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SYNTHELATOR™ - Vasodilator

kidstuff

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hi everyone,

i'm new here and have a couple of questions about one the products your sponsor sells.

i'm interested in the pre-contest vasodilator SYNTHELATOR™ - Vasodilator by synthetek.

my question is.... has anyone used this and gotten the desired effect. AND

what is the REAL way to use this product....
 

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USe the Search function of the board. Synthelator has been around for many years and lots of people used it with good results.

You need to inject it IM 1 hour before you go on stage. As soon as you inj it you will start hyperventilating severely. Within 45 minutes you will have the maddest veins, IF you are carbed up properly.

After you come off stage, make sure you stay carbed up until the evening show, otherwise you will go flat. You don't need another dose for the night show. If you take another one, you will overdose.
 

Ashop

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Works super! Used with competition athletes I work with many times. Veins are explosive like Big A said, carb up properly. Great tool for bodybuilding.
 

kidstuff

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thanks for the responses guys....

what is a good starting dosage for a 200lbs athlete?

and does it matter what muscle i inject it into? (i'd prefer to keep it away from muscles that will require hardcore flexing. i.e. bis, tris, quads, chest)
 

Big L

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Big A said:
USe the Search function of the board. Synthelator has been around for many years and lots of people used it with good results.

You need to inject it IM 1 hour before you go on stage. As soon as you inj it you will start hyperventilating severely. Within 45 minutes you will have the maddest veins, IF you are carbed up properly.

After you come off stage, make sure you stay carbed up until the evening show, otherwise you will go flat. You don't need another dose for the night show. If you take another one, you will overdose.
The whole bottle in one bodypart, or different bodyparts. I will just do a search. Thanks Big A, can't wait to try it, kinda weary about the hyperventilating though.:eek:
 

kidstuff

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yea, i just did a search and found my answers.

man 10ml all at once. why doesn't this product come in a higher concentration?
 

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kidstuff said:
why doesn't this product come in a higher concentration?
Because, generally, it's meatheads using it.

10ml is 400mg. If you inject 500mg, you will pass out. Plenty of people have done that.

So, it's keeping it safe - one whole bottle, 400mg, is the proper dose, without any meathead that thinks more is better having access to more, and banging his head on a toilet bowl as he passes out when he overdoses.

You inject 5ml in each glute. It's water based - you won't even know it's there.
 

Big Bapper

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Viagra

Big A,

I know Synthelator is the best product to use pre-comp but, was doing a lot resarch and was wondering........Would viagra work as as vasodilator in the same way Synthelator does ??
 

dragonfire101

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As soon as you inj it you will start hyperventilating severely.
How long does that last. Sounds a little scary if you don't know its suppose to do that.
 

Big L

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Big A said:
Because, generally, it's meatheads using it.

10ml is 400mg. If you inject 500mg, you will pass out. Plenty of people have done that.

So, it's keeping it safe - one whole bottle, 400mg, is the proper dose, without any meathead that thinks more is better having access to more, and banging his head on a toilet bowl as he passes out when he overdoses.

You inject 5ml in each glute. It's water based - you won't even know it's there.
Thanks Big A!!!!!
 

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Big Bapper said:
Big A,

I know Synthelator is the best product to use pre-comp but, was doing a lot resarch and was wondering........Would viagra work as as vasodilator in the same way Synthelator does ??
I never used Viagra, so I have no idea about it's effects on vascularity. There's lots of people here that use viagra though, so they might chime in.
 

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dragonfire101 said:
How long does that last. Sounds a little scary if you don't know its suppose to do that.
Hell yes it does!

My first ever injection that I did myself was in '92 at a teen comp in another city. I always had a nurse give me the shots until then.
This was my first ever injection on my own. I did it, everything went fine, but as soon as I finished it, the hyperventilation began (noone bothered to tell me about it). I thought I did something really wrong with the injection, and I was dying LOL

I calmed down within the hour (about how long the hyperventilation lasts), just as my father came in the hotel room. He looked at me, he said 'Nervous about the show?' I just nodded LOL

45min to 60min is how long you hyperventilate for.
 

dragonfire101

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45min to 60min is how long you hyperventilate for.
Have you found anything to ease this. I don't think I could bare to hyperventilate this long. Is it a mild hyperventilate like when you cant breath through your nose when you have a cold or one were you just ran a mile as fast as you could and just collasped at the finish line.
 

