Why the "A" in ECA is bad-By str8flexed

[prolangtum]

str8flexed:

I see that alot of you are currently taking ECA stacks before your workouts. May I suggest that you ditch anything containing aspirin (when taken pre workout) let me explain.

When you workout your body sends signals (i.e. releases hormones) which "tell" your cells that damage has occurred. Many of these hormones work by attatching to a receptor and then starting a signal cascade which activates "local messengers" and "secondary" hormones (i.e. prostoglandins and cAMP).
One group of local messengers are called prostoglandins. Prostoglandins are inflamitory hormones which signal the cell that the tissue has been damaged and to begin synthesizing protein. In the case of muscle tissue... lifting causes and inflammatory response to the tissue damage done by lifting. This causes prostoglandins to be synthesized and these prostoglandins continue the messege cascade, "relaying" the message to the nucleus to start DNA transcription, and thus protein synthesis. This is a good thing... it is one of the things that makes us grow.

Now a little about how prostoglandins are synthesized. They are synthesized from an essential fatty acid called Arachnidonic acid. It is called essential because your body cannot produce it from scratch. Most of the arachnidonic acid is made by converting your dietary intake of Linoleic acid to Arachnidonic acid. Most of this arachnidonic acid is stored your cells phospholipid bilayer. When you workout induced hormone (I don't know the specific hormone) attatches to the cell surface receptor, it causes phospholipase 2 to become active. This enzyme then liberates Arachnidonic acid from the phospholipid bilayer. Cyclooxygenase enzymes (COX1 and COX2) then catalyze the conversion of Arachnidonic acid to the eicosinoids PGG2 (via COX1) and this is then converted to PGH2 via COX2.

Aspirin is a covalent inhibitor of these enzymes. This means it actually attatches to the active site via an actual bond. Once it is attatched the enzyme is said to be "inhibited" and can no longer catalyze the reaction. Thus, prostoglandins cannot be synthesized, and the messege will not be sent to the Nucleus to begin protein synthesis. This has been confirmed in several experiments that show COX inhibitor administration (this includes aspirin, acetominophin, and ibuprofin) knock the exercise induced 76% rise in protein synthesis back down to baseline levels.

Thus my suggestion is to not take ECA within 5 hours of your workout. If you feel you must take a stimulant pre-workout, make sure it does not contain aspirin or any derivitave (white willow bark, et. al)

So lets recap...
Hormone signal -> phospholipase 2 active-> release of AA from membrane-> COX conversion of AA to prostoglandins(this is where aspirin stops the pathway) ->signal for protein synthesis-> protein synthesis

Peace

[Jarconis]

good stuff, guess I'll just pop a NYC instead

[trip]

Good post Pro'.

The more I learn, the more I question the reasoning behind lot's of these supps.

[jweave23]

Nice overview!

[monroe]

Very good. I'll just go with some Eph HCL if I really need a boost...Hey pro, how you deal with your 1-test lethargy?

[prolangtum]

4-ad and lots of e-hcl and y-hcl

[monroe]

Originally posted by prolangtum
4-ad and lots of e-hcl and y-hcl

yeah, i just ordered some e-hcl, have to look into y-hcl too. i saw you're somewhere down at 6/7% bf, so its working out good for you

[prolangtum]

Ive always been fairly low bf, but i did slash about 2%

[Zentinel]

Hmmm... Xenadrine uses salicin ("a precursor to asperin"). Is it just as bad?

Zen

[prolangtum]

If it is a COX 2 inhibitor yes, lemme check

[prolangtum]

Originally posted by FitnessBrat
Anyone disagree with this? Just curious.

It has been shown time after time that COX-2 inhibitors are bad for muscle growth, what is there to argue? OF course Im open if you have a valid one.

[Cory]

I just use creatine, get lots of rest, eat clean, and bust my ass in the gym....I typically stay as far away from central nervous system stimulants as possible. Ephedra puts alot of stress on the body and causes elevated levels of cortisol which in turn inhibits hypertrohy and makes the body store fat mainly in the abdomen region.

