N0 Extreme - Technical Specifications


N0 Extreme was designed to be one of the first multi-faceted, extremely potent, pre-workout supplements in existence. This formulation is one of the first of many alternatives to a creatine-free supplement that is highly conducive to muscle growth, while obtaining comparable strength gains to creatine-containing products due to its generation of high ATP levels.

N0 Extreme utilizes nitric oxide boosting from seven different angles, provides carnosine precursors for maximizing ATP levels, supplies pre-workout branched-chain amino acids, and provides an energy boost unlike anything previously designed.

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N0 Stacking Usage N0 Technical Specifications N0 Frequently Asked Questions N0 Testimonials

Arginine-AKG


Key Action:
Arginine-AKG is a rapidly absorbed Nitric Oxide (NO) precursor. It increases vascularity, strength, and muscular growth. As a Tri-Carboxylic Acid (TCA) cycle intermediate, it increases ATP synthesis and enhances the absorption of compounds to which it binds.

Physiological Mechanism:
NO is synthesized from arginine by NO Synthase (NOS). This enzyme couples the terminal nitrogen atom of Arginine with a dioxygen molecule, forming NO. NO then activates cyclic GMP and causes an increase in cellular potassium ions with a decrease in calcium ion concentration, leading to the relaxation of endothelial cells.

N-Carbamylglutamate


Key Action:
N-carbamylglutamate increases the secretion of Arginine and Somatotropin from endothelial cells. It increases NO levels and protein synthesis.

Physiological Mechanism:
No current research has discovered the direct mechanism of N-carbamylglutamate (NCG) in endothelial cells and the release of Arginine and Somatotropin. However, studies have shown that along with the systemic increase of those two compounds after NCG supplementation, dramatic increases in skeletal muscle growth and protein synthesis have occurred.

Citrulline-Malate


Key Action:
Citrulline-Malate is a precursor of Arginine and a NO Cycle intermediate. It enhances endurance and muscle aerobic respiration. As A TCA Cycle intermediate, it increases ATP synthesis and enhances the absorption of compounds to which it binds.

Physiological Mechanism:
Citrulline is converted into Argino Succinate and then back into Arginine in the NO Cycle. Since Malate is an intermediate in the TCA Cycle, once Malate enters the cell, it is quickly metabolized in the mitochondria to produce ATP molecules that the body uses for energy to fuel metabolic processes. One Malate molecule yields three ATP molecules.

Leucine


Key Action:
Leucine is a branched-chain amino acid. It increases protein synthesis and aids the interior hydrogen bonding of proteins.

Physiological Mechanism:
Branched-chain amino acids, such as Leucine, primarily increase protein synthesis, which can occur in many different ways. It increases insulin synthesis and signals for its release. It also activates a Ras-Rhed signaling pathway that increases the rate of mRNA transcription. Additionally, being an amino acid itself, it provides a raw material for the translation of mRNA into proteins.

Beta-Alanine


Key Action:
Beta-Alanine is a precursor of Carnosine. It decreases fatigue and reduces muscle tissue pH levels. It also enhances the body's ability to do additional muscular work and is a Reactive Oxygen Species (ROS) scavenger.

Physiological Mechanism:
Beta-alanine and Histidine are both required for the synthesis of Carnosine. These two amino acids form a dipeptide via the activity of Carnosine Synthase. Carnosine also prevents the peroxidation of the fatty acids that compose cell membranes.

Caffeine


Key Action:
Caffeine is a psychoactive stimulant and diuretic. It reduces fatigue, enhances mental alertness and body coordination, and promotes wakefulness.

Physiological Mechanism:
Caffeine is a very small molecule that is able to cross the blood-brain barrier. It is then able to bind adenosine receptors and act as a competitive antagonist due to its similar molecular shape, which causes an immediate release in Serotonin, Epinephrine, and Dopamine. Caffeine also increases cyclic AMP (cAMP) levels within cells by inhibiting the cAMP-phosphodiesterase enzyme, resulting in an overall increase in cellular ATP levels.

Histidine


Key Action:
Histidine is a precursor of carnosine. It decreases fatigue and muscle tissue pH levels. It also enhances the body's ability to do additional muscular work.

Physiological Mechanism:
Both Histidine and Beta-Alanine are required for the synthesis of Carnosine. These two amino acids form a dipeptide via the activity of Carnosine Synthase. Carnosine also prevents the peroxidation of the fatty acids that compose cell membranes. Histidine is also one of the basic 20 amino acids that aid protein synthesis.

Ornithine-AKG


Key Action:
Ornithine-AKG is a NO Cycle intermediate and is a precursor of Citrulline.