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dragonfire101 said:
Have you found anything to ease this. I don't think I could bare to hyperventilate this long. Is it a mild hyperventilate like when you cant breath through your nose when you have a cold or one were you just ran a mile as fast as you could and just collasped at the finish line.
It's the second one. That's why no asthmatics should use it.
 

StoryOfTheYear

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lol that is some scary sounding shit!! Hey Big A, what causes this?
 

dragonfire101

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Hey Big A, what causes this?
Bronchoconstriction
(adenosine injection) is a respiratory stimulant (probably through activation of carotid body chemoreceptors) and intravenous administration in man has been shown to increase minute ventilation (Ve) and reduce arterial PCO2 causing respiratory alkalosis.


Also Here is some Clinical Pharmacology below on Adenosine if you like to read. It mentions some medications if you are using not to use Adenosine.

Action And Clinical Pharmacology: Adenosine is an endogenous nucleoside occurring in all cells of the body. When injected i.v. adenosine slows atrioventricular (AV) nodal conduction, can interrupt the reentry pathways through the AV node and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff-Parkinson-White syndrome.

Adenosine is antagonized competitively by methylxanthines such as caffeine and theophylline and potentiated by blockers of nucleoside transport such as dipyridamole. Adenosine is not blocked by atropine.

In controlled clinical trials, cumulative 60% and 92% of patients converted to normal sinus rhythm within 1 minute after 6 mg and 12 mg bolus doses of adenosine, respectively. In other controlled clinical trials with bolus doses of 3, 6, 9 and 12 mg some patients with paroxysmal supraventricular tachycardia converted to normal sinus rhythm on 3 mg of adenosine.

Adenosine is not effective in converting rhythms other than PSVT, such as atrial flutter, atrial fibrillation, or ventricular tachycardia to normal sinus rhythm.

Hemodynamics: Adenosine is a potent vasodilator in most vascular beds, except in renal afferent arterioles and hepatic veins where it produces vasoconstriction. The usual i.v. bolus dose of 6 or 12 mg adenosine has no systemic hemodynamic effects. When larger doses are given by infusion, adenosine decreases blood pressure by decreasing peripheral resistance.

Pharmacokinetics: I.V. administered adenosine is rapidly cleared from the circulation through cellular uptake, mainly by erythrocytes and vascular endothelial cells, with a half-life of less than 10 seconds. Intracellular adenosine is rapidly metabolized either via phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in the cytosol. Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool. Inosine formed by deamination of adenosine can leave the cell intact or can be metabolized to hypoxanthine, xanthine and ultimately uric acid.

Since neither the kidney nor the liver are required for the metabolism or elimination of adenosine, the activity of adenosine should be unaffected by hepatic or renal insufficiency.

Indications And Clinical Uses: For the conversion to sinus rhythm of paroxysmal supraventricular tachycardia (PSVT), including that associated with accessory bypass tracts (Wolff-Parkinson-White Syndrome). When clinically advisable, appropriate vagal maneuvers (e.g. Valsalva maneuver) should be attempted prior to adenosine administration.

Adenosine is indicated to aid in the diagnosis of broad or narrow complex supraventricular tachycardia. Although adenosine is not effective in converting atrial flutter, atrial fibrillation or ventricular tachycardia to sinus rhythm, the transient atrioventricular nodal block produced helps diagnosis of atrial activity.

It is essential to ascertain that adenosine actually reaches the systemic circulation (see Dosage).

Adenosine does not convert atrial flutter, atrial fibrillation or ventricular tachycardia to normal sinus rhythm.

Adenosine should only be used with appropriate cardiac monitoring.