[prolangtum]

Originally posted by Cory
I just use creatine, get lots of rest, eat clean, and bust my ass in the gym....I typically stay as far away from central nervous system stimulants as possible. Ephedra puts alot of stress on the body and causes elevated levels of cortisol which in turn inhibits hypertrohy and makes the body store fat mainly in the abdomen region.

any proof to back this up?

[Cory]

Originally posted by prolangtum
any proof to back this up?

Yes there are some studies to prove this....I will have to find them and type them in a post, but you do know that cortisol is a hormone that is released when the body encounters any kind of stress, right? You do know that ephedra is a central nervous system stimulant, which means it puts stress on the bodies organs because it upregulates them, right? And you realize that elevated levels of cortisol inhibit muscle growth and make you store fat to a certain degree, right? I will find the studies and type them in a post. The proof is documented.

[lovetoeat]

Originally posted by Cory
Ephedra puts alot of stress on the body and causes elevated levels of cortisol which in turn inhibits hypertrohy and makes the body store fat mainly in the abdomen region.

You do realize exercise raises cortisol levels?

[lovetoeat]

BTW, ephedrine/ephedra's positive effects on fat loss far out weigh the negatives, there are many, many studies that show this.

[Cory]

Originally posted by lovetoeat
You do realize exercise raises cortisol levels?

Yes I do realize this, but the studies show that cortisol's negative effects on the body due to exercise, are not that much of a concern unless you are over 35. There was an article in the last issue of iron man explaining this and what can be done to help the situation if you are an older body builder.

[Cory]

Originally posted by lovetoeat
BTW, ephedrine/ephedra's positive effects on fat loss far out weigh the negatives, there are many, many studies that show this.

you are right, if the dosage is followed correctly and you give your body a rest from it periodically, then they definately will burn fat very well. The problem is prolonged use and people taking more than the recommended dosage to keep that "up" feeling. It's a stimulant, so eventually the body will develop a tolerance and you won't feel them like you did when you first started using them. That's why people fall into that trap of "needing" them just to get enough energy to train. They fry their adrenals and feel like total shit when they don't have them. I have worked with so many ephedra junkies that want to go to a non-stimulant because they always feel like shit without it and I have to gradually ramp down their dosages and make them drink coffee and then I can slowly start introducing other things like CLA for instance and when they come back to me a few months later they feel so much better, because they are relying on their own natural raw energy...sorry, but central nervous system stimulants suck and are not healthy for the body.
eating properly, getting enough rest, and training hard will give you more than adaquate energy to do whatever you want.

[prolangtum]

CLA is a waste of money IMO.

[Cory]

you should visit the site of the only company that holds the patents on the "real" CLA that actually does work...www.clarinol.com

There have been many clinical studies to prove that the clarinol form of CLA burns fat and builds lean muscle tissue and also enhances cardiovascular health, supports healthy cholesterol levels, promotes healthy immune function and has been used for cancer treatment, and is a great antioxidant. Even if I didn't have to lose any body fat, there is no way I would not be taking it.

[prolangtum]

Ive taken Tonalin CLA, in order to use that name, any company must buy from them. Im aware of the studies, but I can also throw out a few studies disputing it too, as there is always a study disputing something, no matter what the supplement is.

[prolangtum]

This was posted by Rober Thoburn a while back on avant:

Will CLA only help the already-very-fat?

Linda Granlund is a PhD student at the University of Oslo. She participated in the recent conjugated linoleic acid (CLA) study published in the Journal of Lipid Research (Granlund et al. (2003) Trans10, cis12 conjugated linoleic acid prevents triacylglycerol accumulation in adipocytes by acting as a PPARgamma modulator. J Lipid Res, May 16. Ahead of publication.)

Here, she nicely summarizes some isomer-specific issues as she responds to my questions (Grandlund, 2003 personal communication):

"...We did not find that alpha- linolenic acid was an antagonist to PPARgamma, but that the trans10,cis12 CLA isomer was, and that this effect could help explaining the reduced fat accumulation seen after feeding this CLA isomer
to animals.

