Perfect Post-Work Out Consumable

lol...

it makes you think doesnt it , i mean you get guys like "him" on tv shows and wherever else they appear and have nothing but rubbish to say about bodybuilders and some people related to the sport, yet he himself obviously has done bodybuilding to get to the size he is .....i think him and people like him just do this type of thing to gain attention,,,probably has nothing better to do ...

Posted by: adey888

as we are on about post w..out.....there was this guy on tv last night and he was on about bodybuilders saying that we all take supps and yet they are not needed because if you look at our prison systems around the world (esp in america) most of the convicts are built like the hulk and they have to eat whatever they are given and only 3 times a day...he went on to say you dont need anything to bulk and shape yourself ..he said he has never eaten any special foods or taken any POST supps etc , and this guy was huge ..i mean what a beast of a guy ,,,,he was convinced you waste money and time taking any suppliments..

what a character........you could see just by looking at him he is on some serious eating or something (and he said he eats burgers ,,chips (or fries as you americans call them) bacon .everything !!!!!

So a post-work-out 10 stretch will add pounds, What about anti-O's!!!?

So a post-work-out 10 stretch will add pounds, What about anti-O's!!!? (psimonkey)

good one !!!! yeah i think maybe if we all want the perfect build maybe we should do a tenny............

Posted by: PC1

Why does EVERYONE say whey protein pwo? I can see having some whey pwo, but considering whey breaks down faster than the body can assimilate it, a blend containing some whey but other proteins should be optimal.

Hell yeah, Jbol and guys how about a protein blend of whey, egg albumin, soy and fat free milk?

Posted by: adey888

So a post-work-out 10 stretch will add pounds, What about anti-O's!!!? (psimonkey)

good one !!!! yeah i think maybe if we all want the perfect build maybe we should do a tenny............

The Dartmoor cycle!!! 3 on, 1 off.

Posted by: pSimonkey

The Dartmoor cycle!!! 3 on, 1 off.

Years, that is

It will never be the combination of different products which makes you the one you are. We all know that statement to be the correct. But anyway, there are really many products on the market which claim to be THE ONE YOU HAVE TO USE, IF YOU WANT MAXIMAL GROWTH - LOL!

My self do like this;
PRE WORKOUT SHAKE CONSIST;
10g creapure + 5g cee
r-ala 100mg
20g maltodekstrin
10g glutamin peptid
10g bcaa
caffeine, calcium, magnesium, taurine

After workout;
Some whey (50g)
and maltodextrin , the amount depends on what i have done. Its no need for 100g maltodextrin if you have worked out your biceps and calves for 2 set of each.

Piracetam 1000mgs - pill - anti O, increase steroid availability at site "psimonkey"

where did you get this info?

Re: info

Posted by: triguy

Piracetam 1000mgs - pill - anti O, increase steroid availability at site "psimonkey"

where did you get this info?

I have been looking for the original source but alas cannot find it. I wish I had kept it I have been kicking myself for not doing so. I will try again today.

Okay... hoorah.!! It is based on some work by Steve Wm. Fowkes. confirming the cooperation between endogenous steroids and piracetam.

Another interesting ref but to adrenal
MCB 165

Spring 1999

Smart Drugs: Enhancing Cognitive Function with Piracetam

(2-oxo-1-pyrrolidine acetamide)

Piracetam is a psychoactive drug widely used in European and Asian countries for its ability to augment cognitive, learning, and memory abilities, to decrease oxidative and hypoxic stress and to stabilize cells in the blood and CNS (central nervous system). With no known toxicity or addictive properties documented in the past two decades, the drug has been used overseas to address numerous neurological and physical disorders including: myoclonus, Down's syndrome, sickle cell anemia, dyslexia, senile dementia, and others. However, as piracetam is not currently approved by the FDA (Federal Drug Administration) or manufactured by any U.S. pharmaceutical companies, there is very little clinical information and research in the United States. The goal of this paper is to introduce the study of nootropic drugs, summarize current theories on their mechanism of action, and describe relevant applications of piracetam as documented in recent international and domestic research.

The term nootropic, derived from a Greek word meaning "acting on the mind", has been adopted by pharmaceutical companies in recent years to categorize substances similar to that of piracetam, first developed by UCB Laboratories in Belgium under the name Nootropil. (1) In addition to enhanced intelligence and memory, the effects associated with "smart drugs" include improved " sex, relaxation, sleep, immune function and neuroendocrine regulation." (2) Today, overseas sales of piracetam loom in the billions as a growing segment of normal, functioning people are beginning to experiment with nootropics for boosting intelligence and cognitive ability. Although elderly people (especially those suffering from senile dementia and/or Alzheimer's disease) have been the primary target market for nootropics, many have found smart drugs to be very useful in combatting pediatric mental disorders. Nootropics demonstrate extremely low toxicity and tend to work synergistically with other smart drugs like choline, greatly potentiating the individual effects of each other.

