By: Big Cat

Note: The views and comments in this section do not necessarily reflect those of Bodybuilding.com and its owners.

Editorial: What Makes A Champion?

It's early on a Saturday morning, and I'm sitting in the couch watching the TV. I don't watch TV that often, and certainly its not where you would usually find me after a hectic week. 5 extra hours of class this semester, and after 8 hours in a lab, and a 90 minute trip home on days you have to get up at 5:30 in the AM doesn't leave much time to do anything. Usually weekends have various activities as well, and if I do have a Saturday to myself, I normally sleep in.

What got me out of bed was the women's final of the Australian Open. I'm a big sports fan and we don't get much on the TV in the way of sports here unless its two soccer teams no one wants to watch anyway. Two Belgian girls in the final as well, its beginning to become a habit.

Now don't worry, I don't intend to talk to you about the intricacies of the female tennis game, if you ask me they are all a bunch of spoiled brats. But rather the two players and their inherent differences. Kim Clijsters and Justine Henin. It's no lie, I could have predicted the winner before the tournament even started. Eventhough I come from the Dutch speaking part of Belgium, I have a very deep respect for Justine.

She is still a spoiled brat, like the rest of them. But she is a spoiled brat that knows what she wants and is not afraid to go the distance. You see, there are two types of players on the WTA tour. The hard hitters, and the more sophisticated technical players. Even though both hold their own on the court, the game of late has been dominated by the hard hitters.

But what distinguishes a winner from a loser, is the realisation that what you have is not all you can ever get. Not two years ago, Justine was definitely the lesser of the two. She had skill, but lacked variation and she was simply too small. But for little over a year now she has sought the help of renowned coach Pat Etcheberry in Florida.

In just a few short months, Justine has not only resolved her technical shortcomings, she has also packed on an amazing amount of muscle. She used to look like a 2x4, and now she has a really nice body. To achieve what she achieved in such a period of time takes dedication, and dedication requires drive.

Kim on the other hand has leeched of her talent for a long time. She has good reach, a lot of power and she is one of the best baseline tennissers in the game, maybe the best with the exception of possibly Serena Williams. But now there is a new breed of player, cause in the final, Justine served a full 20 miles an hour harder than Kim and scored almost three times the amount of winners.

Nowadays, to be a successful athlete, you not only have to be passionate about your sport, passionate enough to keep doing it every hour of every day, but also dedicated and wilful enough to realize there is more to do than just practice your slice. Justine got in the weight room and fought her demons. The result is not only that she has improved her power and her game through what almost resembled ritual self-punishment, she has come back mentally stronger.

Strong enough to fight marathon matches and come out on top, strong enough to know that she can win when she has too, strong enough to become the world number one and wear that title with pride and defend it.

But what am I saying that you didn't already know? Weight training makes us more self-confident, gives us more strength, gives us a mental edge and teaches us the discipline to walk through life with a smile, no matter what hardships come our way. We know all this. But a big topic at the Australian Open this year was the injuries.

The few players in the game that could actually have prevented an all-belgian final were either absent with injury (Serena Williams, maybe Jennifer Capriati on one of her lighter days) or got injured in the course of the tournament (Amelie Mauresmo). When Steffi Graf was world number one, a tennis player did 12, maybe 13 tournaments a year. Now, these girls easily do 20-25 tournaments a year.

It takes more than talent to survive that schedule and keep winning. And its always easy to look at any tournament and call any victory easy because of the lack of opposition (and that definitely held true at this Aussie Open, both finalists made it there without losing a set), or the condition of the opposition (Both Kim Clijsters and Venus Williams commenced the tournament coming out of injury) but do you ever stop to consider that maybe the reason those left standing at the end don't get hurt BECAUSE they go the extra mile?

Because that too is the merit of the many hours we all spend in the weight room each year. It enables us to cope with extra stress, it enables us to endure more than the rest. And that is our own doing, our own sweat, blood and tears, and not just the talent we are given or the love we have for our sport/hobby. That is what it is all about.

