# Blood Glucose & Bodybuilding



## Raptor (Feb 16, 2010)

Ok so judging by posts i have seen on here and other BBing forums over the last 6 months it seems increasingly popular to be checking your Blood Glucose levels on a regular basis for Bbing purposes, many manipulate glucose levels for whatever reason eg if on a Keto diet and you test too high some use Metformin or even Insulin to help get back down to a low blood glucose level which will ultimately will help push you back in to ketosis faster etc

So i have just bought myself a blood glucose machine as im having my cheat day today.. i have been on very low carbs all week and about an hour ago i had 1/2 a pizza a pack of pringles, and 1/2 a terrys chocolate orange.. just done a test and came out at 128 mg/dl = 7.11111 mmol/l

I'll be eating more carbs tonight and until tomorrow afternoon and then will be slowly pushing myself back in to ketosis, will try and speed this up with a largeish dose of Metformin tomorrow afternoon and then a small daily dose and see what results i get on the meter, im not going out drinking this weekend so its a perfect time to start this experiment... Personally i am finding this very interesting. I know many are sensibly using Insulin for this purpose but while im going out having a drink most weekends i'll give it a miss, maybe when i can give it 100% dedication it will be worth giving a go, but for now im happy with using Metformin to help on blood glucose manipulation, obviously alongside a diet designed to do just that.

I have read some very interesting posts recently, especially from a relatively new member named ausbuilt who has helped me understand many benefits of this topic...

So who else monitors blood glucose? what benefits do you find? and why do you do it?


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## Robbyg (Feb 25, 2008)

I do due to finding out info on here and as i am on keto at present, also will be using met when it comes to help with refeeds


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## Conscript (Sep 5, 2010)

I have just ordered my BG monitor and will be pm'ing the sh1t out of ausbuilt when I have my slin and met.... :thumb:


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## Raptor (Feb 16, 2010)

G-fresh said:


> I have just ordered my BG monitor and will be pm'ing the sh1t out of ausbuilt when I have my slin and met.... :thumb:


Yeah he knows his stuff, also MXD showed me a very very interesting protocol that keeps you in ketosis despite having 150g Carbs per day on a timed keto diet with the use of slin.. very interesting indeed but as i said i'd need to be giving it 100% (no drinking) etc if i was gonna try something like that


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## Conscript (Sep 5, 2010)

The Raptor said:


> Yeah he knows his stuff, also MXD showed me a very very interesting protocol that keeps you in ketosis despite having 150g Carbs per day on a timed keto diet with the use of slin.. very interesting indeed but as i said i'd need to be giving it 100% (no drinking) etc if i was gonna try something like that


I'm usually quite a heavy drinker but I haven't had a drink for 3 weeks now so I'm in the groove and primed to go at the moment, can catch up in the summer when the sun is long and the skirts are short!! 

Protocol?


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## Raptor (Feb 16, 2010)

G-fresh said:


> I'm usually quite a heavy drinker but I haven't had a drink for 3 weeks now so I'm in the groove and primed to go at the moment, can catch up in the summer when the sun is long and the skirts are short!!
> 
> Protocol?


Basically the protocol is 75g Carbs before workout and 75g post workout, slin to be taken with each carb meal... starting off at 2iu and 20g carbs and building up fo 1iu per 10g of carbs... so once your in the groove as much as 7.5iu with the 75g meal, MXD has found that he literally doesn't come out of ketosis and as low as 3.8 an hour after the 2nd meal... so in theory building muscle whilst burning fat. Its a lot more detailed than that but thats the basics, seems very interesting imo


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## ausbuilt (Nov 22, 2010)

The Raptor said:


> Yeah he knows his stuff, also MXD showed me a very very interesting protocol that keeps you in ketosis despite having 150g Carbs per day on a timed keto diet with the use of slin.. very interesting indeed but as i said i'd need to be giving it 100% (no drinking) etc if i was gonna try something like that


Yeah, i thought i was radical until PM'ing with MXD! 

I'm adding PGF2a to my bucket of pharmaceuticals next week, and the general consensus is i need more carbs.. I may try MXD's protocol if I find mine's not coping with the pGF2a..

