Lol.... That's below brosciense level bro...
I agree, there is some data and some reason to think AA would help, the lit is all over the place however, sometimes inflammatory sometimes not, worsening alzheimers progression and potential onset etc..
AA increases the production of prostaglandins, which aide muscle hypertrophy after resistence training. Anti-inflammatories that inhibit COX-1/2 etc reduce this effect.
J Clin Endocrinol Metab. 2001 Oct;86(10):5067-70.
Skeletal muscle PGF(2)(alpha) and PGE(2) in response to eccentric resistance exercise: influence of ibuprofen acetaminophen.
Trappe TA1, Fluckey JD, White F, Lambert CP, Evans WJ.
PGs have been shown to modulate skeletal muscle protein metabolism as well as inflammation and pain. In nonskeletal muscle tissues, the over the counter analgesic drugs ibuprofen and acetaminophen function through suppression of PG synthesis. We previously reported that ibuprofen and acetaminophen inhibit the normal increase in skeletal muscle protein synthesis after high intensity eccentric resistance exercise. The current study examined skeletal muscle PG levels in the same subjects to further investigate the mechanisms of action of these drugs in exercised skeletal muscle. Twenty-four males (25 +/- 3 yr) were assigned to 3 groups that received the maximal over the counter dose of ibuprofen (1200 mg/d), acetaminophen (4000 mg/d), or a placebo after 10-14 sets of 10 eccentric repetitions at 120% of concentric 1 repetition maximum using the knee extensors. Preexercise and 24 h postexercise biopsies of the vastus lateralis revealed that the exercise-induced change in PGF(2alpha) in the placebo group (77%) was significantly different (P < 0.05) from those in the ibuprofen (-1%) and acetaminophen (-14%) groups. However, the exercise-induced change in PGE(2) in the placebo group (64%) was only significantly different (P < 0.05) from that in the acetaminophen group (-16%). The exercise-induced changes in PGF(2alpha) and PGE(2) were not different between the ibuprofen and acetaminophen groups. These results suggest that ibuprofen and acetaminophen have a comparable effect on suppressing the normal increase in PGF(2alpha) in human skeletal muscle after eccentric resistance exercise, which may profoundly influence the anabolic response of muscle to this form of exercise.
In humans, controlled
J Int Soc Sports Nutr. 2007 Nov 28;4:21.
Effects of arachidonic acid supplementation on training adaptations in resistance-trained males.
Roberts MD1, 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.
To determine the impact of AA supplementation during resistance training on body composition, training adaptations, and markers of muscle hypertrophy in resistance-trained males.
In a randomized and double blind manner, 31 resistance-trained male subjects (22.1 +/- 5.0 years, 180 +/- 0.1 cm, 86.1 +/- 13.0 kg, 18.1 +/- 6.4% body fat) ingested either a placebo (PLA: 1 g.day-1 corn oil, n = 16) or AA (AA: 1 g.day-1 AA, n = 15) while participating in a standardized 4 day.week-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.
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. However, no statistically 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 density or MHC type I, IIa, and IIx mRNA expression).
AA supplementation during resistance-training may enhance anaerobic capacity and lessen the inflammatory response to training. However, AA supplementation did not promote statistically greater gains in strength, muscle mass, or influence markers of muscle hypertrophy.
It may enhance capacity but does not seem to really cause much hypertrophy, in fact the blunted inflammatory response would be a bad thing, strength would increase but protein synthesis would be lower.
The wiki page on this shit is a mess also, they cite the same studies over and over and even a fucking poster? who is selling this shit?