Contra-Indications: Second- or third-degree AV block (except in patients with a functioning artificial pacemaker). Sick sinus syndrome (except in patients with a functioning artificial pacemaker). Symptomatic bradycardia (except in patients with a functioning artificial pacemaker). Known hypersensitivity to adenosine. tag_WarningWarnings

Manufacturers' Warnings In Clinical States: Heart Block: Adenosine exerts its effect by decreasing conduction through the AV node and may produce a short lasting first-, second- or third-degree heart block. In extreme cases, transient asystole may result (one case has been reported in a patient with atrial flutter who was receiving carbamazepine). Appropriate therapy should be instituted as needed. Patients who develop high level block on one dose of adenosine should not be given additional doses. Because of the very short half-life of adenosine (<10 seconds), these effects are generally self-limiting.

Rarely, ventricular fibrillation/flutter has been reported following adenosine administration, including both resuscitated and fatal events. In most instances, these cases were associated with the concomitant use of digoxin and, less frequently with digoxin and verapamil. Adenosine should be used with caution in patients receiving digoxin or digoxin and verapamil in combination. Appropriate resuscitative measures should be available.

Patients with atrial fibrillation/flutter and an accessory by-pass tract may develop increased conduction down the anomalous pathway.

Arrhythmias at Time of Conversion: At the time of conversion to normal sinus rhythm, a variety of new rhythms may appear on the ECG. They generally last only a few seconds without intervention, and may take the form of premature ventricular contractions, atrial premature contractions, sinus bradycardia, sinus tachycardia, skipped beats, and varying degrees of AV nodal block. These arrhythmias and conduction disturbances were observed in about 55% of patients.

Bronchoconstriction: Adenosine has been administered to a limited number of patients with asthma and serious exacerbation of their symptoms has been reported in some patients. Respiratory compromise has occurred during adenosine infusion in patients with chronic obstructive pulmonary disease (COPD). Therefore, the use of adenosine should be avoided in patients with COPD or asthma.

Adenosine therapy should be discontinued in any patient who develops severe respiratory difficulties.

Precautions: Pregnancy: Adenosine is a substance naturally present in the body and therefore no fetal effects would be anticipated. However, since it is not known whether adenosine can cause fetal harm when administered to pregnant women, it should not be used during pregnancy unless potential benefits outweigh the potential risks to the fetus.

Children: The safety and efficacy of adenosine in children have not been established.

Drug Interactions: Cardioactive Drugs: Adenosine has been effectively administered in the presence of other cardioactive drugs, such as quinidine, beta-adrenergic blocking agents, calcium channel blocking agents and angiotensin converting enzyme inhibitors, without any change in the adverse reaction profile. Digoxin and verapamil use may be rarely associated with ventricular fibrillation when combined with adenosine (see Warnings). Because of the synergistic depressant effects on the SA and AV nodes, adenosine should be used with caution in the presence of these agents.

Methylxanthines: The effects of adenosine are antagonized by methylxanthines (such as caffeine and theophylline). In the presence of methylxanthines, larger doses of adenosine may be required or adenosine may not be effective.

Dipyridamole: Adenosine effects are potentiated by dipyridamole. Thus, smaller doses of adenosine may be effective in the presence of dipyridamole.

Carbamazepine: Carbamazepine has been reported to increase the degree of heart block produced by other agents. Since the primary effect of adenosine is to decrease conduction through the AV node, higher degrees of heart block may be produced in the presence of carbamazepine.

Adverse Reactions: In controlled clinical trials 268 patients received adenosine. One hundred and two patients (38%) experienced one or more adverse events. These adverse events appeared immediately after administration of adenosine and usually lasted less than 1 minute. The most common adverse reactions were: facial flushing (18%), dyspnea (12%), chest pressure (7%) and nausea (3%).

Cardiovascular: facial flushing (18%), headache (2%), sweating, palpitations, chest pain, hypotension (less than 1%). A variety of arrhythmias and conduction disturbances were observed in about 55% of patients at the time of conversion to normal sinus rhythm (see Warnings).

Respiratory: shortness of breath/dyspnea (12%), chest pressure (7%), hyperventilation, head pressure (less than 1%).