I wish I was recommending my own brand BG meter! LOL but as it is the bayer USB contour keeps me entertained with pretty lines/graphs on my screen


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## Raptor (Feb 16, 2010)

ausbuilt said:


> I'm adding PGF2a to my bucket of pharmaceuticals next week


What does that do mate?


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## Raptor (Feb 16, 2010)

Ok so tonight being my carb up i thought i'd eat loads of carbs.. pizza, choc, crisps, sweets to see how far my blood glucose went up.. just done a test and its up to: 208 mg/dl = 11.55556 mmol/l

11.5 is not good is it? I know i have been on keto all week and this is a rush of glucose in to my system but still its not a good level to be at? Anyway im about to take 1000mg of Metformin and go to sleep to see how this counteracts the carbs from tonight

Will test in the morning and post my results, no doubt i'll be burning some of that glucose in my sleep but will be good to see where i am on waking


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## Huntingground (Jan 10, 2010)

Very interesting Raptor, keep it coming.

Thanks to Ausbuilt too.


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## The Ultimate Warrior (Dec 20, 2010)

Get up you bum and post results, I am very interested in this thread!


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## ausbuilt (Nov 22, 2010)

The Raptor said:


> Ok so tonight being my carb up i thought i'd eat loads of carbs.. pizza, choc, crisps, sweets to see how far my blood glucose went up.. just done a test and its up to: 208 mg/dl = 11.55556 mmol/l
> 
> 11.5 is not good is it? I know i have been on keto all week and this is a rush of glucose in to my system but still its not a good level to be at? Anyway im about to take 1000mg of Metformin and go to sleep to see how this counteracts the carbs from tonight
> 
> Will test in the morning and post my results, no doubt i'll be burning some of that glucose in my sleep but will be good to see where i am on waking


11.5 mmol/L is not bad for that kind of rush.. the question is how long it takes to get to about 6.0-6.5.

the best way to test your bodies insulin/carb response is to do a standard glucose test:

http://en.wikipedia.org/wiki/Glucose_tolerance_test

follow the procedure, in the two hours, pr**k finger(draw blood) and test every 15 mins..

repeat the procedure and take met 500mg with the glucose.

you will see how much faster the met moves your BG levels... and how far... in YOUR body.

See raptor, unless you have impaired Glucose metabolism, you should awake with under 6.1 anyhow... (after 6-8 hour sleep)..

Met is move it down faster than that.. after refeeds (i used to think it was a good idea to take with refeeds on CKD, but then realised you WANT an insulin spike to drive nutrients into cells, and met reduces the spike, which is good on any diet apart from a CKD refeed).


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## Raptor (Feb 16, 2010)

JPaycheck said:


> Get up you bum and post results, I am very interested in this thread!


Ok so i took 1500mg Metformin before sleep at about 4am i was at 11.5 and i have just tested a minute ago at 5.6 (101 mg/dl = 5.61111 mmol/l)

Which is not far off Keto levels if i was to keep it at that level or below, which leads me to believe that the Met did its job last night,

I did sleep which may of burned off some BG but i'll be eating carbs from now until 3:00 in the afternoon as part of my 24 hour carb up

And then i'll do it all over again, i will test in the eve tomorrow after met, i will also test in the morning on sunday and then i'll test again on sunday morning after 40 mins of slow steady cardio


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## ausbuilt (Nov 22, 2010)

The Raptor said:


> What does that do mate?


Prostaglandin PGF2a

by Bryan Haycock

Prostaglandins are part of a class of substances called eicosanoids. Eicosanoids are a group of substances derived from fatty acids and include prostaglandins, thromboxanes, and leukotrienes, all of which are formed from precursor fatty acids by the incorporation of oxygen atoms into the fatty acid chains. This reaction is called oxygenation and is carried out by cyclo-oxygenase enzymes. Prostaglandins and their metabolites have been found in virtually every tissue in the body.

