Discussion in 'HST FAQ' started by Blade, Jan 23, 2003.

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  1. Blade

    Blade Super Moderator Staff Member


    There is so much research showing the benefits of using the stuff it is almost as valuable as protein as far as supplements go.

    It enhances the energy "state" of the cell, it enhances glycogen storage, it enhances protein synthesis, it prevents protein catabolism, it stabilizes the muscle cell membrane (allowing higher faster recovery) and enhances cell volume (hydration state), it increases the number of myonuclei donated by satellite cells when fusing with myofibers - thus increasing the muscle's growth potential (refer to Basics of HST thread).

    Why wouldn't anybody use it? There is now research looking at 5 years of chronic use indicating it is safe.

    It is true that the creatine transporter downregulates itself, but not to the point that no creatine is taken up. If you use 0.03 grams per kilogram (3-5 grams) per day, you will always be loaded and reap the benefits that creatine provides.

    Please keep in mind that creatine was originally marketed to increase your strength dramatically and put 7-10 pounds on you over night (Feels like Deca! Ya, sure it does Bill). This simply isn't going to happen for most people.

    Creatine use will however do alot to optimize your body's ability to adapt to training. That's what a person should use it for. And, it does produce measurable results. Measurable in the lab and in the real world. You just have to be patient, and know what your looking for.

    Creatine is taken up into cells by the creatine transporter. It is a sodium (Na+) dependant transporter. It is estimated that 2Na+ are transported with each Cr molecule.

    The transporter is saturable. Meaning, it can only go so fast no matter how much creatine is present around the cell.

    The creatine transporter is NOT directly effected by glucose, insulin, or caffeine. However, when insulin reaches very high levels, it has been shown to increase the amount of creatine that is taken up into cells. There is no evidence that it increases the total amount that the cell can hold.

    Caffeine does not inhibit the uptake of creatine into cells.

    There is no evidence that "low blood sugar"/hypoglycemia will be effected by creatine supplementation.

    1) Creatine uptake into muscle tissue is limited by the activity of the creatine transporter.
    2) The creatine transporter is "down-regulated" as the level of creatine inside the muscle cell increases.
    3) Creatine only has an effect on muscle cell physiology once it is already inside the cell. Creatine in the blood does nothing for must be inside the cell.
    4) If you load creatine during 5 days (20gm/day), the amount of creatine excreted in the urine goes up DRAMATICALLY by the 3rd day because the muscle cells lose the ability to take in creatine because their transporters are being downregulated.
    5) Creatine uptake appears to be either sodium dependant, or highly regulated by sodium transport. Insulin (from carbs) increases sodium uptake into cells, this is why carbs have been shown to increase creatine uptake.
    6) Exercise increases creatine uptake. If you take some creatine and sit on a staionary bike and only peddle with one leg, the leg you peddle with will take up more creatine than the leg that is not peddling. (hint: take you creatine pre-workout)
    7) Different forms of creatine do not affect creatine uptake. This is because creatine uptake is limited by the creatine itself, not by its form at the time of ingestion. Once the muscle cell is filled up, it won't take any more. Don't let anybody charge you for any special forms of creatine. Monohydrate works as good as any.
    8) Creatine supplementation will result in approximately a 20% increase in phosphocreatine at best.
    9) Some people will have a greater response to creatine if their meat intake was low before. Vegetarians respond beautifully to the stuff.

    Once creatine stores are full in muscle tissue, it doesn't matter whether you take 5 grams or 10 grams, the muscle won't take in any more because it downregulates the creatine transporters until no more creatine can be taken in. Insulin or no insulin, if there are no transporters, no creatine is being taken up into muscle tissue. It is simply being broken down into creatinine and peed out.

    Its hard to say what is optimal. All I can say, is that if you "load" you fill up muscles faster than if you don't. However, in the end, you will still end up with as much creatine in muscle if you don't load, but it will take anywhere from 3-4 weeks to do so. Is faster better? Don't know.

    We also know that if creatine is floating around during exercise, it will be taken up much better than when you take it at rest.

    We also know that insulin, because of its effects on sodium retention, also "facilitates" creatine entry into cells.

    So, putting it all together, whether you load or not, make sure to take creatine before exercise. And, it might further help to take it with something that will icnrease insulin levels, like a preworkout MRP.