In our paper we found that the prevention of fat accumulation could be achieved by 25uM trans10,cis12 CLA in mouse adipocytes, but with as low as 5uM in the human adipocytes. This is a low concentration, and could be achieved in humans. It is shown that the serum concentration of CLA in humans is between 20-70uM, depending of the amount of CLA in the diet. However, this refers to the total CLA concentration, and not the concentration of the 10,12 isomer. The 9,11 CLA isomer is the most abundant in the diet, and will therefore constitute most of the serum concentration.

You will not have the same effect if you have both the CLA isomers (9,11 and 10,12 CLA) at the same time, then the isomers will neutralize each other. The animal studies in which trans10,cis12 CLA has been given separately has the best effect on fat accumulation, however, there are very few human studies with only this isomer, most of the human studies have used a CLA mixture with the two isomers in equal amounts.

Since trans10,cis12 CLA modulates the effect of PPARgamma, and PPARgamma is most abundant in adipose tissue, I guess the best potential is in prevention fat accumulation, not in reducing the fat that is already accumulated."

[prolangtum]

continued:

Par was asking earlier about CLA's effects on PPARalpha null mice, an issue which I address in the thread pasted above, as well as elsewhere on this forum. Below I provide some further comments on this issue.

Many of you may have read the work of Dr. Clifton Baile. He and his colleagues have investigated the effects of CLA on fat cell (adipocyte) apoptosis. Dr. Baile is also involved with an effort to screen for natural products with myostatin-inhibiting properties.

Dr. Mary Anna Della-Fera is one of Dr. Baile's colleagues. Below she comments on the relationship of CLA's 'fat fighting' properties to PPARalpha and PPARgamma (2003 personal communication):

"It is likely that CLA does not affect weight loss and body fat content through it's effects on PPAR alpha. Peters et al (BBA 1533:233, 2001) showed that PPAR-alpha null mice were no different from wild type mice in their response to dietary CLA. Body weight and body fat content were lower in both groups compared to controls and body protein content was higher.

In some experiments PPAR gamma expression was found to be increased, and in others, it was decreased. The effect on PPAR gamma appears to depend on the species, tissue, length of treatment and maybe other factors. For example in 3T3-L1 cells, treatment with CLA 10,12 for 48 hr increased PPAR gamma-2 expression, whereas treatment for 6 days decreased PPAR gamma-2 expression. In another experiment with 3T3 L1 cells, CLA 10,12 decreased mRNA levels of fatty acid synthase, adipocyte lipid binding protein and LPL and reduced PPAR gamma and CEBP alpha levels.

CLA 10,12 has also been found to cause a dose -dependent decrease in expression of steroyl-CoA desaturase 1 gene expression in 3T3-L1 adipocytes. In pigs, dietary CLA treatment was shown to increase PPAR gamma expression in muscle and in intramuscular adipose tissue. CLA isomers have also been shown to increase UCP2 levels in muscle and adipose tissue. The specific mechanism for CLA-induced body fat loss is not yet clear, but may be due to inhibition (or reversal) of adipocyte differentiation. This might also explain the increase in adipocyte apoptosis in CLA-treated mice, since pre-adipocytes are more susceptible to apoptosis triggers than mature adipocytes.

She continues, "There are 2 papers describing loss of body fat in humans treated with CLA (see below). The effects were fairly small. In one study, abdominal diameter was slightly less; in the other study, body fat mass was decreased. Both studies used a mixture of CLA isomers and the quantities were in the 3-6 g/day level. No studies using only the CLA 10,12 isomer in humans have been published. As you know, CLA has other apparent beneficial effects on cancer cell proliferation and inflammation, so it will probably will continue to be tested in humans."

[Cory]

I have read something to that degree, but don't you think that if CLA just inhibited furthur fat storage while eating a clean diet, then you would indirectly burn fat given that you didn't change your diet and exercise regime? Also, the proper way to take CLA and the amounts are very crucial for its efficacy. I read you should take at least 4.6 grams all at one time, preferably in a concentrated clarinol powdered form every day and be very consistant because some people reported that they didn't see significant results until about 3-6 months.