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Antaeus Labs

Thunderbolt

NEW Thunderbolt by Antaeus Labs: Advanced Anabolic Vasodilator! The workout pump isn’t just for show – it provides a valuable effect to your training. Increased blood flow helps supply the muscles with oxygen and nutrients, while speeding removal of cellular waste products that contribute to muscular fatigue. Temporary swelling of the muscles results in stretching of the muscle fascia, which allows for continued muscle growth through a cascade of anabolic signals. The pump is also a powerful motivating factor, by acting as positive feedback on your workout and rewarding your efforts by making you look your best. Antaeus Labs' NEW Thunderbolt isn’t your run-of-the-mill “pump supp” though. We’ve carefully selected the four ingredients we think will make the biggest difference to your workouts and progress in the gym. Each dose of Thunderbolt contains: Kallidinogenase (175 IU) Arginine Butyrate (1500mg) S-Nitrosoglutathione (10mg) -Copper (1mg) There’s a good chance you’re unfamiliar with three of those ingredients, so we’ll guide you through them in more detail. Kallidinogenase Kallidinogenase, also known as kallikrein, is a natural human enzyme and the only pharmaceutical-strength vasodilator legally available as a supplement. Thunderbolt contains kallikrein in recombinant form, and while sensitive to degradation by low pH from stomach acid, we have encapsulated Thunderbolt with enteric-coating to ensure high bioavailability. Mechanism of action: Kallikrein is a serine protease, which cleaves kininogen to release the potent vasoactive kinin peptides bradykinin or kallidin. Kallidin is very similar, and can be converted to bradykinin. Within skeletal muscle, bradykinin promotes glucose uptake and improves blood flow. [1]The pharmaceutical class of drugs known as ACE Inhibitors act on bradykinin to keep it active longer which leads to the normalization of blood pressure and nitric oxide release. Boosting bradykinin also increases vascular permeability, which allows for better nutrient delivery to tissues. Kinins have a very short half-life, as they are destroyed in less than 20secs by through the action of kininases (aminopeptidases) present in the tissues and blood. Hence, kinins are unsuitable for use as exogenously administered agents. In plasma, kininogen is in excess, leaving kallikrein as the limiting factor in kinin formation. Therefore, kallikrein is a far better choice for activating the kinin–kallikrein system. Kallidinogenase is stable for 28 months at room temperature, and about five years if kept refrigerated. [2] Primary effects: Kallidinogenase is a peripheral vasodialator, causing an increase in bloodflow and nutrient delivery to skeletal muscle. [3] Other beneficial effects: Kallidinogenase has significant pro-fertility effects, [4,5,6] is nephroprotective, has diuretic effects via activation of the Bradykinin B2 receptor, and increases bloodflow to the brain. [7] Constitutive over-activation of the Bradykinin B2 receptor has been shown to increase the anabolic response to exercise, so Kallidinogenase may also impart a directly anabolic effect. [8] Arginine Butyrate Mechanism of action: Arginine Butyrate is a histone deacetylase (HDAC) inhibitor, and also activates the nitric oxide pathway. Primary effects: In mouse models of muscular dystrophy arginine butyrate demonstrated beneficial effects including increased muscle strength and increased utrophin expression. [9] Exposure of myoblasts to HDAC inhibitors results in upregulation of follistatin expression. In turn, follistatin binds to and suppresses the activity of myostatin, a TGF-β family member that negatively regulates muscle mass. [10] Other beneficial effects: Arginine’s NO-mediated functions are fairly well known. L-arginine is converted into NO by the enzyme NO synthase (eNOS). Nitric oxide causes relaxation vascular smooth muscle by binding to and activating guanylate cyclase and increasing intracellular levels of cyclic-guanosine 3’,5’-monophosphate, causing vasodilation which lowers arterial pressure. [11] This improves blood flow, which increases the “pump”. Nitric oxide also inhibits platelet aggregation and adhesion. [12] Arginine is also a precursor of creatine, and plays a role in accelerating tissue repair following injuries. [13] S-Nitrosoglutathione S-Nitrosoglutathione (GSNO) mediates the cellular signalling effects of nitric oxide (NO). To date, GSNO has been tested in almost 20 