    There have been no studies to answer the question about creatine cycling. When considering the effects of creatine, I would guess that cycling would not be particularly beneficial, compared to just taking it all the time. Just my opinion though.

    And, there is yet any research to clearly define the time frame for cycling creatine.

    A person is still justified asking whether creatine really needs to be cycled or not. However, I stumbled across a study the other day that measured intramusclar levels of creatine afte loading. They found that levels were slightly higher for the first weeks or so after loading, but then slowly began to decline. So, if there is a particular event where you want as much creatine as possible in the muscle, you may want to go off for 30 days, and then load the week leading up to the event.

    For bodybuilding...we just don't know if there is any real benefit to either rapid loading or cycling it.

    I always take my creatine before training and have never had any cramping or even an upset stomach from it.

    The strength increases seen with creatine supplementation are more a result of fatigue resistance, rather than an increase in neural drive.

    The energy requirements of short duration, high intensity exercise are met primarily through the recycling of ATP and phosphocreatine (PC). Despite the relative importance of this system to performance, relatively little definitive research has been done to elucidate whether this system undergoes significant adaptation. The research which exists suggests that phosphagen and related enzyme adaptations are effected specifically by the type, duration and structure of resistance training.

    Your muscles/body lose creatine everyday at a rate of about 0.03 grams/kg bodyweight/day. So the creatine that is stored in your muscles doesn't just stay there, it is slowly lost at pretty much a constant rate.

    Creatine monohydrate supplementation has been shown to increase creatine-phosphate by about 20%. This is significant and effect the creatine phosphate energy shuttle (which is repsonsible supplying ATP for protein synthesis).

    So, creatine probably wont directly increase your one rep max, but it can increase the number of reps you can get with your 10 rep max. Make sense? Add the creatine to your preworkout protein drink.

    "Twitching" is often caused by Ca++ dysregulation in the muscle cell. The sarcoplasmic reticulum is struggling to sequester all the calcium ions floating around. As this occurs, the calcium ions will cause the fibers to twitch. This can sometimes show up after a change in caffeine intake, along with heavy training. Caffeine is a Ca++ channel agonist.

    This will not hurt your gains, in fact, I have suspected in the past that this will actually lead to muscle hypertrophy through the activation of calcineurin.

    Anyway, you may try using creatine. It helps the muscle fibers relax by making ATP more readily available (when ATP is not available the fibers go into rigor). IF the twitching is driving you crazy, try creatine. If your not quite crazy yet, you can skip the creatine and know that at least the twitching might help those fibers grow. Using the creatine will not "prevent" hypertrophy of course because the real stimulus for hypertrophy occured during your last workout.

    Tachyphylaxis does not really apply to creatine supplementaiton in a classical sense. Creatine doesn't really "push" any physiological system, like say, ephedrine or caffeine. Creatine and the response to oral intake is reduced by decreasing the number and activity of creatine transporters. But this isn't really how the term tachyphylaxis is generally used.

    I don't mean to sound preachy, but...I was told by several people in the industry that unless I did something to my creatine to make it fancy, I would never be able to sell it. They said it needed bells a whistles. I told them, "Why would I make a product that I wouldn't buy myself?" And they would say, "That's different, you know a lot more about this stuff than they do." Well, I didn't do anything fancy to my creatine. I only made sure it was the purest that could be bought and provided the research to support its use, as well as the research to show how best to use it for gains. I didn't fabricate any of the research either. It was done by institutions that have nothing to gain from creatine sales.

    I can tell you that creatine from certain German companies is of high quality. However, the Chinese have actually cleaned up their act and have now began to produce hhigh quality creatine as well. This comes after pressure from large supplement companies for thier creatine to meet other companies standards of purity.

    There is also a US company that sells equally high quality creatine as the Germans. Remember, there is no secret to producing pure creatine. If one company decides to ensure that their raw creatine is pure, it will be just as good as any other company that is producing pure creatine. So, pure is pure, regardles of where it comes from.