Cause in the end, you can look back at any performance and say a win is only a win because more talented players could not compete. But you know what? There will always be someone more talented. In the end, a win is a win because you went the extra mile somewhere along the line. In a field of 8000+ pro players, it is never easy to come out on top, no matter how you look at it.

And maybe that's what we all should realize, every day. That we go the extra mile. We work harder than anyone. And that will always entitle us to say that what we achieve is our own. Don't let anyone ever tell you otherwise. You know how hard you worked and you know if you've done enough or not. And you know you can always do more. And in the end, can we desire any more than that ?

Of course we can, we are bodybuilders. Perfection hasn't been invented yet. Its not good enough to be number one, you have to stay there as long as you can. You have to raise your own bar-It's not good enough to jump as high as the next person, you have to jump as high as you possibly can.

A Review Of Branched Chain Amino Acids And Their Effects On Amino Acid And Glucose Metabolism

A lot of things factor into the equation when we look for maximal growth benefits from our training, nutrition and supplementation. But perhaps none as important as nutrient usage. We address many issues with uptake and availability, which may of course be relevant in making products more cost-effective, but they rarely form a problem when discussing nutrients we find in our daily diets.

Much more important is how the nutrients will affect us once inside the system, and how we can maximize their benefit for our cause. The body has an intricate network of various sensors that can detect the levels of these nutrients in the system and can regulate their fate in this manner. So these nutrients have rather direct effects on their own fate, simply by being present.

Glucose for instance, will regulate its own uptake in various tissues by stimulating insulin in large enough doses. This is no different for amino acids, although they work even more direct. They exert very direct effects not only on factors like insulin, which are important for protein synthesis as well as the uptake of amino acids and glucose, but also on these events themselves.

This goes for a multitude of these amino acids, but today we limit our discussion to the branched chain amino acids, more specifically leucine and isoleucine, which clearly have a profound effect on nutrient uptake and protein synthesis.

Insulin Release

Insulin is a crucial element in this case, not so much because it stimulates amino acid uptake, it does, but because it initiates several pathways that lead to protein synthesis.

Two pathways in particular are very relevant, namely the phosphatodyl-inositol-3-kinase pathway, which regulates glucose uptake through Glucose transporter 4 (GLUT4) translocation as well as enhancing amino acid uptake, and the mammalian target of Rapamycin (mTOR) pathway, downstream of PI3K, which has various cascades needed for muscle anabolism.

Perhaps therefore it is wise to first look at how BCAA's would affect the release of insulin. Leucine has been shown to increase insulin release from the pancreas by itself, but only in conditions of low glucose (1,2). This because insulin release via leucine is mediated by Glutamate dehydrogenase (GDH) activity. GDH is regulated by positive factors (ADP and P) and negative factors (ATP and GTP).

When glucose levels are elevated ATP and GTP will be higher, and consequently ADP and P will be lower, downregulating GDH and inhibiting leucine stimulated insulin release. The leucine metabolite and HMB precursor KIC on the other hand, does still exhibit some effect on insulin release even in high glucose environment, which suggests that they are regulated via a different mechanism.

ATP Molecule

Since leucine and KIC can convert from one to the other, it is safe to assume that increase leucine also leads to increase KIC and may therefore impact insulin release to some extent regardless. This seems evident if we take a second study (3) into consideration that clearly demonstrates that when leucine is administered with glucose, the insulin response is elevated almost 50%. Therefore BCAA use may enhance serum levels of insulin.

Li C, Najafi H, Daikhin Y, Nissim IB, Collins HW, Yudkoff M, Matschinsky FM, Stanley CA. Regulation of leucine-stimulated insulin secretion and glutamine metabolism in isolated rat islets. J Biol Chem. 2003 Jan 31;278(5):2853-8. Epub 2002 Nov 19.

Gao Z, Young RA, Li G, Najafi H, Buettger C, Sukumvanich SS, Wong RK, Wolf BA, Matschinsky FM. Distinguishing features of leucine and alpha-ketoisocaproate sensing in pancreatic beta-cells. Endocrinology. 2003 May;144(5):1949-57.

