ARNIE

there goes slick willy again!

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hackskii

Well, can you blame him bro, he is only trying to make a few bucks:love:

Now where was that study that Bill suggested they build 1 to 2 pounds of muscle a week?
How did he know that was all muscle and not fat?:confused:
Funny, many threads the guys suggest they got nothing from it.
Maybe it was fat pounds.....lol....

I would venture to say that it has its place in the vegatarian diet or mabye guys that eat no meat or eggs, other than that I see no reason to supplement AA.
Fish oils on the other hand I totally recommend supplementing daily and for ever.
My health is important to me, if I am going to jack myself I might as well use gear as this I know works, and it isnt much if any more expensive....lol......
I dont need any scientific studies backing that one up to support it, or some killer media hype either.....haaa haaaaa

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Scott


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thestudbeast

So how much AA is optimal according to molecular? For example should a vegan take more x-factor than a meat eater and should someone on the anabolic diet take less or none at all.

So simple equation of: amount in diet + X-factor dose = optimal amount

How much AA should we have according to you guys?

phosphate bond

It is tough to say but that 1 gram per day of AA Bill gave to the experimental group did show "strong trending" reductions in IL-6 (IL-6 levels correlate with silent inflammation)

So I think there may be something to giving additional AA (beyond the typical diet) to people as long as people are weight training.

Keep in mind there is a lot of talk about omega 6 to three ratios here, but if you look on page 56 (or is it page 64) of Udo Erasmus's book "The fats that Heal, the fats that Kill" you will see that these ratios are upside down in wild meat. Wild meat actually has less saturated fat, but a stronger AA:EPA/DHA ratio. Wild meat and heavy physical exercise is what humans have evolved on so consider this with any argument here. Saturated fat does impact insulin secretion and insulin resistance also (not to mention silent inflammation if either of these two get out of hand)

Like I was saying you definitely need series 2 prostaglandins (from localized muscle contractions) if you ever hope to activate glycogen sythetase. (stimulating CAMP to break down glycogen and then eventually lowering cAMP allows that enzyme to work correctly)

hackskii

Lets not demonize saturated fats here, many feel they have a bad rap and this has perpetuated myth's over the years to make saturated fats the bad guy.
Yes they can effect blood sugar levels, but all foods eaten together determine the glycemic load of that meal.

There are in fact more than a dozen different types of saturated fat, but you predominantly consume only three: stearic acid, palmitic acid and lauric acid.

It’s already been well established that stearic acid (found in cocoa and animal fat) has zero effect on your cholesterol levels, and actually gets converted in your liver into the monounsaturated fat called oleic acid.

The other two, palmitic and lauric acid, do raise total cholesterol. However, since they raise “good” cholesterol as much or more than “bad” cholesterol, you’re still actually lowering your risk of heart disease.

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Scott


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phosphate bond

Saturated fats are only "bad" for people who have a supply and demand problem. Anytime excess free fatty acids are in the bloodstream they affect the secretion of insulin at the pancreas (resulting in a delayed but over-secretion curve when in the presence of glucose at the same time).

Now bodybuilders do not normally have this problem because they have large muscles (high demand for oxidizing fat) and low adipose levels (low supply of fat). Now in this case any saturated fats eaten will do usually cause a rise in plasma levels of fatty acids (because they are oxidized or disposed of promptly)

What we are talking about here is the average american (a target of the Zone Diet). These people are the reverse and high satuared fat affects them differently than someone Bodybuilding. For one thing they have higher insulin levels and thus acetly-COA carboylase is activated in muscle (rather than oxidative phosphorylation). For this reason they have a hard time converting fatty acids into ATP (malonyl COA produced from Acetyl COA carboylase blocks carnitine from transporting fatty acid into the mitochondria)

In these cases (because of excess saturated fat relative to their ability to oxidize it) there can be a set-up scenario for hyperinsulinemia and silent inflammation. Then all this Dr. Barry Sears "bad prostaglandins" stuff kicks in because of the poor energy state resulting from the hyperinsulinemia.

Its not Arachidonic acid that causes "silent inflammation" it is a poor energy state that causes it. You can't repair anything without ATP and the cells in your body know this. That is why they send out all these little messanger chemicals like IL-6 to help correct the situation.

That is the irony about obese people (targeted by the Zone Diet) is that they are over-eating, but are poorly converting there food into energy.

hackskii

The reason why I posted that was because you were giving the impression that we should avoid saturated fats and supplement AA, I guess this is part of your arguement to lower saturated fats in the diet and increase AA for those that lift weights.
Same can be made for saturated fats along with meats that in weight lifters I do not believe that AA needs to be supplemented.
Bill on another post on this thread talked about cholesterol from eggs could be a problem.
I disagree. Overall cholesterol is effected but not the ratio of HDL to LDL, thus overall risk is not a factor.

I am aware that saturated fats have an impact on insulin, but fish oils and olive oil have a neutral effect. Not only that but fiber slows digestion lowering spiking of blood sugar as well as insulin spiking.
So, a diet that has meat, vegetable fiber, and some good oil wont be an issue with insulin responce, as the glycemic load wont be much of a factor, even for those that dont exercise. Fish oils aid better than any other fat for insulin sensitivity.
Also for those just sitting on the couch burn almost all fat and hardly any glucose/glycogen.