    Keep in mind that high quality (pure) creatine costs more than cheap impure creatine. So there is alwyas a temptation for companies who don't really know or care "who they are as a company" to just go for the cheap stuff without regard for quality.
  2. Blade

    Blade Super Moderator Staff Member

    What Bryan uses

    I use (in order of priority):

    1) Protein powders
    2) Creatine
    3) EFAs (fish oil)
    4) 1/2 multi vit/mineral per day

    When I can afford it, I'll use:

    HMB (well suited for HST, but less useful with traditional training methods)

    Ipriflavone or methoxy-7 (for the effects on calcium and tendons, not muscle) I don’t take it (when I take it) for its purported effects on muscle, but because it has been demonstrated to reduce collagen protein breakdown. Ipriflavone also increases calcium uptake from the gut. Those are the only two reasons I use it. As for toxicity, it has been shown to affect the immune system to a non-significant degree. For those concerned about this effect they should not take it.

    EFA before CLA Just because CLA is more expensive

    Also, CLA can't exactly "replace" EPA as far as nutritional needs go. But it does do the same job on fat cells (through PPARs)
  3. Blade

    Blade Super Moderator Staff Member


    Here are the reasons to take glutamine.

    1) Immune support. Supplemental use of glutamine, either in oral, enteral, or parenteral form, increases intestinal villous height, stimulates gut mucosal cellular proliferation, and maintains mucosal integrity. It also prevents intestinal hyperpermeability and bacterial translocation, which may be involved in sepsis and the development of multiple organ failure. One study reported that athletes reported fewer incedences of upper respiratory tract infections while supplementing with glutamine (2 grams) after they ran.

    2) Gastrointestinal support. 70-80% of orally administered glutamine is absorbed into the cells of your GI tract. It remains there and is metabolised by those cells without ever reaching the blood stream (image). In sicknesses such as sepsis it has been shown to help improve survival because of improved GI tract function.


    Thats pretty much it.

    There is no real benefit for someone looking to build bigger muscles. That 10% of dietary glutamine that gets past the GI tract is taken up by the liver where it is converted into sugar (gluconeogenesis) and stored as glycogen in the liver.

    Don't let in-vitro research fool you into thinking oral glutamine will have an effect on a healthy individuals muscle mass. Yes, glutamine does regulate protein synthesis to a certain extent under some situations. However, you can't make it happen by taking it orally. Don't let ads with some pro-bodybuilder holding a bottle of glutamine fool you. Even if that pro-bodybuilder is taking isn't doing anything for him either.

    Here are a couple good "in-vivo" research studies to start with:

    1. Candow DG, Chilibeck PD, Burke DG, Davison KS, Smith-Palmer T. Effect of glutamine supplementation combined with resistance training in young adults. Eur J Appl Physiol. 2001 Dec;86(2):142-9.

    2. Antonio J, Sanders MS, Kalman D, Woodgate D, Street C. The effects of high-dose glutamine ingestion on weightlifting performance. J Strength Cond Res. 2002 Feb;16(1):157-60.

    Keep in mind that if you are eating protein powders, especially any thing with whey in it, you are getting plenty of glutamine. The question of glutamines worth in the newsletter centered on its effect on building mass and/or strength, not anything to do with the gastrointestinal track.

    In short, only 47-50% of orally administered glutamine can be expected to make it past the liver and other organs, into the blood stream. And only about 10% can be expected to reach extracellular spaces.[Bowtell JL, Gelly K, Jackman ML, Patel A, Simeoni M, Rennie MJ. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. Journal of Applied Physiology. 1999 Jun;86(6):1770-7] Now, this is the main argument against glutamine. 90% of the glutamine you take orally never even makes it to your muscles. This isn't to say it is wasted. Your GI tract loves glutamine from reasons explained earlier. If you are having intestinal problems nothing is better. If you are trying to increase protein synthesis by loading glutamine, it isn't going to work.
  4. Blade

    Blade Super Moderator Staff Member

    Ephedrine and Caffeine

    Ephedrine is a sympathomimetic, which means it acts to increase sympathetic activity. As a sympathomimetic, ephedrine acts to stimulate the sympathetic nervous system. It does this by causing pre-synaptic nerve terminals to release norepinephrine, or what is commonly called noradrenaline (NA), into the synaptic space. It also has the effect of increasing circulating adrenaline (Adr), the body’s chief beta-2 agonist. Noradrenaline, once released into the synaptic space, interacts with adrenergic receptors on the surface of adipocytes (plain old fat cells). This initiates a sequence of events within the adipocyte that increases lipolysis.