Anthony JC, Anthony TG, Kimball SR, Jefferson LS. Signaling pathways involved in translational control of protein synthesis in skeletal muscle by leucine. J Nutr. 2001 Mar;131(3):856S-860S.

Stimulation And Enhancement Of PI3K

One of the immediate downstream targets of the insulin receptor is Phosphatodyl-inositol-3-Kinase (PI3K). BCAA's effect PI3K, both directly and by enhancing the action of insulin. The effects on PI3K can be important for several things, including mTOR related anabolism, but as we will see later, BCAA's exert an effect on mTOR that may be independent of PI3K, so its probably not worth discussing here.

But PI3K also affects protein kinase B and C, both control the uptake of glucose into the cell by allocating the Glucose transporter 4 (GLUT4) to the cell membrane. PI3K, although certainly not the only factor, also enhances amino acid uptake into the cell (1). In this regard it appears that leucine is more effective than its metabolite KIC, in promoting glucose uptake.

It seems to do so independent of insulin, through a PI3K/PKC dependent mechanism (2). This means that leucine directly, without needing insulin present, can activate PI3K. Its role in this regard is highly synergistic (3) with insulin. When insulin stimulates PI3K, leucine will amplify the signal for protein synthesis at the level of peptide initiation. So apart from stimulating insulin release, it displays synergistic effects in enhancing its action at the post-receptor level.

Leucine is not alone in this, that other BCAA, isoleucin exerts similar effects (4) , showing increased glucose uptake via PI3K activation, but without leading to activated mTOR, as we will see later, this is different from leucine, which can activate mTOR. Oddly enough the glucose uptake does not necessarily lead to increased glycogen synthesis if insulin is not present.

McDowell HE, Eyers PA, Hundal HS. Regulation of System A amino acid transport in L6 rat skeletal muscle cells by insulin, chemical and hyperthermic stress. FEBS Lett. 1998 Dec 11;441(1):15-9.

Nishitani S, Matsumura T, Fujitani S, Sonaka I, Miura Y, Yagasaki K. Leucine promotes glucose uptake in skeletal muscles of rats. Biochem Biophys Res Commun. 2002 Dec 20;299(5):693-6.

Layman DK. Role of leucine in protein metabolism during exercise and recovery. Can J Appl Physiol. 2002 Dec;27(6):646-63.

Doi M, Yamaoka I, Fukunaga T, Nakayama M. Isoleucine, a potent plasma glucose-lowering amino acid, stimulates glucose uptake in C2C12 myotubes. Biochem Biophys Res Commun. 2003 Dec 26;312(4):1111-7.

Stimulation And Enhancement Of mTOR

Further downstream PI3K via PKB can activate mTOR. Insulin works in this manner. But both for leucine and isoleucine, the PI3K mediated pathways were through PKC, and independent of mTOR. But that does not mean that leucine does not exert effects on mTOR. So what is the benefit of this mTOR? Well it has two direct modes of action upon activation.

The first is to activate p70S6 Kinase (S6K) by phosphorylating it. S6K, as its name suggests phosphorylates S6 protein in a ribosomal subunit, which has been shown to lead to increased protein synthesis (1). At the same time it will deactivate 4E-BP1, a binding protein. This frees up the substrate of 4E-BP1, namely eIF-4E. This initiation factor has also been shown to increase protein synthesis.

Leucine has been shown to increase protein synthesis via activation of mTOR and its downstream targets (2,3). It seems to do so quite effectively, and independently of insulin or IGF-1 (the most common activators of mTOR), in skeletal muscle and adipose tissue, as well as the liver, but not in other tissues (4). And it does this quite effectively as well, seeing as how chronic administration shows no downregulation of the mTOR pathways, or increased metabolism of leucine.