Piracetam is among the most popular of the smart drugs due to its reported efficacy in enhancing cognitive ability and alleviating various ailments among normal and disease-afflicted individuals. The exact mechanism of action for piracetam is still undetermined but believed to affect many physiological systems simultaneously.

Initial research into the structure of piracetam suggested that a GABAergic (gamma amino butyric acid, a neurotransmitter) mechanism was at work, as piracetam resembles the GABA derivative, pyroglutamate. However, no evidence has been found to confirm this hypothesis.

"Piracetam is very similar in molecular structure to the amino acid pyroglutamate. Piracetam and pyroglutamate have the same "base" chemical structure, the 2-oxo-pyrrolidine, but they differ by the side chain. Pyroglutamate is 2-oxo-pyrrolidine carboxylic acid, and piracetam is 2-oxo-pyrrolidine acetamide." (3)

Later attempts to analyze the chemical structure of piracetam were more successful and provided some insight into its psychoactive effects. Analysis of piracetam-type drugs by X-ray diffraction, NMR spectroscopy and evaluation of molecular dynamics indicate that the structural properties of the molecule affect the amnesia-reversal (memory associated) activity of piracetam. Unlike many neurotransmitters, the lipophilicity of piracetam and associated ability to cross the blood-brain barrier were not considered relevant to its psychoactive effects or amnesia-reversal activity. Many psychoactive substances have lipophilic ("lipid loving") structures that facilitate their passage into the brain.

"The conformational properties of a number of rigid and flexible piracetam-type cognition enhancers have been assessed by X-ray diffraction, NMR spectroscopy, and ab initio and high-temperature-quenched molecular dynamics (QMD) calculations. The structures of the preferred conformers in solution derived from 1H-NMR spectral analysis were in good agreement with those found by QMD calculations. Interestingly, the calculation of the average molecular lipophilicity potential on the water-accessible surface of the selected conformers was helpful in interpreting the partitioning behavior observed by measuring octanol-water partition coefficients and capacity factors in reversed-phase high-performance liquid chromatography. While lipophilicity does not play a relevant role, the distance between polar groups, accounted for by the distance between carbonyl oxygens, emerges as a factor, among others, which should influence the amnesia-reversal activity of piracetam-type nootropics." (4)

Early research on piracetam's mechanism of action in rats led scientists to hypothesize that the cognitive enhancing qualities of piracetam are related to its effects on adrenal steroids. One study found that removing the adrenal glands of rats that had previously been administered piracetam inactivates any effect of the associated effects on learning and cognition. (5) Another study involving adrenalectomized rats confirmed hypothesis of piracetam moderation by adrenal steroids, rats would not respond to piracetam at any dosage. (6) Further research in this area suggested that piracetam's mechanism of action may be due to intervention in steroid-sensitive gene transcription/protein synthesis. (7) This area of animal research has diminished/lost attention due to recent research using piracetam as a treatment for many different types of disorders in humans.

Recent human research has finally started to shed light on the mechanism(s) and effects of piracetam. Elderly psychiatric patients have been administered piracetam for years to improve memory (8) and treat Alzheimer's disease and multi-farct dementia. The synergistic effect of choline with piracetam was not observed in the elderly (9) but PET (positron emission tomography) experiments have verified improved glucose metabolism in piracetam-using AD patients. (10) These studies and others have collectively led scientists toward a cholinergic mechanism of action and/or influence on ion transport..

Although the exact details of piracetam metabolism haven't been deduced, a recent review of piracetam and other structurally related nootropics indicate piracetam potentiates an increase of sodium/calcium influx or decrease in potassium efflux during neurotransmission. Many common psychoactive pathways such as muscarinic, dopaminergic, GABAergic receptors show no affinity when piracetam is used.