    The process of lipolysis is under feedback control which attenuates lipolysis at several levels. A couple of the chemicals involved in attenuating the effectiveness of ephedrine are phosphodiesterases and adenosine. As you might expect, these are the chemicals that we will try to minimize with caffeine while using ephedrine as a fat loss agent.

    Caffeine is a methylxanthine. Caffeine possesses the ability to inhibit phosphodiesterases within the cell and has even been shown to have the ability to prevent some re-uptake of norepinephrine. Another property of caffeine is adenosine receptor blockade. There is some question as to weather oral caffeine ingestion actually significantly inhibits phosphodiesterases but it does seem to inhibit adenosine action in vivo. Both of these properties make it potentially useful as an adjunct to ephedrine to enhance fat loss.

    Caffein does temporarily decrease insulin sensitivity. So does anything else that is "lipolytic". I have read the study(s).

    Exercise was shown to negate (reverse) the effect of the caffeine. This is because of what is called non-insulin dependant glucose uptake.

    Anything that stimulates the release of noradrenaline or adrenaline will decrease insulin sensitivity. Even an increase in blood levels of released fatty acids will decrease insulin sensitivity. Its called the glucose fatty acid cycle, or the Randle Cycle. This is because the fat cell's "machinery" is not designed to store and release fuel at the same time. This would be counter productive. The only exception is exercise, where the body wants to release fuel from fat cells at the moment, but increase its ability to take in fuel to replace what it lost from muscle as fast as possible afterwards (or "during" exercise in the case of muscle tissue).

    No need to panic about caffeine and insulin sensitivity. Its effects on insulin sensitivity have been known for a long time.

    Keep carbs relatively low while using ephedrine. Insulin counter acts the effects of ephedrine and will ultimately hinder fat loss if carbs remain too high. This does not mean you must go on a ketogenic diet. If total calories are low enough carbs become less of an issue. But if you are trying to keep muscle by lowering calories only slightly, the carbs will sabotage ephedrine’s action.

    Ephedrine and Clenbuterol have two different, yet similar mechanisms of action. Nevertheless, don’t use Clenbuterol and ephedrine at the same time, or even in an alternating fashion. Both drugs work through the beta-adrenergic receptor, however, Clenbuterol will shut down beta-receptors within a few weeks. Taking ephedrine at that time will do little for you. Better to use ephedrine from the start of your diet, only switching to Clenbuterol no further than 3 weeks out from the contest.

    In order to get the most benefit from ephedrine on muscle loss, adjust your dosing schedule to every 2 hours. This will enhance the duration and consistency of beta-adrenergic activity. Be sure to adjust the amount you take each time in order to maintain the total amount taken over the course of a day. For example, instead of taking 20 mg ephedrine and 200 mg caffeine 3 times daily, take 10 mg ephedrine and 100 mg caffeine 6 times daily.

    E/C was never intended to be cycled. Clen was never intended to be used chronically, but instead only as needed.

    People often confuse E/C with Clen because they both involve the beta-2 receptors. Clen is a potent specific agonist to the receptor and causes rapid downregulation of the receptor. E/C is NOT a specific agonist, but instead works in a round about way to increase circulating norepinephrine and epinephrine. The caffeine is also an adenosine inhibitor.

    It has been demonstrated that E/C actually get more effective over time. This has been attributed to an increase in thyroid receptors.

    E/C is notorius for rebound "hunger" though, so taper off over a long period of time, starting first with the caffeine, then the ephedrine.

    For mild appetite control, ephedrine can be used alone with good results.

    The Primer will ensure that you get the desired effect from the caffeine/ephedrine. The effects are tied to pathway tyrosine>norep/ep>dopamine.

    With or without carbs you will still get the emotional and stimulatory effect of E/C. You just don't get the lipolytic effect as long as the insulin is high from carbs. The effect of insulin on E/C induced lipolysis is significant, but it does not mean that it completely negates the effects of E/C.

    If you use E/C too long without food it won't provide that positive sense of "lift". It will only make you feel anxious. Supplementing with additional tyrosine seems to help as well.

    The caffeine can also really cause havoc on your stomach. It gives lots of people significant pain (sometimes nausea) after a while of taking it on an empty stomach.