The discovery of prostaglandins and determination of their structure began in 1930, when Raphael Kurzrok and Charles Lieb, both new York gynecologists, observed that human seminal fluid stimulates contraction of isolated uterine muscle. A few years later in Sweden, Ulf von Euler confirmed this report and noted that human seminal fluid also produces contraction in intestinal smooth muscle and lowers blood pressure when injected into the blood stream. It was Von Euler who came up with the name prostaglandin for this mysterious substance. The name prostaglandin seemed appropriate because he thought it originated in the prostate gland. Today, we know that prostaglandin production is not limited to the prostate, in fact, there is virtually no soft tissue in the body that doesn't produce them. The name, however, has stuck with us through the years. If Von Euler had known his name for prostaglandins would still be with us into the next millennia, I'm sure he would have chosen to name them "Von Eulers" or "UVEs" instead of prostaglandins. By 1960, several specific prostaglandins had been isolated in pure crystalline form and their structures determined. Because our concern with prostaglandins involves primarily PGF2a, and perhaps PGE2, we will not go into detail about the myriad of other prostaglandins. Just know that prostaglandins are abbreviated "PG". The additional letter and numerical script indicate the type and series. The various types differ in the functional group present in the five-membered ring.

While scientists were studying the structure of these new compounds, other research was being done to determine their role in human physiology and their potential as drugs. Initially these compounds were extremely expensive to synthesize and/or isolate in sufficient quantities for research. In 1969, the price of prostaglandins dropped dramatically with the discovery that the gorgonian sea whip, or sea fan, is a rich source of prostaglandin-like materials. Now however, there is no need to rely on natural sources because chemists have developed highly effective laboratory methods for the synthesis of almost any prostaglandin or prostaglandin analog.

Endogenous production from Arachidonic Acid

Prostaglandins (PGs) are not stored in the tissues of your body. PGs are produced in response to some physiological trigger. The starting material for PG synthesis are unsaturated fatty acids that have 20 carbon structures. The fatty acid that is used to make PGF2a is arachidonic acid.

Functions of prostaglandins in the body

Prostaglandins are classified as autocrine (effecting the same cell that produced it), as well as paracrine (effecting adjacent cells), regulators. They do not really fit into the category of hormones, nor are they neurotransmitters, instead they are simply considered as a corollary of the endocrine system.

The following are some of the regulatory functions of prostaglandins in various organs and systems of the body:

Inflammation & Pain - PGs promote many aspects of the inflammatory response. They are involved in the sensation of pain associated with inflammation and vasoconstriction and/or dilation, and the development of fever. PGs, when injected directly into the hypothalamus, induce fever. Anecdotally, the use of PGF2a also induces a rise in body temperature presumably by interacting with the hypothalamus as well.

Reproductive systems. PGs may play a role in ovulation and corpus luteum function in the ovaries and in contraction of the uterus. Excessive PG production may be involved in premature labor, endometriosis, dysmenorrhea (menstrual cramps), and other gynecological disorders. PGs are often given to induce labor.

Gastrointestinal tract - The stomach and intestine produce PGs. PGs are believed to inhibit gastric secretions and influence gastric motility as well as fluid absorption. Drugs such as aspirin that inhibit prostaglandin production can lead to overproduction of gastric secretion. This predisposes the person to gastric ulcers.

Respiratory System - PGs can cause vasoconstriction as well as vasodilation of blood vessels within the lungs, depending on which PGs are being produced. PGs also cause both dilation and constriction of bronchial smooth muscle. PGs as well as other eicosanoids may play a role in asthma.

Blood vessels - Some PGs are vasoconstrictors, others are vasodilators. The overall effect is determined by which PG is present in greater concentration.

Blood clotting - Thromboxanes, also a product of cyclo-oxygenase, are produced by blood platelets. These eicosanoids promote platelet aggregation and vasoconstriction. Prostacyclin, produced by vascular endothelial cells, inhibits platelet aggregation and causes vasodilation.

Kidneys - PGs are produced in the medulla of the kidneys and cause vasodilation, resulting in increased renal blood flow and increased excretion of water and electrolytes in the urine. In particular, high potassium intake has been shown to selectively increase PGF2a excretion in animals.