"The piracetam-like nootropics are capable of achieving reversal of amnesia induced by, e.g., scopolamine, electroconvulsive shock and hypoxia. Protection against barbiturate intoxication is observed and some benefit in clinical studies with patients suffering from mild to moderate degrees of dementia has been demonstrated. No affinity for the alpha 1-, alpha 2-, beta-, muscarinic, 5-hydroxytryptamine-, dopamine, adenosine-A1-, mu-opiate, gamma-aminobutyric acid (GABA) (except for nefiracetam (GABAA)), benzodiazepine and glutamate receptors has been found. The racetams possess a very low toxicity and lack serious side effects. Increased turnover of different neurotransmitters has been observed as well as other biochemical findings, e.g., inhibition of enzymes such as prolylendopeptidase. So far, no generally accepted mechanism of action has, however, emerged. We believe that the effect of the racetams is due to a potentiation of already present neurotransmission and that much evidence points in the direction of a modulated ion flux by, e.g., potentiated calcium influx through non-L-type voltage-dependent calcium channels, potentiated sodium influx through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor gated channels or voltage-dependent channels or decreases in potassium efflux. Effects on carrier mediated ion transport are also possible." (11)

Because of these effects on ion transport, many U.S. physicians and scientists actively discourage the use of piracetam for diseases such as DS (Down's syndrome/ trisomal disorder). This apprehension is based on theoretically elevated seizure risk and the lack of long-term, clinical research in the United States. The vast majority of DS victims and parents who administer piracetam to their children have yet to be discouraged as nearly three decades of clinical studies overseas have failed to support any indication of toxicity to seizure victims.

"This is of special concern due to a higher-than normal incidence of seizures in DS individuals. The basis of these allegations of seizure risk is enhanced cellular calcium influx from piracetam, an in vitro (test tube) finding whose applicability to real life must be seriously questioned in the face of decades of clinical experience to the contrary [see SDN v5n8p10]. In fact, piracetam has mild anti-seizure activity, and it protects against memory and cognitive deficits caused by seizures." (12)

For nearly three decades, piracetam has exhibited extremely low toxicity in research with humans. Although extremely large doses of piracetam have been administered to humans in clinical studies, average daily doses for normal people range between 800-4000 milligrams, which is a rather large amount for a psychoactive substance.

"The classical measure of drug toxicity, the LD-50 (the dose causing death for 500f test animals), is not applicable; standard dosing methods (oral, intravenous injection, intraperitoneal injection) cannot deliver enough piracetam to kill laboratory animals. Doses of greater than 20g/day have been given to people suffering from myoclonic seizure disorders, without serious side effects [Karacostas et al., 1993]. The recommended dose of piracetam for infants with myoclonic seizures is 10-20g/day (approximately 1-2 rounded tablespoons), a phenomenally high dose by normal drug standards." (13)

The documented efficacy and extremely low toxicity of piracetam also make it a lucrative nootropic for private industry, especially the various analogues under development such as vinpocetine, aniracetam, pramiracetam, oxiracetam, and others. These drugs have been under intensive research and development during this past decade. The piracetam analogues also demonstrate the low toxicity associated with nootropics and in some cases, even greater efficacy.

Alarmist opinion regarding the safety of nootropics has quieted over the past few years as piracetam has been acknowledged as the drug of choice for treating myoclonus, a seizure-like condition characterized by uncontrollable muscle twitching or jerking. (14) A nationwide multi-institution study in Japan found:

"Piracetam was effective in myoclonus, especially that of cortical origin, in both monotherapy and polytherapy. Piracetam also had positive benefits on gait ataxia and convulsions but not on dysarthria, and feeding and handwriting improved much more significantly. Psychologically significant improvement was seen in decreased motivation, sleep disturbance, attention deficit, and depression, all of which might be possibly secondary benefits associated with improvement of myoclonus. There was no positive correlation between clinical and electrophysiological improvement. Tolerance was good, and side effects were transient. However, hemtological abnormalities observed in at least two patients in the present study should be kept in mind when relatively large doses of piracetam are administered, especially in combination with other antimyoclonic drugs." (15)

These desirable effects have been associated with alterations in lipid membrane fluidity within the brain. Membrane fluidity is an indicator of permeability, influenced by many factors such as cholesterol content, fatty acid profile, and degree of lipid peroxidation. Higher levels of cholesterol content, fatty acid saturation (hydrogenation) and peroxidation (form of oxidative stress) cause lipid membranes to become rigid and impermeable. Piracetam has already been shown to alleviate oxidative stress caused by excess hydrogen peroxide and increase membrane fluidity in the brain.