    Unfortunately synephrine can't replace ephedrine. They work by different mechanisms and have a different adrenergic agonist profile.

    The benefits of E/C while bulking is a nutrient partitioning effect. Your metabolic rate stays greatly elevated and your strength is augmented by the caffeine. You should take E/C every two hours at half dose regardless of what diet you are using.

    Precaution should always be used with E/C though. They are both drugs and can have serious side effects in some individuals.
  5. Blade

    Blade Super Moderator Staff Member

    CLA and EFAs

    Try to get 2-6 grams per day of EPA+DHA. The FDA has only approved 2 grams per day because of the ability of omega-3s to thin the blood (reduce clotting). However, if you are not at risk of bleeding abnormalities, anywhere up to 6 grams per day is beneficial. The burping WILL stop if you take them consistantly. Takes about a week for the burps to stop.

    Keep in mind that omega-3s will be preferentially oxidized (burned for fuel), so a lot of what you supplement on a low carb diet will be burned as energy before it can be stored in fat cells where it does its magic. Whenever possible, take your fish oils after a meal or after carbs. The carb load to the liver will decrease the oxidation of the fatty acids and allow more to pass through into the blood for storage. This is good when it comes to omega-3s and CLA.

    CLA can't exactly "replace" EPA as far as nutritional needs go. But it does do the same job on fat cells (through PPARs)

    It's going to take about 6-10 grams per day of CLA to notice any effect. If you use CLA while bulking it may help nutrient partitioning. CLA and Omega-3s should be taken "all" the time. They aren't supplements that you take every now and then. It has to be constant so that they can have time to change the environment within the body. This only happens as CLA are incorporated into fat cells. Unfortunately, the CLA is preferentially oxidized as it enters the liver, so you have to take enough to not only let the liver burn some, but also have enough to get into circulation and be deposited into fat cells.

    As with EFAs I suggest you take CLA with carbs (or after a meal). The rise in insulin may prevent the immediate oxidation of the CLA, and enhance the delivery of it to subcutaneous fat cells.

    The delivery of "fat" to fat cells may not seem like a good idea at first, but CLA and Omega-3s activate PPARs once in fat cells. This is good, and is what leads to the change in body composition over time.

    Regular use of CLA will change your "tendency" to gain and lose fat. It will basically make your fat cells act as if you had a genetic predisposition to leanness. The mechanism is pretty interesting.

    Here is a bit of info on CLA.

    CLA is a naturally occurring fatty acid found primarily in beef and dairy fats. The reason that it is found primarily in beef and dairy products is because CLA is formed from linoleic acid by bacteria in the gut of cows (or herbavors). The cows then absorb the CLA and it becomes incorporated into lipids in the cows, including milk lipids.

    How does it work?

    CLA increases fat oxidation.
    (West, D. B., J. P. DeLany, P. M. Camet, F. Blohm, A. A. Truett, and J. A. Scimeca. Effects of conjugated linoleic acid on body fat and energy metabolism in the mouse. Am. J. Physiol. 275 (Regulatory Integrative Comp. Physiol. 44): R667-R672, 1998)

    CLA has been shown to increase certain enzymes responsible for fatty acid beta-oxidation. This means that the body’s ability to burn fat goes up significantly with CLA supplementation.

    Inhibition of triglyceride uptake into fat cells.
    (Park, Y., K. J. Albright, W. Liu, J. M. Storkson, M. E. Cook, and M. W. Pariza. Effect of conjugated linoleic acid on body composition in mice. Lipids 32: 853-858, 1997)

    The best way to get fat is to send the fat you eat straight to the fat cell to be stored. This is generally what happens when we eat fat, however CLA supplementation has been shown to decrease the enzyme necessary for fat cells to take up fat and triglycerides from the blood. This fat is then more apt to be taken up by muscle tissue where it can be burned for fuel. In fact, CLA also increases the muscles ability to burn fat as fuel as mentioned previously.