CNS: lightheadedness (2%), dizziness, tingling in arms, numbness (1%), apprehension, blurred vision, burning sensation, heaviness in arms, neck and back pain (less than 1%).

Gastrointestinal: nausea (3%), metallic taste, tightness in throat, pressure in groin (less than 1%).

Symptoms And Treatment Of Overdose: Symptoms and Treatment: No cases of overdosage associated with the use of adenosine have been reported. It is unlikely that the true overdosage will occur because adenosine has a short half-life (<10 seconds) and is dosed by a rapid bolus injection. If prolonged adverse events associated with the use of adenosine occur, treatment should be individualized and directed toward the specific event. To date, no patient has required administration of adenosine antagonists such as aminophylline to counteract adverse events associated with the use of adenosine.

In clinical studies on the use of adenosine as a diagnostic agent in imaging, less than 0.1% of the patients exposed to adenosine were described as having severe, prolonged, adverse events. These prolonged adverse events were treated with aminophylline after discontinuation of the adenosine infusion. The usual concentration of aminophylline used was 1.25 mg/mL (125 mg in 100 mL) administered i.v. over 5 to 6 minutes. An additional 1.25 mg/mL (125 mg in 100 mL) can be administered, but clinical experience has demonstrated that this is rarely required.
 
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Big A

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dragonfire101 said:
Bronchoconstriction
(adenosine injection) is a respiratory stimulant (probably through activation of carotid body chemoreceptors) and intravenous administration in man has been shown to increase minute ventilation (Ve) and reduce arterial PCO2 causing respiratory alkalosis.


Also Here is some Clinical Pharmacology below on Adenosine if you like to read. It mentions some medications if you are using not to use Adenosine.

Action And Clinical Pharmacology: Adenosine is an endogenous nucleoside occurring in all cells of the body. When injected i.v. adenosine slows atrioventricular (AV) nodal conduction, can interrupt the reentry pathways through the AV node and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff-Parkinson-White syndrome.

Adenosine is antagonized competitively by methylxanthines such as caffeine and theophylline and potentiated by blockers of nucleoside transport such as dipyridamole. Adenosine is not blocked by atropine.

In controlled clinical trials, cumulative 60% and 92% of patients converted to normal sinus rhythm within 1 minute after 6 mg and 12 mg bolus doses of adenosine, respectively. In other controlled clinical trials with bolus doses of 3, 6, 9 and 12 mg some patients with paroxysmal supraventricular tachycardia converted to normal sinus rhythm on 3 mg of adenosine.

Adenosine is not effective in converting rhythms other than PSVT, such as atrial flutter, atrial fibrillation, or ventricular tachycardia to normal sinus rhythm.

Hemodynamics: Adenosine is a potent vasodilator in most vascular beds, except in renal afferent arterioles and hepatic veins where it produces vasoconstriction. The usual i.v. bolus dose of 6 or 12 mg adenosine has no systemic hemodynamic effects. When larger doses are given by infusion, adenosine decreases blood pressure by decreasing peripheral resistance.

Pharmacokinetics: I.V. administered adenosine is rapidly cleared from the circulation through cellular uptake, mainly by erythrocytes and vascular endothelial cells, with a half-life of less than 10 seconds. Intracellular adenosine is rapidly metabolized either via phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in the cytosol. Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool. Inosine formed by deamination of adenosine can leave the cell intact or can be metabolized to hypoxanthine, xanthine and ultimately uric acid.

Since neither the kidney nor the liver are required for the metabolism or elimination of adenosine, the activity of adenosine should be unaffected by hepatic or renal insufficiency.

Indications And Clinical Uses: For the conversion to sinus rhythm of paroxysmal supraventricular tachycardia (PSVT), including that associated with accessory bypass tracts (Wolff-Parkinson-White Syndrome). When clinically advisable, appropriate vagal maneuvers (e.g. Valsalva maneuver) should be attempted prior to adenosine administration.

Adenosine is indicated to aid in the diagnosis of broad or narrow complex supraventricular tachycardia. Although adenosine is not effective in converting atrial flutter, atrial fibrillation or ventricular tachycardia to sinus rhythm, the transient atrioventricular nodal block produced helps diagnosis of atrial activity.

