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Arachidonic acid

What is arachidonic acid?

Arachidonic acid is an important fatty acid that is consumed in small amounts with our normal meals. It is mainly found in the fatty parts of meat and fish (mostly in raw meat). Therefore, vegetarians usually have lower levels of arachidonic acid in their bodies than those who eat everything. The intake is rather low even in meat eaters, according to what was actually found here. For example, the visible fat content of beef contains between 20 and 180mg of arachidonic acid per 100 grams of fat! (almost a quarter of a pound)! . The amount of arachidonic acid in lean meat is lower. This particular fatty acid is only found in small amounts; the average Western diet provides each of us with only 230 milligrams of this important nutrient every day. If this arachidonic acid is only slightly detected in lean meat, bodybuilders who adhere strictly to a low-fat diet could also consume less. Knowing the importance of this important nutrient to our bodies, we should all start paying more attention to its intake. Because we think it could be of great benefit to us all to have a little more of it.

Arachidonic acid is considered an "essential" fatty acid because it is an absolute must for the proper functioning of the human body. In this case, it is vital for the working of the prostaglandin system. More specifically, it is the raw material used by the body to assemble a major series of hormones, which as a whole refer to dienolic prostaglandins (the main prostaglandin is found in Mammals4). This includes the prostaglandins PGF2 and PGF2a, which are the primary focus of our studies. The body's ability to release normal amounts of these prostaglandins is therefore directly dependent on the availability of this fatty acid. This is of crucial importance for the athlete as, among other important physiological functions, prostaglandins are entirely responsible for protein conversion and muscle mass gain. They act precisely in the nucleus responsible for muscle growth and are responsible for regulating the direct, local (muscular) effects of physical exertion.

Prostaglandins and anabolism

Prostaglandins begin to exert their powerful effects on muscle growth immediately after physical exertion. More specifically, it is the stretch stimulus triggered by overstretched muscle contraction that first triggers the local build-up of these hormones. In turn, they play a crucial role in what goes on in your muscles in the following days of recovery. A study published in the American Journal of Physiology in 1990 looked quite closely at the relationship between prostaglandins, protein turnover and the growth effects of exercise5. In this study, skeletal muscle cell preparations were incubated under stretch stimuli to replicate the stimuli during exercise. The protein throughput was then measured by quantifying the uptake of the labeled amino acid phenylalanine in muscle tissue. During the first 5 hours of stimulation, prostaglandin levels PGF2 and PGF2a increased by 101% and 41% respectively (PGF2 is linked to the destructive effect of exercise). PGF2a remained elevated over 48 hours and corresponded to a 52-98% longer-term increase in protein buildup. Additional, further studies point to PGF2a specifically because it is the protein most closely linked to the enhancement of skeletal synthesis of muscle proteins.

Prostaglandin PGF2alpha and PGE2 - The core regulators of protein synthesis

Studies using drugs that prevent the conversion of arachidonic acid into prostaglandins may help us better understand why these hormones are so important for muscle development. One such study was published in March 2002. It involved a group of 24 recreationally active young men who were given maximum OTC doses of ibuprofen (1,200mg/day) or acetaminophen (4,000mg/day) and induced to exercise. These two popular over-the-counter painkillers are known to work by blocking the enzyme responsible for prostaglandin synthesis. The change in amino acid was measured over 24 hours after the exercise bout, which allowed the researchers to determine what effect, if any, these drugs had on protein buildup or breakdown. It was found that both the ibuprofen and acetaminophen significantly mitigated the normal increase in protein synthesis after exercise, which differed by 76% from baseline in the group taking placebo alone. A subsequent study under the same conditions and with the same people showed that both drugs blocked the normal increase in PGF2a in particular13.These studies together show us how strongly prostaglandins actually support the basic process of muscle growth. Without them, there is no muscle growth, it's as simple as that.

Triggering during exercise

The role that arachidonic acid plays in muscle growth must be considered far greater than just that of a precursor to prostaglandins. Skeletal muscle tissue does not have the ability to actually store prostaglandins. Therefore, arachidonic acid is the only local source of PGF2a, which is stored in the outer phospholipid layer of each cell. More importantly, it is the stretching of muscle fibers during intense exercise that triggers the release of arachidonic acid and converts it into active prostaglandins. The release of arachidonic acid is therefore the very first trigger in a long cascade that controls the rebuilding and strengthening of muscle tissue after exercise. A study carried out by the Rowett Research Institute in the UK illustrates this relationship. Here the researchers used similar muscle incubation and stretching techniques to those used in the 1990 American Journal of Physiology study to demonstrate that it is the release of arachidonic acid, rather than stored prostaglandins, which act as the main stimulus for protein build-up. Their work was correctly summarized by the participants when they noted: "...the link between mechanical movement and protein synthesis...is most simply explained by the assumption that unbound arachidonic acid is released during stretching, stored within cells and continues to be converted into prostaglandins". Two additional studies by Palmer and colleagues at the Rowett Institute support the same conclusion.