    CLA increases insulin sensitivity
    (Houseknecht, K. L., J. P. Vanden Heuvel, S. Y. Moya-Camarena, C. P. Portocarrero, L. W. Peck, K. P. Nickel, and M. A. Belury. Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat. Biochem. Biophys. Res. Commun. 244: 678-682, 1998)

    The reason CLA has been labeled a “partitioning agent” is because of its ability to shift the flow of nutrients away from fat tissue and towards muscle tissue. So you are starving the fat and feeding your muscle, the end result being an increase or maintenance of muscle and a reduction in fat.

    CLA acts to reduce body fat stores by chronically increasing metabolic rate.
    (West DB, Blohm FY, Truett AA, DeLany JP. Conjugated linoleic acid persistently increases total energy expenditure in AKR/J mice without increasing uncoupling protein gene expression. J Nutr. 2000 Oct;130(10):2471-7.)

    Treatment with CLA chronically increases basal metabolic rate. Over time this elevation leads to significant reductions in fat mass. The exact mechanism by which CLA raises energy expenditure has yet to be elucidated but could act through PPARs.
  6. Blade

    Blade Super Moderator Staff Member


    An understanding of HMB is critical if you are to get any benefit from it.

    How does HMB affect muscle mass and strength? It isn’t through anabolism, and it appears not to be directly through anticatabolic mechanisms either. If you recall the pathway for leucine metabolism, you’ll notice that the fate of ingested HMB is mainly as HMG-CoA, a substrate for cholesterol synthesis. It appears that cholesterol synthesis may be a rate-limiting step in membrane repair after intense training. Keep in mind that muscle cells do not use circulating cholesterol for membrane repair. They must manufacture cholesterol from scratch (i.e. through the HMG-CoA pathway).

    HMB won’t help if you are not training in such a way as to cause microtrauma to the cell membrane. HST however does cause frequent microtrauma and I personally have felt subjective benefits from HMB supplementation. Mostly, a sense of faster recovery and less noticeable “stiffness” in the morning after.

    Take it in divided doses evenly spaced. Take at least one dose right before and another right after training. This is to take advantage of blood flow to the muscle.

    I DO recommend HMB. It won't do much for guys who have been using the same weight for months without any gains, but for HST it is perfectly suited. It will help keep you lean too.

    If you do decide to use it, use it during the entire cycle. 3-4 grams per day is a suitable dosage depending on your weight. If you are over 200 pounds I would recommend 4 grams. HMB's effectiveness does not increase with escalating doses above ~4 grams. Try to split it up throughout the day as much as possible. Make sure to take some right before training when blood flow to muscle is highest.

    HMB does not interact with any other supplements so it can be taken whith any or all other supplements.

    It won't do anything during Strategic Deconditioning so don't take it then.

    HMB appears to be converted mostly to beta-hydroxy-beta-methylglutaryl CoA (HMG-CoA). HMG-CoA is then used to make cholesterol within cells. This is important for muscle cells in that they cannot use cholesterol from the blood.

    Here is where much of the misunderstanding about HMB comes in. HMB has NOT been shown to directly inhibit protein breakdown, and certainly does not cause protein synthesis. A study done in 1997 looked at the effects of giving lambs high doses of HMB (Br J Nutr. 1997 Jun;77(6):885-96). To their surprise, HMB did not have any effect on protein catabolism or anabolism. In essence, HMB didn’t do squat under normal conditions.

    So, if you are expecting HMB to "build" muscle you are going to be disappointed. If the "noticeable effect" you are looking for is anabolism, you are going to be disappointed.

    However you’ll notice that the fate of ingested HMB is mainly to be converted to HMG-CoA, a substrate for cholesterol synthesis. It appears that cholesterol synthesis may be a rate-limiting step in membrane repair after intense training.

    HMB significantly decreased the exercise-induced rise in muscle breakdown as measured by urine 3-methylhistidine and CK during the first 2 wk of exercise. In the studies showing an effect of HMB on muscle breakdown, the differences between the HMB group and the placebo group tend to decline over a period of about 3-4 weeks until at about 4-5 weeks there is no difference in the above markers of damage, including 3-MH. This reflects the fact that, if the cholesterol mechanism is true, HMB serves to facilitate rates of growth only when membrane integrity is a limiting factor. This generally occurs during the first two to three weeks of a new or unaccustomed exercise program. After that, muscles become resistant to further damage (repeated bout effect, or rapid training effect) induced by that particular program (loading regimen) and HMB supplementation loses its usefulness.

