essential nutrient it is proposed to reduce depressions even though this is not substandiated in the medical literature.


MYOTROPIC PHOSPHATE & OROTROPIC FUSION


Magnesium Orotate is magnesium bound to orotic acid, a key intermediate in the biosynthesis of pyrimidine nucleotides (a building block of the “letters” of your DNA code, and of RNA, the messenger that delivers the instructions from the DNA to the cellular machinery that assembles cellular proteins based on DNA’s commands). Animal models had shown that heart failure increases the demand for RNA for the biosynthesis of proteins needed to repair the heart. So Soviet cardiologists reasoned that, since orotate is needed for biosynthesis of RNA precursors, supplemental orotate might speed the recovery of heart muscle function. Results of numerous experiments involving animals and humans have borne this out. Magnesium is added to orotate since magnesium acts as a cofactor for the enzyme responsible for the production of RNA precursors by orotate. As an added benefit, orotate inreases the bioavailability of magnesium.


Might the same effect apply to skeletal muscle as heart muscle? In one study a group of triathletes, some were given magnesium orotate (MO) and others placebo. At the end of the trials, creatine kinase, a marker of muscle tissue breakdown, was significantly lower in the MO group. Blood acidity dropped in the MO group, and the blood of the MO group was more highly oxygenated than in the controls. (24).


Potassium Orotate, like Magnesium Orotate, is highly bioavailable and readily delivers potassium to tissues where it is needed. Potassium’s most important roles include the transmission of nerve impulses, contraction of muscles, production of energy, maintenance of intracellular tonicity and regulation of blood pressure. Evidence suggests that diets high in potassium may help to protect against hypertension, strokes, cardiovascular disease and quite possibly other degenerative diseases. Modern diets do not contain as much potassium as the diets of our primate ancestors, so there is reason to believe modern humans could benefit from potassium supplementation. This is especially true among bodybuilders who often use diuretics that flush potassium from the system


Calcium Phosphate serves several purposes in the body. Phosphate in the form of calcium phosphate is readily absorbable. One action of calcium phosphate is to act as a buffer, lowering the acidity of blood and allowing for enhanced athletic performance. Another role played by phosphate is to replenish ATP and phosphocreatine within cells. When the cell in question are muscle, this could lead to increased work capacity.


The third mechanism proposed for the ergogenic of phosphate supplementation effect is attributed to the possible increase of 2, 3-diphosphoglycerate (2,3-DPG) with increased intake of phosphate. 2,3-DPG shifts the oxyhemoglobin dissociation curve to the right, thus allowing a greater unloading of oxygen at the tissue level (25). It should be noted that some earlier studies have supported these results, while others contradict them.


Sodium citrate & Sodium Bicarbonate are two widely used buffers, compounds that neutralize the acidifying effect of lactic acid buildup during exercise. Numerous studies involving high intensity exercise have proven the efficacy of these buffers as ergogenic aids due to the establishment and maintenance of an elevated pH level during exercise (26).



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