Exercise and AS concentrations

To make things a little more difficult for athletes, both animal and human studies show that exercise reduces the stock of arachidonic acid in skeletal muscle tissue. One such study divided individuals into an active and a highly sedentary (inactive) group, with both groups receiving the same standardized diet with the same composition of fatty acids and arachidonic acid (total food intake varied only slightly between the groups). The inactive group showed a 5% increase in the concentration of arachidonic acid over the course of the study, whereas the active group showed a moderate, 7-8% depletion of this fatty acid. This was despite the fact that the active group actually consumed on average 13% more food compared to the inactive group, which can be explained by a slightly higher intake of fatty acids. Since dienolic prostaglandin synthesis is inextricably linked to the amount of available arachidonic acid, lower levels can only lead to less arachidonic acid released during stretching during failed movements. Likewise, this leads to less muscle-building PGF2a, which is produced to enhance muscle protein synthesis.

Charging AS

In June 2001, a paper was published in the journal "Lipids" which reviewed the many medical studies over the past few decades regarding the sources of arachidonic acid in the body. Among other things, this paper discussed several studies that looked at the effect of short-term diets rich in arachidonic acid. In reviewing animal and human data, the authors consistently indicated a sharp increase in the levels of arachidonic acid in various tissues of the body with increased supplementation than the normal diet could provide. In one such series of studies, people consumed 1.7 grams of arachidonic acid daily for 50 days. This comprehensive study found that this amount of arachidonic acid in the diet nearly doubled the amount of arachidonic acid in plasma phospholipids and also significantly increased the levels of this fatty acid in platelets, red blood cells and lipoid tissues.

Another study looked in particular at the effects that high concentrations of arachidonic acid could have on the prostaglandin system. The researchers exposed the bodies to high levels of arachidonic acid by asking people to take 6 grams a day for 2-3 weeks in its ethyl ester form. The researchers found a considerable retention of arachidonic acid in the lipoids of all tissues measured. There was also an increase in the output of prostaglandin metabolites during the study period (in particular, they looked at the E-series of prostaglandin metobolites). In 3 of the 4 subjects studied, the increase in prostaglandin production was a remarkable 47%, indicating a dramatic improvement in the rate of build-up of these hormones. The authors concluded that the addition of the fatty acid precursor greatly enhances prostaglandin biosynthesis and function.

Safety appendix

For those who may experience immediate cardiovascular symptoms when consuming a "raw meat" food such as arachidonic acid, we would like to refer you to a 1997 study which looked very closely at the effects of high doses on blood lipoprotein and lipoid levels, which were known to be risk factors for cardiovascular disease. This study again included a consumption of 1.7 grams per day and ran over a period of 50 days. Noting that the subjects consumed the fatty acids at a concentration eight times higher than the average Western diet, the researchers found no adverse effects on plasma cholesterol or overall triglyceride concentrations. Both good (HDL) and bad (LDL) cholesterol levels remained unaffected during the study period. From this we can conclude that taking larger amounts of arachidonic acid will increase its contribution to tissue phospholipids. The increase in the responsiveness of the prostaglandin system depends on this fatty acid. It does not appear to increase the risk of cardiovascular disease (assuming you are healthy when you start). However, this product is not recommended if you have diabetes, asthma, high blood pressure, high cholesterol, heart disease, are pregnant or have an inflammatory disease. Consult your doctor before using it if you are taking any medication or suffer from any condition where raw meat intake is prohibited.

What the research is trying to tell us

The above studies on prostaglandins and arachidonic acid have been taken from many different areas of medical research and combine together to reveal the role this nutrient will play as a muscle-building supplement. They reveal unfulfilled promises and the typical "yet another useless supplement" scenario, yet a scientifically well-supported method for increased muscle growth. To summarize what we have learned from their research, we can highlight several very important key points. Prostaglandins are the actual main stimulators for protein build-up after exercise. The build-up of prostaglandins depends on the availability of arachidonic acid. The body stores arachidonic acid in muscle tissue but no active prostaglandins. Arachidonic acid is released from the outer phospholipid layer of muscle cells during exercise-induced stretching. Once unbound, it is rapidly converted into active prostaglandins. Exercise lowers the level of arachidonic acid in muscle tissue. Ingestion of arachidonic acid in larger than normal amounts will result in greater retention of this fatty acid in body tissues, which should have increased production of anabolic prostaglandins in response to exercise.