Protein synthesis - PGs are known to be regulators of protein synthesis in skeletal muscle. PGE2 and PGF2a being involved in protein breakdown and protein synthesis rates respectively. Stretch induced hypertrophy of skeletal muscle is in part regulated by prostaglandins. More on the role of PGs in protein synthesis in later sections.

Adipogenesis - PGF2a directly inhibits adipogenesis. You should not be surprised to hear that yet another prostaglandin serves to induce adipogenesis, namely PGJ2. PGJ2 derivatives function as activating ligands for peroxisome proliferator-activated receptor (PPAR), a nuclear hormone receptor that is central to fat cell proliferation. PGF2 blocks adipogenesis through activation of mitogen-activated protein kinase (the same kinase involved in insulin action), resulting in inhibitory phosphorylation of PPAR. Both mitogen-activated protein kinase activation and PPAR phosphorylation are required for the anti-adipogenic effects of PGF2. So you have PGs within the cell telling the fat cell to divide while at the same time you have other PGs, such as PGF2a, at the outside preventing it from taking place.

Current uses of PGF2a

Humans - PGF2a is not currently FDA approved for use in humans. Products containing PGF2a should be considered hazardous to women and must be handled with extreme care. PGF2a is readily absorbed through the skin and may result in birth defects and/or instantaneous abortion. Prostaglandins of use today in humans are of the "E" class and are administered to women for abortion or to induce labor. Prostaglandins are also used for impotence in men. In such case it (PGE1) is injected directly into the penis.

Animals - PGF2a has been tested in a wide range of animals from monkeys to horses. In most cases the side effects are increased body temperature, vomiting and diarrhea, bronchial constriction, confusion, loss of coordination, tachycardia, and low blood pressure just to name a few. PGF2a is nontoxic with a serum half life of only minutes.

PGF2a is currently used in animal husbandry to manage breeding. It is used commonly as dinoprost in the form of a tromethamine salt. Upjohn makes a version called Lutalyse® as a sterile solution for subcutaneous and intramuscular injection. It's purpose is to synchronizing ovulation in cattle by sequential injection of several hormones along with PGF2a. A hormone selected from the group consisting of gonadotropin releasing hormone (GnRH), luteinizing hormone (LH), or human chorionic gonadotropin (hCG) is administered to an open cow during an estrous cycle in order to stimulate follicle development. PGF2a is then administered to initiate corpus luteum regression about five to eight days after administration of the GnRH, LH or hCG. A second dose of GnRH, LH or hCG is then administered concomitantly with the PGF2a injection or up to about three days after the PGF2a injection. This second dose of hormone functions to stimulate the ovulation of a dominant follicle and the cow is then breed within one day of the administration of the second dose of hormone.

The Role of PGF2a in Muscle Growth

After that brief introduction into prostaglandins, we can now begin to discuss more specifically the role of prostaglandins in muscle growth. In a nutshell, mechanical stimulation (i.e. intermittent stretch) results in the production and efflux of two prostaglandins, PGE2 and PGF2a. PGE2 increases protein degradation where as PGF2a increases protein synthesis. Muscle hypertrophy is usually achieved by an increase in protein synthesis as well as a proportionately smaller increase in degradation. The simultaneous release of both PGE2 and PGF2a creates this condition.

It is well known that mechanical stretch, without any electrical activity, is sufficient to induce muscle hypertrophy. Recent studies have shown that the mechanism by which mechanical stretch leads to prostaglandin production and ultimately muscle growth, involves G proteins embedded in the cell membrane. These G proteins increase the amount of cyclo-oxygenase, the enzyme responsible for making prostaglandins from arachidonic acid. Skeletal muscle cyclooxygenase generates PGE2 and PGF2 alpha at a ratio approximately equal to one.

The exact mechanism by which PGF2a increases protein synthesis is not entirely clear. That's just a spineless way of saying, "I don't know the exact answer to that!" We are free to speculate though. It may involve short phase protein synthesis and/or long phase protein synthesis.