It acts both on the eIF-4E pathway (5) and the S6K pathway. In that latter pathway, as with PI3K, it shows a highly synergistic action (6). Leucine alone increased its action 4-fold, and insulin increased it 8-fold, but the combination of insulin with leucine increased it 18-fold. Again showing the benefits for leucine in a high glucose/insulin environment.

But while it shows some effectiveness on its own in this regard, it still requires insulin to be at its best. But do not despair, even in low insulin surroundings leucine appears to be quite effective at increasing protein synthesis, although through a mechanism that is not fully understood (7)

Dufner A, Thomas G. Ribosomal S6 Kinase signalling and the control of translation. Exp Cell Res. 1999 Nov 25; 253(1) : 100-9

Anthony JC, Anthony TG, Kimball SR, Jefferson LS. Signaling pathways involved in translational control of protein synthesis in skeletal muscle by leucine. J Nutr. 2001 Mar;131(3):856S-860S.

Lynch CJ, Patson BJ, Anthony J, Vaval A, Jefferson LS, Vary TC. Leucine is a direct-acting nutrient signal that regulates protein synthesis in adipose tissue. Am J Physiol Endocrinol Metab. 2002 Sep;283(3):E503-13.

Lynch CJ, Hutson SM, Patson BJ, Vaval A, Vary TC. Tissue-specific effects of chronic dietary leucine and norleucine supplementation on protein synthesis in rats. Am J Physiol Endocrinol Metab. 2002 Oct;283(4):E824-35.

Anthony JC, Anthony TG, Kimball SR, Jefferson LS. Signaling pathways involved in translational control of protein synthesis in skeletal muscle by leucine. J Nutr. 2001 Mar;131(3):856S-860S.

Greiwe JS, Kwon G, McDaniel ML, Semenkovich CF. Leucine and insulin activate p70 S6 kinase through different pathways in human skeletal muscle. Am J Physiol Endocrinol Metab. 2001 Sep;281(3):E466-71.

Anthony JC, Reiter AK, Anthony TG, Crozier SJ, Lang CH, MacLean DA, Kimball SR, Jefferson LS. Orally administered leucine enhances protein synthesis in skeletal muscle of diabetic rats in the absence of increases in 4E-BP1 or S6K1 phosphorylation. Diabetes. 2002 Apr;51(4):928-36.

Sensitization To Insulin

We have already seen that leucine and isoleucine exhibit highly synergistic actions with insulin in regards to glucose and amino acid uptake. In regards to glucose uptake, they do far more than this. Several amino acids have been shown to increase glucose uptake by allocating the GLUT4 transporter to cell compartments that are more sensitive to insulin.

Meaning that in a cell with high concentrations of these amino acids, more GLUT4 will be released upon stimulation by insulin, resulting in higher uptake of glucose into the cell. Leucine was shown to be the amino acid most capable of doing this (1). Now many may wonder what the benefit of this is. Because this has no direct effect on amino acid uptake.

Indeed, but it should further effect protein synthesis by multiple pathways. Energy is needed for protein synthesis to take place. So a cell with adequate amino acids will want to increase its glucose levels. First of all increased glucose may lead to increased glycogen stores, and for every gram of glycogen a cell stores, it also stores 2.7 grams of water.

This causes the cell to swell, and cell swelling has been shown to increase protein synthesis. This is the same principle behind the use of sugared up creatine, the combination being sure to drive a great deal of water into the cell. On the other hand, glucose uptake also results in a more positive energy balance, so more ATP. mTOR, discussed in the previous paragraph, is also an ATP sensor (2), so high ATP levels would also trigger higher increases in mTOR activity.

Bogan JS, McKee AE, Lodish HF. Insulin-responsive compartments containing GLUT4 in 3T3-L1 and CHO cells: regulation by amino acid concentrations. Mol Cell Biol. 2001 Jul;21(14):4785-806.