"In vitro preincubation of brain membranes of aged mice with piracetam (0.1-1.0 mmol/L) enhanced membrane fluidity, as indicated by decreased anisotropy of the membrane-bound fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Piracetam had similar in vitro effects on brain membranes of aged rats and humans, but it did not alter brain membrane fluidity in young mice. Chronic treatment of young and aged rats with piracetam (300 mg/kg once daily) significantly increased membrane fluidity in some brain regions of the aged animals, but had no measurable effect on membrane fluidity in the young rats. The same treatment significantly improved active avoidance learning in the aged rats only. It is suggested that some of the pharmacological properties of piracetam can be explained by its effects on membrane fluidity." (16)

Hypoxia (a condition of low oxygen levels in the tissues caused by hypobaric conditions, decreased oxygen-carrying capacity of the blood, and impaired circulation) has been treated with piracetam because of its protective effects from lipid peroxidation.

Medical applications are being researched in Russia including improvement of metabolic and hormonal indices disturbed by collateral damage from heart disease (17) and treatment of hypoxia-related damage from prostaglandin synthesis (powerful hormones created by oxygen free radicals and polyunsaturated fatty acids). (18) Vast amounts of anecdotal evidence among athletes, academics, elderly people, and parents with children afflicted by DS (developmental delays in closing of heart muscle wall cause de-oxygenated blood to circulate resulting in chronic hypoxia) support piracetam's usefulness in treating hypoxia-related symptoms.

However, the treatment of Down's Syndrome remains the center of controversy regarding the applications of piracetam. A recent presentation at by the Pediatric Academic Societies in San Francisco included a study reporting that piracetam does not enhance cognitive abilities in moderate to high-functioning 7-13 year-old children with DS.

"Piracetam, a drug reported to enhance cognitive performance in many neurobehavioural conditions, has become popular in the treatment of children with Down Syndrome (DS). However, reports of its efficacy in DS have been anecdotal, not from evidence-based studies. Some caregivers have noted no effect of piracetam, while others claim substantial improvement in cognitive functioning. To address the need for objective analysis, we conducted a double-blind placebo-controlled crossover study assessing the cognitive and behavioral effects of piracetam in children with DS... Piracetam did not show significant effects over placebo on any outcome measure (ANCOVA, covariate was age at baseline). All significant interactions (p's < 0.05) with drug order or the covariate were examined further to ensure drug effects were not being masked. That analysis did not alter the results. Piracetam administration was associated with CNS stimulatory effects: aggressiveness (n=4), agitation (n =3), sexual arousal, (including masturbation in public, n=2), irritability (n=1), and poor sleep (n=1). Conclusion. Piracetam has received a great deal of attention in the popular press purporting its efficacy in improving cognitive function in children with Down Syndrome. In this study, we were unable to substantiate these claims, even at doses associated with adverse effects. Neither cognitive nor behavioural measures demonstrated improvement under piracetam. Due to the serious adverse effects, it is unlikely that larger doses can be tolerated."(19)

This study is a serious departure from the consensus; many users feel that piracetam is fated to wallow in FDA limbo until politically profitable. However, many U.S. doctors and scientists refer to piracetam as "the drug in search of a disease", another discredited panacea to be shunned.

As piracetam has not been approved by the FDA, many ethical and political arguments surround the unadvised administration of piracetam to children afflicted by ailments such as: aphasia/stroke, Down's Syndrome, sickle cell anemia, myoclonus, and learning disorders. The ethical considerations surrounding the administration of substances not approved by the FDA and in general, the right to supplement with alternative therapies, have been examined by the popular media over the last few years with much fanfare and very little actionable research. The range of arguments and sentiment presented by critics of smart drugs tend to mirror those who criticize alternative/complementary medicine, a topic far beyond the scope of this paper. Now, unfortunately, due to the conservative nature and underlying profit motive of private industry, drug companies such as UCB Laboratories no longer have the latitude to fund or conduct studies on controversial topics such as DS.

Fortunately, because nootropics exhibit favorable activity in cognitive enhancement and are relatively safe, piracetam has fared reasonably well within this tumultuous context of science and politics. With orphan drug status as a treatment for myoclonus, and a study of piracetam and Ts65dn mice (an animal model for trisomy 21) currently underway at John Hopkins, U.S. research is finally starting to pick up speed. A new study assessing the feasibility of piracetam and school-aged children has gained attention at Kennedy-Kriger Institute in an effort to raise awareness for the possible application of piracetam and possibly acquire funding for a large-scale study by the FDA. In addition, with adequate media coverage and an American manufacturer, the expected profitability of piracetam may eventually speed the FDA approval process, illuminating the future of piracetam and its users in the United States.

References

1) Dean, Ward M.D.; Morgenthaler, John, Smart Drugs & Nutrients, 1990.