Even ketogenic diets like Atkins work exceptionally well for the couch potato. I have no problem with fats, I do feel that the problem really lies in simple sugars, processed foods, transfats and hydgrogenated oils, not saturated fats.
Some of the most energy I ever had (with the exception of the zone), was on a ketogenic diet.
high fat diets are not the problem, high fat diets with diet high in carbohydrates is a problem, and for most low fat diets are not healthy.

I dont think eating saturated fats makes one prone to hyperinsulinemia.
Sears suggests against Saturated fats, but that is about one of the only positions that I do not agree with him on.
Many studies Atkins posted suggested in better lipid profiles on a ketogenic diet. At least in the beginning anyway....lol

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Scott


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thestudbeast

Yes some interesting points Scott, it's amazing how our countries with such poor health try to put the blame on saturated fat. As our diets have changed to vegtable fats and refined carbs so our health has plumeted to all time lows. Yet the top 4 countries in the health stakes all eat diets rich in saturated fat.

If you look at the Insulin index you clearly see that products high in saturated fat like beef can not be compared to refined carbs in terms of insulin release and it is the combo like Hack's mentioned of saturated fat and refined carbs that give the large sustained release of insulin. This has been proven in practice by the anabolic diet, Vince Gironda's teachings, the plaeo diet etc etc.

I think the most conclusive exidence of wether AA should be in our diets will be to look at what our ansesters (sp) ate like PB has hinted at. The problem is knowing how much AA would have been in wild meat. Remember that organ meat was given priority in hunter gatherer times, in fact when a pack of wolves or lions catch a prey the first thing they go for is the liver and organ meats. Eggs again would have been eaten along with red meat, so the sources would have been there. If AA is present in reasonable quantities in wild animals livers it will no doubt turn out all the boffins have got it wrong again!

winger

Bump for Bill!

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TH&S

My sentiments exactly...

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D: 220 | B: 110 | S: 170 | Target: 550

Tinytom

This thread is fcuking awesome.!!!!!

wealth of info I never knew.

Cheers guys

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Sponsored by Extreme Nutrition - Almost an unfair advantage

hackskii

This study looks familiar.

J Int Soc Sports Nutr. 2007 Nov 28;4(1):21 [Epub ahead of print] Links
Effects of arachidonic acid supplementation on training adaptations in resistance-trained males.Roberts MD, Iosia M, Kerksick CM, Taylor LW, Campbell B, Wilborn CD, Harvey T, Cooke M, Rasmussen C, Greenwood M, Wilson R, Jitomir J, Willoughby D, Kreider RB.
ABSTRACT: BACKGROUND: To determine the impact of AA supplementation during resistance training on body composition, training adaptations, and markers of muscle hypertrophy in resistance-trained males. METHODS: In a randomized and double blind manner, 31 resistance-trained male subjects (22.1 +/- 5.0 yrs, 180.0 +/- 0.1 cm, 86.1 +/- 13.0 kg, 18.1 +/- 6.4% body fat) ingested either a placebo (PLA: 1 g * d-1 corn oil, n = 16) or AA (AA: 1 g * d-1 AA, n = 15) while participating in a standardized 4d * wk-1 resistance training regimen. Fasting blood samples, body composition, bench press one-repetition maximum (1RM), leg press 1RM and Wingate anaerobic capacity sprint tests were completed after 0, 25, and 50 days of supplementation. Percutaneous muscle biopsies were taken from the vastus lateralis on days 0 and 50. RESULTS: Wingate relative peak power was significantly greater after 50 days of supplementation while the inflammatory cytokine IL-6 was significantly lower after 25 days of supplementation in the AA group. PGE2 levels tended to be greater in the AA group. No significant differences were observed between groups in body composition, strength, anabolic and catabolic hormones, or markers of muscle hypertrophy (i.e., total protein content or MHC type I, IIa, and IIx protein content) and other intramuscular markers (i.e., FP and EP3 receptor activity or MHC type I, IIa, and IIx mRNA expression). CONCLUSIONS: AA supplementation during resistance-training may enhance anaerobic capacity and lessen the inflammatory response to training. However, AA supplementation does not promote greater gains in strength, muscle mass, or influence markers of muscle hypertrophy.

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Scott


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phosphate bond

Fish oils definitely lower insulin secretion (evidenced by reduced C-petide levels) but not blood sugar in type II diabetics. So I am not sure how they are helping with glucose disposal. You can improve insulin sensitivity two ways. One ways is to lower insulin secretion. The Other way is to improve insulin action. Ideally you want both effects. This is why some books I have seen have recommended caution for people people with diabetes to take Fish oil (in high amounts). You can find the actual studies on Pubmed. Some are conflicting as usual but the info is there.

Now some of these diets like Atkins have a lot of saturated fat in them, but not lots of glucose at the same time. Its when you combine carbs with saturated fat that insulin resistance can be a problem when energy expenditure is lower than intake.

thestudbeast

The type of carb is also an issue, for example the Japs eat rice and pork/eggs together and don't suffer and the swiss eat dairy lactose/saturated fat with out negative health consiquences (they are the top two healthiest countries in the world)

But in general we agree on this topic.



Is it Moleculars position that AA is inflamitory in the muscle during exersize and then works as an anti inflamitory there after?

hackskii

Or better asked, why were the muscle biopsies not taken immediatly after training, instead of a fasting state 48 hours after exercise in the Baylor Study?
Surely this would have a huge impact on the outcome?
Why assume that AA was responsible solely for the lowering of IL-6?

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Scott


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