Dennis PB, Jaeschke A, Saitoh M, Fowler B, Kozma SC, Thomas G. Mammalian TOR : a homeostatic ATP Sensor. Science 2001 Sep 1; 15(17): 2203-8

Valine

We have seen many of the effects of leucine and isoleucine on insulin-dependent and independent uptake of glucose and amino acids, as well as their role in enhancing protein synthesis. But wasn't there a third Branched Chain amino acid as well? Of course, its called valine. It may not be immediately relevant to this discussion, as there is no real evidence of valine playing a key role in any of those processes.

But all three of the BCAA's seem to be the rate-limiting step in one process or another and should always be taken together. So what real benefit does valine have? Well one thing that came up was that valine has been shown to reduce fatty acid synthase in adipocytes by 40% (1). That means it exerts a negative effect on adipogenesis and may help to keep you leaner and less hungry.

This is definitely a positive thing since leucine and isoleucine increase glucose uptake by the fat cell as well, which would otherwise lead to increased fat mass. Valine also has potent effects in reducing cholesterol. Again, this could have something to do with balancing out the effects of leucine. That leucine analog, KIC, converts to HMB and HMB in turn converts to HMG-CoA.

This particular nutrient increases cholesterol synthesis in the muscle cell. This is needed for increased stability and integrity of the membrane, which protects it when damaged, allowing for better and faster repair. Particularly useful to the athlete, and probably the reason behind the few minor successes experienced with HMB. Valine is probably a fail-safe mechanism to be able to eliminate this excess cholesterol, by turning it to bile acid (2).

Taylor WM, Halperin ML. Effect of valine on the control of fatty acid synthesis in white adipose tissue of the rat. Can J Biochem. 1975 Oct;53(10):1054-60.

Ohara M, Doi H, Hayasi M, Satomi S. Administration of L-valine lowered plasma cholesterol by accelerating the conversion of cholesterol into bile acid. Clin Nutr. 2003 Aug;22(S1):S57.

Conclusions

BCAA's, and leucine especially, have been established as a supplement with great benefit to the bodybuilder, specifically in regards to increased post-exercise recovery (1) and reduction of post-prandial protein degradation (2) (and much more effective at it that its often over-used metabolite glutamine).

The gist of this has been known for a long time, but still it seems BCAA's are all but forgotten by todays bodybuilder, left on the shelf to rot in favour of supplements that appear in glossy ads that make promises the cannot deliver. Consider this a re-appreciation of the concept of BCAA use with updated material. I Highly advise people to add some additional BCAA's to their post-workout shake. The ideal ratio's are 2:1:2 leu:iso:val.

Anthony JC, Anthony TG, Layman DK. Leucine supplementation enhances skeletal muscle recovery in rats following exercise. J Nutr. 1999 Jun;129(6):1102-6.

Nagasawa T, Kido T, Yoshizawa F, Ito Y, Nishizawa N. Rapid suppression of protein degradation in skeletal muscle after oral feeding of leucine in rats. J Nutr Biochem. 2002 Feb;13(2):121-127.

Alcohol And Bodybuilding

This question remains one of the most posed questions. Frankly I don't see the appeal of alcohol that people want to binge on it so frequently at the cost of coherence, appearance and health. Sure, a few drinks on a special occasion can be tolerated, it is after all part of our social culture to drink at certain events. But to athletes the use of alcohol is not advised, and if you cannot abstain from use, then you would still do wise not to extend your use of alcohol beyond these social events.

Just recently the question was raised whether or not 1AD could be combined with regular drinking binges. I pretty much fell out of my chair that anyone would even dare ask such a question as it portrays extreme stupidity and lack of ambition. The truth is, the answer has nothing to do with the use of any supplement at all, it's simply not a good thing.

Here I want to present you with just a few factors that alcohol will influence. These are just studies I happened to come across, if you wilfully research the subject you'll find a great deal more negative effects of alcohol on your metabolism. But I'm going to give you these, so the next time someone asks if alcohol is detrimental to their gains you can answer with a resounding yes. And this is why.

First, this is highly relevant to todays topic on BCAA's, alcohol appears to inhibit leucine's effect on mTOR (1). Having just explained the relevance of this protein synthesis, the leucine resistance induced by alcohol at this level would have grave consequences on your potential to make gains.