2 phases of protein synthesis Modulation

Modulation of protein synthesis rates occurs at two levels, the short phase and the long phase. The short phase alteration in protein synthesis rates occurs by altering the activity of existing ribosomes and/or eukaryotic initiation factors (eIFs). This happens within minutes of the appropriate physiological trigger. The long phase modulation of protein synthesis happens by way of increasing the number of myonuclei. This mechanism involves hormones and growth factors such as HGH and IGF-1 bringing about the activation of myogenic stem cells. This can take several days to effect protein synthesis rates. This is a simplified view but for our purposes it is sufficient.

The role of PGF2a in short phase protein synthesis in muscle tissue is speculative at best. In non-muscle tissue, prostaglandins effect calcium fluxes, plasma membrane ionic channel activities, and cyclic nucleotide levels. All of which are important regulators of protein synthesis rates in muscle. PGF2a has been shown to interact with the S6 small ribosomal subunit, increasing its potential to form the ribosomal initiation complex with the large subunits. It is also plausible that PGF2a may effect the activity of eIFs.

Initiation of translation (the binding of mRNA to the ribosomal pre-initiation complex) requires group 4 eukaryotic initiation factors (eIFs). These initiation factors interact with the mRNA in such a way that makes translation (the construction of new proteins from the mRNA strand) possible. Two eIFs, called eIF4A and eIF4B, act in concert to unwind the mRNA strand. Another one called eIF4E binds to what is called the "cap region" and is important for controlling which mRNA strands are translated and also for stabilization of the mRNA strand. Finally, eIF4G is a large polypeptide that acts as a scaffold or framework around which all of these initiation factors and the mRNA and ribosome can be kept in place and proper orientation for translation. There is yet no direct evidence to confirm that PGF2a works through this mechanism however.

Long term modulation of protein synthesis involves the activation of myogenic stem cells or satellite cells. If you recall, when a muscle is stretched it not only produces PGF2a, but also PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is how existing muscle cells increase the number of nuclei they contain. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications on growth and development as well as stretch induced hypertrophy.

The role of other hormones, drugs and diet in the action of PGs.

Because prostaglandins are signaling molecules that get their message across through multi step signal transduction pathways, they are susceptible to modulation by several chemical, hormonal, and dietary factors. I will do my best to shed some light on the subject without bogging you down with meaningless terms and jargon. It is well to remember that the action and interaction of prostaglandins in the human body is complex.

Cortisol

Cortisol effects the production of prostaglandins in muscle tissue by at least two mechanisms. First, cortisol by way of lipocortins, inhibits the action of phospholipase A2. Phospholipase is necessary in order to make arachidonic acid available for PGF2a production. Cortisol also inhibits the production of cyclo-oxygenase mRNA content within cells. As mentioned earlier, cyclo-oxygenase is the enzyme that converts arachidonic acid into prostaglandins. So cortisol inhibits muscle growth by preventing the production of PGF2a in response to training (mechanical stimulation) and eating (insulin action).

Insulin

As eluded to above, insulin stimulated protein synthesis is linked to the production of phospholipases which lead to increased availability of arachidonic acid. This is a two edged sword. Increased availability of arachidonic acid can increase the amount of PGF2a thereby increasing protein synthesis. On the other hand, arachidonic aid directly suppresses GLUT4 production which is the chief glucose transporter in skeletal muscle. High levels of arachidonic acid can reduce glucose transport by up to 50%. It could be that insulin action is more dependant on the cAMP antagonist, cyclic PIP (prostaglandylinositol cyclic phosphate), a proposed second messenger for insulin and alpha-adrenoceptor action, than on PGF2a. PGE2 however is a different story. Prostaglandin E, myo-inositol and one phosphate are components of cyclic PIP. So increased production of PGE2 may increase insulin mediated glucose transport through this mechanism. Taking this into consideration, exogenous PGF2a should not be considered to replace insulin.