Physiological Mechanism:
Ornithine-AKG is formed from Arginine and, with carbamyl phosphate, forms Citrulline. Citrulline is then converted into Argino Succinate and then into Arginine for the additional production of NO.

Isoleucine


Key Action:
Isoleucine is a branched-chain amino acid. It increases protein synthesis and aids the interior hydrogen bonding of proteins.

Physiological Mechanism:
Branched-chain amino acids, such as Leucine, primarily increase protein synthesis, which can occur in many different ways. It increases insulin synthesis and signals for its release. It also activates a Ras-Rhed signaling pathway that increases the rate of mRNA transcription. Additionally, being an amino acid itself, it provides a raw material for the translation of mRNA into proteins.

Valine


Key Action:
Valine is a branched-chain amino acid that increases protein synthesis and aids the interior hydrogen bonding of proteins.

Physiological Mechanism:
Branched-chain amino acids, such as Valine, primarily increase protein synthesis, which can occur in many different ways. It increases insulin synthesis and signals for its release. It also activates a Ras-Rhed signaling pathway that increases the rate of mRNA transcription. Additionally, being an amino acid itself, it provides a raw material for the translation of mRNA into proteins.

Arginine-Picamilon


Key Action:
Arginine-Picamilon is a rapidly absorbed NO precursor. It increases vascularity, strength, muscular growth, and cerebral blood flow and is a Gamma-amino butyric acid (GABA) receptor agonist.

Physiological Mechanism:
Picamilon works by increasing cerebral blood flow. Since Picamilon is composed of Niacin and GABA, it creates vasodilation and increases blood flow to areas of the brain where GABA receptors are present. This effect results in an increase in awareness, mood, and memory.

Norvaline


Key Action:
Norvaline is an inhibitor of Arginase. It decreases the body's ability to limit NO Synthesis.

Physiological Mechanism:
Both Arginase and NOS are enzymes that compete for the ligand Arginine. Norvaline lacks the methyl group from Valine and the diaminomethylideneamino group from Arginine. However, Norvaline can bind and inhibit the activity of Arginase, while not affecting NOS. This result causes an increase in Arginine levels and, therefore, an increase in NO.

Theobromine


Key Action:
Theobromine is a stimulant with vasodilating and bronchodilating properties. It also reduces blood pressure.

Physiological Mechanism:
Similar in structure to Caffeine, Theobromine functions within the cell by inhibiting cAMP-phosphodiesterase enzymes and preventing the breakdown of cAMP. The increased concentrations of cAMP are phosphorylated and yield high amounts of ATP that result in the stimulant effects associated with Theobromine.

Magnesium Tashinoate


Key Action:
MTB increases the release of NO Cycle metabolites from endothelial cells.

Physiological Mechanism:
MTB acts via a direct interaction with constitutive NOS (cNOS), a calcium-dependent version of NOS. MTB is responsible for the release of NO metabolites, such as nitrate and nitrite, and their conversion to NO, which is a completely different NO-producing mechanism from Arginine.

Methyltyramine


Key Action:
Methyltyramine increases the release of stored monamines, such as Dopamine, Norepinephrine, and Epinephrine.

Physiological Mechanism:
Methyltyramine is a methyl group donor; in its active form, Tyramine, causes an increase in the release of Norepinephrine from synaptic vesicles. This result causes vasoconstriction and increased heartbeat.

Methylsynephrine


Key Action:
Methylsynephrine increases energy levels and ATP synthesis. It enhances the stimulation of adrenaline and is structurally similar to Ephedrine.

Physiological Mechanism:
Methylsynephrine is a methyl group donor and both an alpha- and beta-adrenergic agonist. It directly stimulates adenylyl cyclase, which produces cAMP from ATP, and increases overall energy levels. It is also a slight bronchodilator.

Oxovanadium


Key Action:
Oxovanadium is a synthetic compound that mimics the functions of insulin and prevents insulin resistance.

Physiological Mechanism:
Oxobis (picolinato) vanadium IV, or Oxovanadium, functions similarly to insulin and increases insulin sensitivity. The effects of Oxovanadium significantly reduce blood glucose levels and increase glycogen synthesis in skeletal muscle.

Vinpocetine


Key Action:
Vinpocetine improves memory and cognitive function. It enhances the delivery of nutrients to muscles.

Physiological Mechanism:
Vinpocetine enhances memory and cognitive function by inhibiting the Ca (2+)-calmodium-dependent cyclic GMP-phosphodiesterase enzyme, which then causes an increase in cGMP levels in the vascular endothelial cells of the brain. This vasodilating effect in the brain increases cerebral blood flow and, thus, improves neural function.