Thunderbolt

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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 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.

Ingredient Breakdown

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]

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]

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.

Recommended Dosage

Take 3-6 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.

WARNING

Not for use by individuals under the age of 18 years. Do not use if pregnant or nursing. Keep out of the reach of children. Do not consume this product if you have a medical condition and/or taking any prescription medication. Do not exceed recommended servings. Do not use this product if you are at risk or are being treated for high blood pressure, kidney, thyroid or psychiatric disease, anxiety, depression, seizure, enlarged prostate or stroke. Before beginning any supplement or training program always consult a physician first.

“These statements have not been evaluated by the Food & Drug Administration (FDA). This product is not intended to diagnose, treat, cure, or prevent any disease. ALWAYS consult your physician before taking supplements.”

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