Dietary Fatty Acids

Dietary fatty acids significantly effects prostaglandin production. Diets high in omega-3 fatty acids (fish oil, flax oil) decrease prostaglandin production. Diets high in omega-6 fatty acids (corn oil) increase prostaglandin production. Once again you have pros and cons with trying to manipulate PGF2a production with your diet. By increasing omega-3s, you get lower levels of PGF2a and probably a less intense stimulus of protein synthesis immediately after you workout. On the other hand by increasing omega-3s you reduce inflamation, pain, increase GLUT4 content, and a whole host of other factors related to cardiac risk. I don't think its as clear cut as Dr. Sears (Zone Diet) would have you believe. Trying to manipulate the diet to control prostaglandin kinetics is fraught with complexity making black and white statements difficult to support.

NSAIDs

NSAIDs are non-steroidal anti-inflammatory drugs. An example of such drugs are aspirin, ibuprofen (Motrin), naproxen sodium (Anaprox, Alleve). There are several more but these are the most common to consumers. NSAIDs work by inhibiting the activity of cyclooxygenase. By blocking cyclooxygenase you block prostaglandin production. These drugs have been shown to improve nitrogen balance under conditions of severe physical stress such as after surgery. The effect is abolished when PGE2 is infused linking PGE2 production with the catabolic effect of stress. In the case of PGF2a, the use of NSAIDs also blocks its production in that PGE2 and PGF2a are normally produced in a 1:1 ratio from the same precursor. Using NSAIDS while using exogenous PGF2a may improve the anabolic effect by reducing PGE2 in the presents of elevated PGF2a shifting the ratio towards anabolism.

PGF2a + IGF-1: The ultimate cocktail for localized muscle growth?!

Say good by to lagging body parts forever. It is a special time to be a bodybuilder. With the advent of PGF2a as a localized anabolic agent along with the newly available rhIGF-1 which has also been shown to build muscle where you want it, the future for genetically challenged bodybuilders looks bright indeed. A brief refresher course on locally injected IGF-1. Non-exercised muscle, when injection with 0.9 - 1.9 micrograms/kg/day of rhIGF-1 was shown to mimic the effects of physically loading the muscle. Much the same effect PGF2a but by different mechanisms. With local IGF-1 injections there is an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 needed are extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.

Now add PGF2a to the mix and whalla! You can virtually mimic the mechanical stimulus of training without even picking up a weight. You have PGF2a to accelerate short term protein synthesis by activating ribosomes and/or eIFs and thereby translation, as well as IGF-1 to activate satellite cells to bind and donate additional nuclei to boost the amount of mRNA to be used by the ribosomes. Because the mechanism of action is different, the two compounds should compliment each other delivering results beyond what either one alone could produce.

Are these compounds going to replace traditional training? Not in the near future. The use of site injectable drugs only reaches the surface musculature. Deeper muscles are only stimulated to grow with traditional training. For strength athletes, strength is dependant on neuromuscular training which is not enhanced by simple muscle hypertrophy without actual lifting in a coordinated fashion. Are these compounds going to replace traditional anabolics? No. The reason is basically the same as with training. Deeper muscle groups are only reached by systemically administered anabolics that are carried throughout the entire body. In addition, androgens are needed to influence genetic expression in favor of whole body skeletal muscle growth. Are these compounds going to change the face of bodybuilding? It is very likely that they will, depending on their availability and cost. I would hope that as competitors become educated about these alternatives that we will no longer see implants in top level competitors. It would also be nice to see people have an option when it comes to pumping their muscles full of "stuff" in hopes that it will improve their symmetry. No doubt the future will bring us even more new and exciting drugs like non-steroidal androgens and compounds that alter the expression of myostatin (GDF8). Once again, it is an exciting time in the science of bodybuilding, perhaps now more than any other time since the introduction of testosterone.

from:

http://www.basskilleronline.com/prostaglandin-pgf2a.shtml


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## Raptor (Feb 16, 2010)

ausbuilt said:


> 11.5 mmol/L is not bad for that kind of rush.. the question is how long it takes to get to about 6.0-6.5.
> 
> the best way to test your bodies insulin/carb response is to do a standard glucose test:
> 
> ...