2) Dean, Ward M.D.; Morgenthaler, John; Fowkes, Steven Wm. Smart Drugs II, The Next Generation, 1993.

3) Dean, Ward M.D.; Morgenthaler, John Smart Drugs & Nutrients, 1990.

4) Altomare, C.; Cellamare, S. X-ray crystal structure, partitioning behavior, and molecular modeling study of piracetam-type nootropics: insights into the pharmacophore, Journal of Medicinal Chemistry 38(1):170-9, 1995.

5) Mondadori, C. Do piracetam-like compounds act centrally via peripheral mechanisms? Behav. Brain Res. 435:310-14, 1987.

6) Mondadori, C. et al. Blockade of the nootropic action of piracetam-like nootropics by adrenalectomy. Behav. Brain Res. 34:155-58, 1989.

7) Mondadori, C. Involvement of a steroidal component in the mechanism of action of piracetam-like nootropics. Behav. Brain Res. 506:101-108, 1990.

8) Chouinard, G. et al. Piracetam in elderly psychiatric patients. Psychopharm 81:100-106, 1983.

9) Corona, GL. Et al. Clinical and biochemical responses to therapy in Alzheimer's disease and multi-infarct dementia. Dur. Arch. Psychiatr. Neurol. Sci. 239:79-86, 1989.

10) Heiss WD et al. Abnormalities of energy metabolism in Alzheimer's disease studied with Positron Emission Tomography. Ann NY Acad Aci, 1991.

11) Gouliaev A.H.; Senning A. Piracetam and other structurally related nootropics. Brain Res. Rev., 19:180-222, 1994.

12) Fowkes, Stephen WM. The Case for Piracetam in Down's Syndrome. Smart Drug News V.5(9):1, 1997.

13) Fowkes, Stephen WM. The Case for Piracetam in Down's Syndrome. Smart Drug News V.5(9):2, 1997.

14) Dulac O. et al. Myoclonus and epilepsy in childhood: 1996 Royamount meeting. Epilepsy Research 30:91-106, 1998.

15) Ikeda, A et al. Clinical trial of piracetam in patients with myoclonus: Nationwide multiinstitution study in Japan. Movement Disorders 11(6): 691-700, 196.

16) Muller, WE et al. Effects of piracetam on membrane fluidity in the aged mouse, rat and human brain. Biochem. Pharmacology 53:135-140, 1997.

17) Fowkes, Stephen WM. The Case for Piracetam in Down's Syndrome. Smart Drug News V.5(9):5, 1997.

18) Fowkes, Stephen WM. The Case for Piracetam in Down's Syndrome. Smart Drug News V.5(9):6, 1997.

19) Lobaugh, NJ et al. [abstract] Piracetam does not enhance cognitive abilities in moderate to high-functioning 7 to 13 year-old children with Down Syndrome. Presented at the PAS/SPR meeting, May 3, 1999; publication pending.

My post shake is all this in one:

Protein 25G
Carbs 41G (malo, dex)
Vit. C 100mg
Vitamin E 200mg
calcium 150mg

Works good for me :O
Mag. 240mg
sodium 220mg
Potassium 121mg
L-glut 1,000mg
L-Leucine 2,000MG

If my workout is real hardcore, I'll double the serving :O Pretty cheap drink mix,

My pre-workout nutrition:

30g whey isolate
150g banana

My post-workout nutrition:
30g whey hydrollisate
170g pine-apple
2g creatine monohydrate
(followed an hour later by the same post workout shake)

Changing only my pre and postworkout nutrition (before: preworkout: oatmeal/milk, postworkout: whey isolate + dextrose)and keeping the rest of my diet and training exactly the same has had noticable positive effects on my body-composition, so this seems to work for me.

Since even with whey isolate, which is supposed to be a fast acting protein, it takes 2 hours for the amino acids hit the bloodstream the pre-workout nutrition is IMO even more important than the post workout nutrition. This is also the reason btw why I use hydrolisate instead of concentrate or isolate.

I personally don't believe in the need for fast carbs in post nutrition. My reasons for this are:
Since the amino acids of the protein in the postworkout shake take a long time to peak in the blood, that would mean the glucose/insulin peak in the blood is long gone when amino acids begin to enter the bloodstream.
For strength sports there is no need to replenish glycogen stores fast. Over a 24 hour period they will be replenished anyway just by eating carbs as you would normally do.

Fast carbs to enhance creatine uptake are also a bad idea IMO since it takes a long time (80 minutes) for creatine to peak in the bloodstream.