It is essential to ascertain that adenosine actually reaches the systemic circulation (see Dosage).

Adenosine does not convert atrial flutter, atrial fibrillation or ventricular tachycardia to normal sinus rhythm.

Adenosine should only be used with appropriate cardiac monitoring.

Contra-Indications: Second- or third-degree AV block (except in patients with a functioning artificial pacemaker). Sick sinus syndrome (except in patients with a functioning artificial pacemaker). Symptomatic bradycardia (except in patients with a functioning artificial pacemaker). Known hypersensitivity to adenosine. tag_WarningWarnings

Manufacturers' Warnings In Clinical States: Heart Block: Adenosine exerts its effect by decreasing conduction through the AV node and may produce a short lasting first-, second- or third-degree heart block. In extreme cases, transient asystole may result (one case has been reported in a patient with atrial flutter who was receiving carbamazepine). Appropriate therapy should be instituted as needed. Patients who develop high level block on one dose of adenosine should not be given additional doses. Because of the very short half-life of adenosine (<10 seconds), these effects are generally self-limiting.

Rarely, ventricular fibrillation/flutter has been reported following adenosine administration, including both resuscitated and fatal events. In most instances, these cases were associated with the concomitant use of digoxin and, less frequently with digoxin and verapamil. Adenosine should be used with caution in patients receiving digoxin or digoxin and verapamil in combination. Appropriate resuscitative measures should be available.

Patients with atrial fibrillation/flutter and an accessory by-pass tract may develop increased conduction down the anomalous pathway.

Arrhythmias at Time of Conversion: At the time of conversion to normal sinus rhythm, a variety of new rhythms may appear on the ECG. They generally last only a few seconds without intervention, and may take the form of premature ventricular contractions, atrial premature contractions, sinus bradycardia, sinus tachycardia, skipped beats, and varying degrees of AV nodal block. These arrhythmias and conduction disturbances were observed in about 55% of patients.

Bronchoconstriction: Adenosine has been administered to a limited number of patients with asthma and serious exacerbation of their symptoms has been reported in some patients. Respiratory compromise has occurred during adenosine infusion in patients with chronic obstructive pulmonary disease (COPD). Therefore, the use of adenosine should be avoided in patients with COPD or asthma.

Adenosine therapy should be discontinued in any patient who develops severe respiratory difficulties.

Precautions: Pregnancy: Adenosine is a substance naturally present in the body and therefore no fetal effects would be anticipated. However, since it is not known whether adenosine can cause fetal harm when administered to pregnant women, it should not be used during pregnancy unless potential benefits outweigh the potential risks to the fetus.

Children: The safety and efficacy of adenosine in children have not been established.

Drug Interactions: Cardioactive Drugs: Adenosine has been effectively administered in the presence of other cardioactive drugs, such as quinidine, beta-adrenergic blocking agents, calcium channel blocking agents and angiotensin converting enzyme inhibitors, without any change in the adverse reaction profile. Digoxin and verapamil use may be rarely associated with ventricular fibrillation when combined with adenosine (see Warnings). Because of the synergistic depressant effects on the SA and AV nodes, adenosine should be used with caution in the presence of these agents.

Methylxanthines: The effects of adenosine are antagonized by methylxanthines (such as caffeine and theophylline). In the presence of methylxanthines, larger doses of adenosine may be required or adenosine may not be effective.

Dipyridamole: Adenosine effects are potentiated by dipyridamole. Thus, smaller doses of adenosine may be effective in the presence of dipyridamole.

Carbamazepine: Carbamazepine has been reported to increase the degree of heart block produced by other agents. Since the primary effect of adenosine is to decrease conduction through the AV node, higher degrees of heart block may be produced in the presence of carbamazepine.

Adverse Reactions: In controlled clinical trials 268 patients received adenosine. One hundred and two patients (38%) experienced one or more adverse events. These adverse events appeared immediately after administration of adenosine and usually lasted less than 1 minute. The most common adverse reactions were: facial flushing (18%), dyspnea (12%), chest pressure (7%) and nausea (3%).