Yeah i'll be doing all sorts of tests on my blood glucose and my bodies efficiency... im convinced that my bodies efficiency is not optimal, and i also notice that after carbs i often feel exhausted, for example.. yesterday afternoon after my 1st lot of carbs (1/2 a meat feast pizza, a tube of pringles and 1/2 a terrys chocolate orange) i literally fell in to a deep sleep for 90 mins and felt extremely lethargic for about 2 hours despite having 10 hours sleep the night before..

Also cheers for the PGF2a article will have a read


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## dtlv (Jul 24, 2009)

ausbuilt said:


> Yeah, i thought i was radical until PM'ing with MXD!


Haha, known Max for a few years, great guy who NEVER does anything by half!!!



ausbuilt said:


> Prostaglandin PGF2a
> 
> by Bryan Haycock
> 
> ...


That's a really good article there, nice find. Reps for posting that.


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## ausbuilt (Nov 22, 2010)

Dtlv74 said:


> Haha, known Max for a few years, great guy who NEVER does anything by half!!!
> 
> yeah he really made me think!! I like that
> 
> That's a really good article there, nice find. Reps for posting that.


oh thanks! I never pretend to know it all (or anything really) i just read everything I can... then put it into practice to see if the theory works in real life.. I don't want to cross post, but search for "lutalyse" on here, and i will be posting everything i do / use. Going to start transdermal application next week on my abs/love handles


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## dtlv (Jul 24, 2009)

ausbuilt said:


> oh thanks! I never pretend to know it all (or anything really) i just read everything I can... then put it into practice to see if the theory works in real life.. I don't want to cross post, but search for "lutalyse" on here, and *i will be posting everything i do / use*. Going to start transdermal application next week on my abs/love handles


Yeah, am a nerd too reading everything in site and trying most of it out afterwards 

Am glad that you'll be open about what you are using - I see far too many people who use assistance on this forum and others talking up a diet or training protocol, citing how amazing their gains have have, but failing to mention how the 'assistance' they have had has massively contributed and modified the effect. This lack of honesty often results in very misleading advice to natties.


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## The Ultimate Warrior (Dec 20, 2010)

very interesting indeed!!!! Keep us informated mate.


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## Raptor (Feb 16, 2010)

JPaycheck said:


> very interesting indeed!!!! Keep us informated mate.


Will do mate, been suffering all day lol.. tried some Superpump 250 before my workout... was good at the time but the come down for me is terrible, not eaten since 1:00 lol! Had a mega sesh in the gym and been wasted all day from one sachet, damn stims really do fcuk me up!

Will have to extend todays carb up as i was gonna have an indian today


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## ausbuilt (Nov 22, 2010)

Dtlv74 said:


> Yeah, am a nerd too reading everything in site and trying most of it out afterwards
> 
> Am glad that you'll be open about what you are using - I see far too many people who use assistance on this forum and others talking up a diet or training protocol, citing how amazing their gains have have, but failing to mention how the 'assistance' they have had has massively contributed and modified the effect. This lack of honesty often results in very misleading advice to natties.


True, I see all the drugs as just tools, and I see no difference to taking an aspirin if I have a headache.. but the moral decisions are individual. I think the number one issue for natties generally is cortisol and its effects; apart from AAS you have to rely on super short workouts, and some other means of combating morning peak cortisol levels (after all this is why natties are size limited- cortisol stops anabolism past a certain point). I hear 7 Oxo is meant to be useful for this, but I have no experience as I have never considered dieting without AAS...


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## Raptor (Feb 16, 2010)

Ok so i have just tested at 5.2 and im going for 40 mins cardio.... hope to at least get below 5.0

Tbh i was at 5.2 at monday morning, and not eaten no carbs so not sure why its sticking... but hey ho

As said im still in ketosis


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## maccer (Jul 11, 2007)

That is some peoples baseline mate. When I was testing myself all the time and low carb I would wake and be from 4.8 to 5.6. The meters have variance as well, if you used 3 different metres you would get 3 different results! What matters is knowing your baseline to work off.

Also sometime your bg is higher when you wake due to cortisol being higher in the am.


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## Papa Lazarou (Jul 4, 2007)

5.3mmol/L was my waking baseline on a GH blast, mid 4's for normal.


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