    HST is characterized by a constant increase in load following a period of Strategic Deconditioning. Therefore, when followed with the appropriate frequency, you stay just ahead of the structural recovery curve. This keeps you constantly in a state of muscle damage. This appears to be the only time when HMB is useful.

    In traditional routines you use the same weight until you can add more because your strength has increased. I’ve seen guys use the same weight on their lifts workout after workout for months or even years at a time. Their muscle tissue is tuff as shoe leather and there virtually NO structural damage to the tissue after any workout. They simply walk out of the gym with their butt kicked but with no new muscle to show for it…for months at a time! HMB facilitates “recovery” from frequent heavy bouts of training typical of HST. I have experienced increased exercise tolerance when using it. No I didn’t measure anything, I just felt better and stronger with fewer aches and pains.

    I haven’t even began to talk about the benefits of the calcium in HMB with respect to fat cell metabolism: (J Am Coll Nutr. 2002 Apr;21(2):146S-151S.; FASEB J. 2000 Jun;14(9):1132-8.; FASEB J. 2001 Feb;15(2):291-3.; J Am Coll Nutr. 2001 Oct;20(5 Suppl):428S-435S; discussion 440S-442S.)
  7. Blade

    Blade Super Moderator Staff Member


    Antioxidants significantly reduced erk1/2 and had no effect on p38...I personally have stopped the high-dose antioxidants. It’s true that antioxidants have been shown to decrease the signal for hypertrophy. Will taking an antioxidant after training have a "significant" detrimental effect? I don't know. I'm the type that avoids anything that has been shown to reduce hypertrophy so I only take antioxidants during SD or on the second day of rest (weekend).

    Ginseng: If you are buying a product because you want it to increase the amount of muscle and/or strength that you have. Ginseng won't give it to you.

    If you are buying ginseng for a spiritual or "back to nature", or "I'm experimenting with Chinese traditions" reason, then once again, do whatever you want. But if you are buying ginseng to get big, save your money.

    Green tea has compounds that block COMT. I stopped using as much green tea when I found that they were anti-androgenic. They not only block androgen at the receptor, thay also apear to downregulate androgen receptors.
    Green tea is basically an anti-endocrine factor. It seems to reduce the effects of all steroid hormones. I don't mean to freak anybody out, it's just that the flavones (especially epigallocatechin gallate) are well known to reduce the actions of endogenous androgens (and estrogens) as well as even lowering testosterone levels themselves.

    Anyway, my point is that, you may never see any significant effect of drinking green tea on muscle gains. Then again, we know that it is having an antagonistic effect, however small, in a direction oposite to what we want with respect to testosterone.

    Cultures that consume a lot of green tea of also known to have fewer androgenic "manifestations" both normal (body hair, muscle mass, etc) as well as fewer pathologic manifestations (prostate problems, and other cancers associated with steroid hormones).

    Fat is a different story. It clearly helps fat loss by altering catecholamine metabolism and probably a few other things.

    If Udo's Choice is your only source of fat in the diet, it’s great. I tend to get some fat of various kinds in the food I eat so the "ideal ratio" of fats in Udo's is no longer ideal when combined with the other fats in my diet. Instead I just want to add some that I may be low in. CLA I take only for its effects on PPARs.

    Myostatin inhibitors: Myoblast is a product by Cytodyne. It contains a sulfated sugar extracted from seaweed. This heparin-like extract will bind to the myostatin protein in-vitro (colum). Similar products are being sold by Biotest and Champion Nutrition.

    Because this extract was shown to bind to the myostatin protein in-vitro (not published, nor peer reviewed research), it is being sold as a myostatin blocker called CSP3 or Myozap.
    What does it do? Nobody knows yet.

    Are there any side effects? Nobody really knows yet. It will probably thin the blood if taken in high enough doses.

    I used it for 8 weeks...nothing happened accept a bit of stomach upset. Well, actually something interesting did happen. I have a heart murmur (irregular heart beat) and strangely enough, after 8 weeks of the sea weed it went away. Go figure. I did notice a slight effect on my heart rate when I first began taking it (stimulant effect), but that was it. There is evidence of some compounds that have a favorable effect on irregular heart beat, maybe this is a new one.