In a second instance I came across a study that showed alcohol diminished system A amino acid transport (2), which would seriously cripple your ability to transport amino acids into the cell. Without amino acids, no protein synthesis can take place.

Apart from this, it has been known for some time that alcohol intake also increases estrogen levels (3). And while I am a firm believer in the ability of estrogen to enhance androgen related gains, an increase in estradiol without an increase in androgens is anything but beneficial. And fact is, testosterone is actually decreased by alcohol (4).

This same study also demonstrated a reduction in IGF-1. This also leads to increased voluntary alcohol consumption (5) and ultimately just worsens the problem. There is further evidence showing it may enhance post drinking catabolism by increased levels of plasma cortisol (6).

This is just a small grasp of effects that alcohol has on your body and gains. There is a lot more evidence for those willing to look, I seem to remember things like 'alcohol increases Fatty acid synthase' and the like.

In short, it doesn't take a genius to realize that alcohol does not mix with bodybuilding and will exert a severely negative effect on your ability to grow, your health, your ability to maintain muscle mass and your level of body-fat percentage. The only uses for alcohol in my opinion, are for transdermal delivery of hormones.

Lang CH, Frost RA, Deshpande N, Kumar V, Vary TC, Jefferson LS, Kimball SR. Alcohol impairs leucine-mediated phosphorylation of 4E-BP1, S6K1, eIF4G, and mTOR in skeletal muscle. Am J Physiol Endocrinol Metab. 2003 Dec;285(6):E1205-15. Epub 2003 Aug 26.

Jones CR, Srinivas SR, Devoe LD, Ganapathy V, Prasad PD. Inhibition of system A amino acid transport activity by ethanol in BeWo choriocarcinoma cells. Am J Obstet Gynecol. 2002 Jul;187(1):209-16.

Emanuele NV, LaPaglia N, Steiner J, Kirsteins L, Emanuele MA. Effect of chronic ethanol exposure on female rat reproductive cyclicity and hormone secretion. Alcohol Clin Exp Res. 2001 Jul;25(7):1025-9.

Rasmussen DD, Sarkar DK, Roberts JL, Gore AC. Chronic daily ethanol and withdrawal: 4. Long-term changes in plasma testosterone regulation, but no effect on GnRH gene expression or plasma LH concentrations. Endocrine. 2003 Nov;22(2):143-50.

Ford MM, Eldridge JC, Samson HH. Determination of an estradiol dose-response relationship in the modulation of ethanol intake. Alcohol Clin Exp Res. 2004 Jan;28(1):20-8.

Linkola J, Fyhrquist F, Ylikahri R. Renin, aldosterone and cortisol during ethanol intoxication and hangover. Acta Physiol Scand. 1979 May;106(1):75-82.

Leptin: The Vindication Commences

As was to be expected when one targets any new hype, it did not take long for hurtful and spiteful comments to pop up about my latest column regarding leptin, and the concerns I wanted to raise. (although the comments did come from the man that has most to benefit from maintaining the hype, so no surprises there). As I aptly pointed out in column number 2, profit is often more important than addressing genuine concerns.

But it has already begun. It will not even take as long as I thought before I'm proven right. Surprisingly enough it did not come from my comments on whether or not we could raise leptin sufficiently or even whether or not increased leptin is beneficial or detrimental, but rather the concern I raised that leptin will eventually drop and that the longer you spend with elevated leptin levels, the worse the outcome for final fat loss, muscle retention and in keeping the fat off.

The reason being that while leptin was maintaining most functions, it was also efficiently eliminating the systems that would govern these functions when leptin is lowered. And oddly enough it was this, the least substantiated of my claims, that was the first to be validated.

One study reported, and I quote :

"Low initial leptin levels and large declines in serum leptin were associated with a large 1-yr weight loss in both genders. Leptin levels (baseline or changes) were not independently associated with the changes in insulin, cortisol, or thyroid hormones. Our results may indicate that leptin by itself could be of minor importance for the neuroendocrine response to severe caloric restriction in humans."