Cardiovascular: facial flushing (18%), headache (2%), sweating, palpitations, chest pain, hypotension (less than 1%). A variety of arrhythmias and conduction disturbances were observed in about 55% of patients at the time of conversion to normal sinus rhythm (see Warnings).

Respiratory: shortness of breath/dyspnea (12%), chest pressure (7%), hyperventilation, head pressure (less than 1%).

CNS: lightheadedness (2%), dizziness, tingling in arms, numbness (1%), apprehension, blurred vision, burning sensation, heaviness in arms, neck and back pain (less than 1%).

Gastrointestinal: nausea (3%), metallic taste, tightness in throat, pressure in groin (less than 1%).

Symptoms And Treatment Of Overdose: Symptoms and Treatment: No cases of overdosage associated with the use of adenosine have been reported. It is unlikely that the true overdosage will occur because adenosine has a short half-life (<10 seconds) and is dosed by a rapid bolus injection. If prolonged adverse events associated with the use of adenosine occur, treatment should be individualized and directed toward the specific event. To date, no patient has required administration of adenosine antagonists such as aminophylline to counteract adverse events associated with the use of adenosine.

In clinical studies on the use of adenosine as a diagnostic agent in imaging, less than 0.1% of the patients exposed to adenosine were described as having severe, prolonged, adverse events. These prolonged adverse events were treated with aminophylline after discontinuation of the adenosine infusion. The usual concentration of aminophylline used was 1.25 mg/mL (125 mg in 100 mL) administered i.v. over 5 to 6 minutes. An additional 1.25 mg/mL (125 mg in 100 mL) can be administered, but clinical experience has demonstrated that this is rarely required.

Good read, but that's just straight adenosine. AMP (adenosine monohosphate) as in Synthelator, has a MUCH longer life and as such overdosage happens easily - I've seen it first hand.

And I'm glad I read that, as I forgot - the vasuclarity effects will not happen at maximum if the person using it is not fully carbed up and if he is using caffeine.

So for it to work properly, the user has to not be on any caffeine and has to be fully carbed up.
 

dragonfire101

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Good read, but that's just straight adenosine. AMP (adenosine monohosphate) as in Synthelator, has a MUCH longer life and as such overdosage happens easily - I've seen it first hand.
I noticed that, but when i searched for info it kept on referring to the straight adenosie for its definition. I did come across one abstract with adenosine monohosphate for the use of shingles with a recommend daily dose at 160-200mg.

In you exxperince can one use less say just 200mg to maybe decrease the hyperventilation and still get vasuclarity effects if fully carbed up and if he is using caffeine, or is the higher amonut needed for a higher body weight. I figured one should take the least possible that they could obtain vasuclarity with. Maybe one can take smaller dosages divided 1-2 hr apart to reduce this hyperventilation.
Unles hyperventilation is inevitable with any dose.
 
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Big A

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dragonfire101 said:
I noticed that, but when i searched for info it kept on referring to the straight adenosie for its definition. I did come across one abstract with adenosine monohosphate for the use of shingles with a recommend daily dose at 160-200mg.

In you exxperince can one use less say just 200mg to maybe decrease the hyperventilation and still get vasuclarity effects if fully carbed up and if he is using caffeine, or is the higher amonut needed for a higher body weight. I figured one should take the least possible that they could obtain vasuclarity with. Maybe one can take smaller dosages divided 1-2 hr apart to reduce this hyperventilation.
Unles hyperventilation is inevitable with any dose.
Unfortunately, the vascularity is dose dependant. Basically, the more is injected, the more vascularity one ends up with. The people that have overdosed and as such passed out for a few minutes, when they woke up they were insanely vascular.

BTW, the user should be carbed up and NOT using caffeine!
 

bulldog21

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Big A said:
BTW, the user should be carbed up and NOT using caffeine!
Does that apply to other pre comp "tools" as well? Like if someone were to use ephedra or clenbuterol they should abstain from those the morning of the show to be able to administer vasodiolator?
 

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