    It didn't make me grow though. Believe me, I understand all the research (had access to unpublished research), so i didn't take it blindly.

    The active compound is a sugar molecule with a sulfur group on it, so it is no surprise if none of it even made it past my gut.

    Yes, I was using the same material that Biotest has.
    If it ever is going to work, the active fraction must be isolated and administered in a way that bypasses the gut. Until then, odds are not very good that you will experience any added muscle growth from using it. However, I am hopeful that supplements based on this mechanism will evolve from these first generation compounds. In all likelyhood, you will see other compounds emerge with greater binding affinity and with better absorption properties.

    Psyllium Husk is a waste of money - all the research on fat absorbers demonstrate that they don't work.
    Forskolin: For people who may be unfamiliar with Forskolin, here is a brief review.

    Forskolin is an extract of the roots of the Ayurvedic herb Coleus forskohlii. Forskolin has been shown in-vitro to increase the level of cAMP in cells. Forskolin-induced elevation of cAMP levels in cells leads to blood vessel dilation, inhibition of mast cells (and hence reduction in allergic inflammation), increase in thyroid hormone secretion, and stimulation of fat release from fat cells. Forskolin has other properties as well, including inhibition of the pro-inflammatory substance known as platelet-activating factor (PAF) and inhibition of the spread of cancer cells. Research into coleus’s other constituents has been sparse. Keep in mind that Sabinsa is making all of the claims concerning Forskolin's effects on body composition. They have a major interest in bodybuilders using it instead of ephedrine. Not that I mind companies educating customers about a product, but they should use peer-reviewed research that is available to the public to do so.

    Forskohlii raises intracellular cAMP plays which plays major role in causing fat breakdown and release from fat stores. Companies are adding Forskohlii to weight loss products in order to appease people who don’t want to use ephedrine. What people don’t realize is that Forskohlii acts "post receptor" and therefore is less specific than ephedrine. In other words, Forskohlii does not rely on beta-adrenergic receptors to increase cAMP levels. Forskolin acts on ALL cells with adenylate cyclase, not just those sensitive to noradrenalin. For example, forskolin is traditionally used in Ayurvedic medicine to lower blood pressure. Ephedrine on the other hand raises blood pressure. Obviously the effects are not the same, even though each drug eventually leads to increased cAMP levels in various tissues. Therefore, you can’t rely on Forskohlii only affecting cells sensitive to adrenergic stimuli.

    I haven't heard from anyone who has experienced much from forskolin. The old ephedrine/caffeine combination thus far has no equal, even clen falls short.

    Octacosanol is a sugar alcohol made from sugar cane wax, and has nothing to do with IGF-1. It's also present in wheat germ oil. It interferes with cholesterol synthesis which might be good if you have a problem with cholesterol, but it will do nothing for muscle growth. In fact, it might actually hamper it slightly if it interferes with the muscle's ability to produce cholesterol for cellular repair.

    There is no medical research to back up their claims. Using wheat germ oil as a "tonic" is as old as the hills but it has no effect whatsoever on muscle growth.

    Furhtermore, a thorough analysis of studies has not supported the claim that wheat germ oil is an effective performance aid. This evidence was used successfully by the Federal Trade Commission to ban advertising claims that wheat germ could improve endurance, strength, and vigor. So this company simply changed the name they were calling it and said it will grow muscles.

    They should be ashamed for making false claims and deceptive advertising.

    Saw Palmetto binds and blocks the activity of the androgen receptor as well. This binding is not terribly strong, but it does happen. So saw palmetto is an anti-androgen both because it appears to reduce the activity of 5-alpha reductase but also because it binds the androgen receptor intself.

    Theanine is the only thing I have come across that seems to temper the effects of caffeine.

    Ipriflavone may really help if you need actual tendon effects. Ipriflavone decreases catabolism of collagen proteins which, over time should help to strengthen tendons/ligaments.

    It is important to remember that your problem may not be the strength of your tendons or ligaments, but the length of them. Sometimes injuries can altern the length of ligaments and tendons, causing laxicity (looseness) in the joint. Sometimes this is called subluxation. You can't fix this without surgery to shorten the ligaments.

    Scar tissue can also cause pain where a tendon slides against the surface of a joint or bone.

    Glucosamine and chondroitin deal primarily with cartilage.
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