You don't have extremely high leptin levels, so if you could experience a fast drop as well, it would be an indication of a potentially successful diet. By using these products, provided they work, you could be negatively affecting your fat loss efforts by attenuating the drop, staying on higher leptin levels longer than you have too, and if you were taking these products from the very beginning, you may have even increased you initial leptin levels.

It's never fun when you have to report bad news, but at least being right (again) will make the insults people sling at my head for telling the truth and raising genuine concerns that much easier to swallow. And in the process hopefully save some people a lot of money.

Torgerson JS, Carlsson B, Stenlof K, Carlsson LM, Bringman E, Sjostrom L. A low serum leptin level at baseline and a large early decline in leptin predict a large 1-year weight reduction in energy-restricted obese humans. J Clin Endocrinol Metab. 1999 Nov; 84(11): 4197-203.

Do Not Use Taurine While Dieting

It has come to my attention that some people have been adding taurine to their diets to decrease cramping from clenbuterol or other beta-adrenergic agonists. Whether or not there is any merit to this, I really don't know. I haven't seen any data one way or the other. I assume there must be some truth to the rumour or people wouldn't be doing it. Then again...

Regardless however, supplementing extra taurine during a diet is not advisable. It is indeed true that beta-adrenergic agonists like clenbuterol and ephedrine will reduce taurine levels, no question about it. But did anyone ever stop to think that maybe this has a reason? Your protein intake should stay the same, roughly, which means that these compounds are actively reducing taurine levels.

If anyone had bothered to look these things up for a few seconds they would have known it is with good reason. Taurine may inhibit fat loss in different ways. First of all it will increase insulin sensitivity. I didn't even need to state that, it has been used in supplements with varying success for that exact same reason. If we know that many effective fat loss aids work primarily by lowering insulin resistance (Growth hormone, noradrenaline, etc), we already know this is not a bright idea.

This lowers the threshold at which glycogen is stored again. This will increase chance of gaining fat during cheat days due to enhanced sensitivity of fat cells to insulin, and limit fat lost on dieting days since the extra stored glycogen will have to be burned again before you start burning fat again.

This is however the least of your concerns. Taurine is also known to reduce Thyroid levels. Studies have demonstrated that a high platelet level of taurine will reduce T3:T4 ratio in men. This would slow down your metabolic rate, meaning you use less calories than you would otherwise. Obviously this will result in less fat lost for the same amount of calories eaten.

Taurine may also reduce cAMP production in certain animals. The extrapolation in this case is a far fetch, but something I would like to see tested in humans. Since the cAMP acts as a second messenger in the process of lipolysis, the process of releasing fatty acids from their glycerol backbone, making them available for burning, this will reduce the amount of fat released and consequently the amount of fat burned.

This all fits nicely into the picture that free form amino acids should not be frequently used on a diet. As with carbohydrates, quickly absorbed sources create higher peak levels that also decline faster. This almost always leads to a favourable situation for a lower metabolism.

When dieting you will opt for carbohydrate sources that absorb slower, so they have less of an effect on factors influencing food intake. The same holds true for protein. You should opt for protein sources with a more anti-catabolic character, that release slower, such as casein.

Haber CA, Lam TK, Yu Z, Gupta N, Goh T, Bogdanovic E, Giacca A, Fantus IG. N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress. Am J Physiol Endocrinol Metab. 2003 Oct; 285(4): E744-53. Epub 2003 Jun 10.

Baskin SI, Klekotka SJ, Kendrick ZV, Bartuska DG. Correlation of platelet taurine levels with thyroid function. J Endocrinol Invest. 1979 Jul-Sep; 2(3): 245-9.

Hayakawa Y, Downer RG, Bodnaryk RP. Taurine inhibits octopamine-stimulated cAMP production.. Biochim Biophys Acta. 1987 Jun 15; 929(1): 117-20.

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