clinical trials, examining its efficacy in treating a variety of conditions – including topical use as a treatment for female sexual dysfunction. [14] Mechanism of action: Although GSNO is often described as a “NO donor”, rather than being denitrated like traditional nitrate drugs (e.g. glyceryl trinitrate) which decompose to produce NO, GSNO is capable of donating the nitroso moiety to other molecules, though a reaction called S-nitrosylation. [15] This ability to directly transfer NO+ protects the NO moiety from attack by free radicals. [16] Primary effects: GSNO has vasodilatory effects on the vasculature, specifically of the arteries. [17] Unlike nitrates, S-nitrosothiols do not cause tolerance with long-term continuous use. [18] While NO itself is very short lived, GNSO acts as a stable intracellular pool of NO which allows the beneficial effects of NO stimulation to sustain over a longer period of time. Other beneficial effects: GSNO, and associated nitrosothiols like S-nitrosocysteine, contribute to the regulation of breathing, heart rate, blood pressure, and vascular muscle tone. [19,20,21] GSNO inhibits platelet aggregation, [22] probably via degradation to NO and glutathione disulfide by the cell-surface protein disulfide isomerase (csPDI). [23] GSNO also has neuroprotective properties (via up-regulation of the antioxidative thioredoxin system), and may encourage wound repair through enhanced collagen formation. [24,25] Copper Copper potentiates the vasodilatory and antiplatelet actions of GSNO. Mechanism of action: Copper ions are important catalysts in the decomposition of low molecular weight nitrosothiols (like GSNO) by superoxide dismutase (Cu/Zn SOD). [26] Primary effects: Copper enhances the anti-platelet aggregation properties of GSNO. [27] Other beneficial effects: Copper deficiency has been shown to block acetylcholine-mediated vascular smooth muscle relaxation. [28,29,30] Get a shocking pump with new Antaeus Labs Thunderbolt!!! References: [1] Wicklmayr M, Dietze G, Brunnbauer H, Rett K, Mehnert H. Dose-dependent effect of bradykinin on muscular blood flow and glucose uptake in man. Hoppe-Seyler’s Z Physiol Chem. 1983 Jul;364(7):831–3. [2] Tanimoto T, Fukuda H, Kimura T. [Long-term stability of Kallidinogenase Reference Standard]. Eisei Shikenjo Hokoku. 1989;(107):119–20. [3] Ogawa K, Ito T, Ban M, Motizuki M, Satake T. Effects of kallidinogenase on urinary kallikrein excretion and plasma prostanoid concentrations in patients with essential hypertension. Experientia. 1986 Sep 15;42(9):1014–5. [4] Kamidono S, Hazama M, Matsumoto O, Takada KI, Tomioka O, Ishigami J. Kallikrein and male subfertility. Usefulness of high-unit kallikrein tablets. Andrologia. 1981 Apr;13(2):108–20. [5] Saitoh S, Kumamoto Y, Shimamoto K, Iimura O. Kallikrein in the male reproductive system. Arch Androl. 1987;19(2):133–47. [6] Izzo PL, Canale D, Bianchi B, Meschini P, Esposito G, Menchini Fabris GF, et al. The treatment of male subfertility with kallikrein. Andrologia. 1984 Apr;16(2):156–61. [7] Wang Chang-lin, Zhu You-ling. Clinical effect of urinary kallidinogenese compined with citicoline on treating acute carotisal cerebral infarction. Anhui Medical and Pharmaceutical Journal 2009-01. [8] Popadic gacesa JZ, Momcilovic M, Veselinovic I, Brodie DA, Grujic NG. Bradykinin type 2 receptor -9/-9 genotype is associated with triceps brachii muscle hypertrophy following strength training in young healthy men. BMC Musculoskelet Disord. 2012;13:217. [9] Vianello S, Yu H, Voisin V, Haddad H, He X, Foutz AS, et al. Arginine butyrate: a therapeutic candidate for Duchenne muscular dystrophy. FASEB J. 2013 Jun;27(6):2256–69. [10] Verdin E. Histone Deacetylases: Transcriptional Regulation and Other Cellular Functions. Springer; 2007. [11] Tapiero H, Mathé G, Couvreur P, Tew KD. I. Arginine. Biomed Pharmacother. 2002 Nov;56(9):439–45. [12] Radomski MW, Palmer RM, Moncada S. The anti-aggregating properties of vascular endothelium: interactions between prostacyclin and nitric oxide. Br J Pharmacol. 1987 Nov;92(3):639–46. [13] Witte MB, Barbul A. Arginine physiology and its implication for wound healing. Wound Repair Regen. 2003 Dec;11(6):419–23. [14] Souto S, Palma P, Fregonesi A, Palma T, Reis LO. Vascular modifications of the clitoris induced by topic nitric oxide donor gel–preliminary study. J Sex Med. 2011 Feb;8(2):484–8. [15] De Souza GFP, S. Ferreira E da, Baldim V, de Oliveira MG. Metabolic fate of S-nitrosoglutathione after oral administration: Where does NO go? Nitric Oxide. 