Dosage in sport

Athletes up to 100 kg take 750 mg arachidonic acid per day. From 100 kg up to 1 gram daily. The dose should be taken with meals and preferably divided (3-4 times a day). Take arachidonic acid for 50 days and then take a break of at least 50 days before using it again. Because arachidonic acid dramatically increases protein synthesis in trained muscles, you will need to increase your daily protein and calorie intake to gain muscle mass. This often falls in the range of 500-1000 calories daily. It depends on the body's ability to convert arachidonic acid into active prostaglandin and therefore 100% effective. This conversion can be hindered by the consumption of various medications, supplements or foods. Here is a list of what you should reduce while taking arachidonic acid:

  • Pain relievers that contain acetaminophen, ibuprofen or aspirin
  • NSAIDs (non-steroidal anti-inflammatory drugs)
  • Omega 3 fatty acids
  • Flax and fish oil supplements
  • N-acetyl cysteine (NAC)
  • Conjugated Linoleic Acid (CLA)
  • Avoid regular consumption of products high in omega 3 fatty acids or anti-inflammatory nutrients such as cold water fish, peanut butter and sesame seeds, olives

Important: Remember to drink at least 2 liters of water daily while taking arachidonic acid.

Side effects

Arachidonic acid is also a precursor for the formation of various eicosanoids (prostaglandins, thromboxanes and leukotrienes). These are important for smooth muscles and for inflammatory and immune reactions, among other things. Arachidonic acid is also found in sperm and is required for the production of testosterone.

But be careful: excessive amounts of arachidonic acid can have undesirable effects. These include an increased risk of atherosclerosis and involvement in inflammatory processes (e.g. rheumatism, allergies, joint pain). Normally it is almost impossible to get these side effects within such a short time (50 days). You would have to take such high doses of arachidonic acid for several years without a break to cause such side effects. If this is the case, you could proceed as follows:

Counterpart omega-3 fatty acids

Omega-3 fatty acids such as eicosapentaenoic acid, on the other hand, have a positive effect on inflammation. Like arachidonic acid, it is mainly absorbed through food and is mainly found in certain vegetable oils and sea fish. Eicosapentaenoic acid is very similar in structure to arachidonic acid. It influences the formation and metabolism of arachidonic acid in several ways and thus also its conversion into inflammation-promoting secondary products. In order to shift the ratio of the two fatty acids in favor of eicosapentaenoic acid, fish should be included in the diet several times a week instead of meat. In particular, cold-water fish such as sardines, tuna, herring, mackerel or salmon contain a lot of eicosapentaenoic acid and thus reduce inflammatory activity. You could also take supplements such as omega 3 fatty acids, flax and fish oil, N-acetyl cysteine (NAC), conjugated linoleic acid (CLA) or olive oil.

Antioxidants against oxygen radicals

Inflammatory processes are accompanied by an increased formation of free oxygen radicals. These aggressive particles activate the enzymes involved in the release (figure, reaction a) and conversion (figure, reaction c) of arachidonic acid and thus promote the formation of inflammatory prostaglandins and leukotrienes. In addition, oxygen radicals attack structure-giving molecules in cartilage, tendons and joints and thus contribute directly to the disease process. Antioxidants counteract these processes by scavenging oxygen radicals. The most important antioxidants are vitamins E and C as well as selenium and zinc. Inflammatory diseases such as rheumatoid arthritis require an increased intake of these substances.

Vitamin E reduces the release of arachidonic acid from the cell membranes and reduces the activity of enzymes that are necessary for the formation of inflammation-promoting leukotrienes and prostaglandins. It also has a regulating effect on immune processes that release inflammation-promoting substances and activate cartilage-degrading enzymes.

Vitamin C regenerates vitamin E, which is itself oxidized when scavenging oxygen radicals, i.e. in the course of its antioxidant effect. In addition, vitamin C plays an important role in the biosynthesis of the structural protein collagen and is therefore essential for the regeneration of cartilage and bones.

Selenium also has an antioxidant effect. It is necessary for the activation of the enzyme glutathione peroxidase, which regenerates oxidized vitamin C.

Zinc is a cofactor for the enzyme superoxide dismutase, which is also involved in antioxidant processes.

Micronutrients against osteoporosis ...

Rheumatoid arthritis impairs bone metabolism and in many cases leads to a decrease in bone density (osteoporosis). The problem is exacerbated by prolonged treatment with cortisone. To counteract osteoporosis, an increased intake of calcium, vitamin D and vitamin K as well as vitamins C and B6 is necessary.

Calcium is an important component of bones. Vitamin D promotes the absorption of calcium and its incorporation into the bones. Vitamin K is involved in the synthesis of osteocalcin, which regulates the mineralization of bones. Vitamin C and vitamin B6 promote, among other things, the cross-linking of structural proteins in cartilage.

Cardiovascular diseases Studies have shown that many people with rheumatoid arthritis have an elevated homocysteine level. Homocysteine, a waste product of protein metabolism, is considered a risk factor for diseases of the cardiovascular system. Vitamins B6 and B12 act as a co-factor for an enzyme that breaks down homocysteine. In this way, together with folic acid, they regulate the homocysteine level to a healthy level.