2012 Jul 15;27, Supplement:S35. [16] I. Miller MR, Megson IL. Recent developments in nitric oxide donor drugs. Br J Pharmacol. 2007 Jun;151(3):305–21. [17] Broniowska KA, Diers AR, Hogg N. S-Nitrosoglutathione. Biochimica et Biophysica Acta (BBA) – General Subjects. 2013 May;1830(5):3173–81. [18] Miller MR, Roseberry MJ, Mazzei FA, Butler AR, Webb DJ, Megson IL. Novel S-nitrosothiols do not engender vascular tolerance and remain effective in glyceryltrinitrate-tolerant rat femoral arteries. Eur J Pharmacol. 2000 Nov 24;408(3):335–43. [19] Chen Q, Sievers RE, Varga M, et al. Pharmacological inhibition of S-nitrosoglutathione reductase improves endothelial vasodilatory function in rats in vivo. J Appl Physiol. 2013;114(6):752-60. [20] Lipton AJ, Johnson MA, Macdonald T, Lieberman MW, Gozal D, Gaston B. S-Nitrosothiols signal the ventilatory response to hypoxia. Nature. 2001 Sep 13;413(6852):171–4. [21] Ohta H, Bates JN, Lewis SJ, Talman WT. Actions of S-nitrosocysteine in the nucleus tractus solitarii are unrelated to release of nitric oxide. Brain Res. 1997 Jan 23;746(1-2):98–104. [22] Davisson RL, Travis MD, Bates JN, Lewis SJ. Hemodynamic effects of L- and D-S-nitrosocysteine in the rat. Stereoselective S-nitrosothiol recognition sites. Circ Res. 1996 Aug;79(2):256–62. [23] De Belder AJ, MacAllister R, Radomski MW, Moncada S, Vallance PJ. Effects of S-nitroso-glutathione in the human forearm circulation: evidence for selective inhibition of platelet activation. Cardiovasc Res. 1994 May;28(5):691–4. [24] Broniowska KA, Diers AR, Hogg N. S-Nitrosoglutathione. Biochimica et Biophysica Acta (BBA) – General Subjects. 2013 May;1830(5):3173–81. [25] Rauhala P, Andoh T, Chiueh CC. Neuroprotective properties of nitric oxide and S-nitrosoglutathione. Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):91–5. [26] Achuth HN, Moochhala SM, Mahendran R, Tan WTL. Nitrosoglutathione triggers collagen deposition in cutaneous wound repair. Wound Repair Regen. 2005 Aug;13(4):383–9 [27] Burg A, Cohen H, Meyerstein D. The reaction mechanism of nitrosothiols with copper(I). J Biol Inorg Chem. 2000 Apr;5(2):213–7. [28] Gordge MP, Meyer DJ, Hothersall J, Neild GH, Payne NN, Noronha-Dutra A. Copper chelation-induced reduction of the biological activity of S-nitrosothiols. Br J Pharmacol. 1995 Mar;114(5):1083–9. [29] Schuschke DA, Saari JT, Miller FN. A role for dietary copper in nitric oxide-mediated vasodilation. Microcirculation. 1995 Dec;2(4):371–6. [30] Schuschke DA, Percival SS, Saari JT, Miller FN. Relationship between dietary copper concentration and acetylcholine-induced vasodilation in the microcirculation of rats. Biofactors. 1999;10(4):321–7. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease Supplement Facts Serving Size: 3 Capsule Servings per container: 30 Amounts per serving %DV Arginine Butyrate 150mg ** S-Nitrosoglutathione 10mg ** Kallidinogenase 1.75iu ** Cooper( (As copper L-Aspartate) 1mg ** **(DV)Daily Value Not Established Other Ingredients: Hypromellose, Microscrystalline cellulose, Silicon Dioxide. Thunderbolt Directions: Take 3 capsules 25 minutes prior to training. For best results, take on an empty stomach, with 12-16 ounces of water or your favorite pre-workout drink, and keep well-hydrated during excersise. Thunderbolt WARNING: This product is intended to be consumbed by healthy adults 18 years of age or older. It is designed for individuals interested in bodybuilding who generally do not have health problems. Consult with a licensed physician before using this product, especially if you are taking any prescription, over the counter medication, dietary supplement product, or if you have any preexisting medical condition including but not limited to: high or low blood pressure, high or low cholesterol, cardiac arrhythmia, stroke, heart, liver, kidney or thyroid disease, seizure disorder, psychiatric disease, osteoporosis, diabetes, difficulty urinating due to prostate enlargement or if you are taking a MAO-B inhibitor or any other medication. Do not take this product if you have been diagnosed with prostate cancer, testicular cancer or breast cancer. Discontinue use 2 weeks prior to surgery. Discontinue use and immediately consult your heath care professional if you experience any adverse reaction to this product. Do not exceed recommended serving. Do not use if safety seal is broken or missing. This product should not be taken by women. KEEP OUT OF REACH OF CHILDREN.
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