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.

J Int Soc Sports Nutr. 2007;4:21.

PubMed: http://www.ncbi.nlm.nih.gov/pubmed_arachidonic_acid

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 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.

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. 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).

CONCLUSION:

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.

Opening Comments

The other day I got a request to do an article on arachidonic acid (AA) supplementation. Now, to be completely honest, I haven’t heard much about arachidonic acid in terms of supplementation for muscle and strength gains, although I am familiar with the lipid and its role within the inflammatory response. So, I figured why not, could be interesting. As it turns out, arachidonic acid research, in terms of supplementing for muscle hypertrophy, strength, etc. in humans, is quite scarce. To my knowledge this is the only study to look at arachidonic acid supplementation on muscle protein synthesis – contrary to what some supplement companies may have you think.  Furthermore, this study attempts to look AA’s effects on body composition and strength, two factors I’m sure many of you are interested in improving. I will first start with a short history of the literature surrounding AA – as it pertains to weightlifting – and then jump right into the above study wherein I will touch upon the strengths and weaknesses of the study and my views on/potential implications for AA supplementation.

Arachidonic Acid: A Quick Review of the Literature

Arachidonic acid (AA) is an omega-6 polyunsaturated fatty acid (PUFA) – denoted 20:4 ω-6 – found naturally in foods and in membrane phospholipids of humans. Contrary to what some people think, AA is not an essential fatty acid. The human body can effectively make enough AA through various enzymatic pathways which I will not get into. AA is converted into a group of eicosanoids known as prostaglandins (PGs). PGs play an important role in regulating the inflammatory response as well as other immune responses in the human body. It is estimated that the average 70kg man (~154lbs) contains about 50-100g AA spread throughout various tissues and membranes [1], although it is thought that the AA status of the body is dependent upon dietary intake [1] as well as activity level [2-3]. An interesting study from 2000 saw that the fatty acid profile of skeletal muscle differed between endurance-trained and sedentary individuals – with less AA and in the trained group – even though the fatty acid composition of the diet was similar [3]. This implies that physical activity may play a more important role than diet in terms of the fatty acid composition of cell membranes.

Early in vitro and animals studies demonstrated that PGs (and therefore AA) are implicated in the inflammatory response of muscles after mechanical stimulation (comparable to that of resistance exercise) as well as the rates of protein synthesis and degradation in both skeletal and cardiac muscle [4-7]. Because AA is converted to prostaglandins (PGs) via the COX-2 pathway – the same pathway inhibited by non-steroidal anti-inflammatory drugs (i.e. Ibuprofen, acetaminophen) – it is thought that commonly used pain killers (Advil, Tylenol, etc.) could potentially inhibit the necessary myogenic inflammatory response needed for muscle protein synthesis. Reaffirming this notion, a study done by Trappe et al. showed that subjects supplemented with normal doses of NSAIDs prior to resistance training completely eliminated PG synthesis of the inflammatory response as well as muscle protein synthesis following the exercise protocol [8]. Paired to together with research showing that 1.5g of AA/day for a month and half significantly increased PG synthesis [9], AA has now been implicated as a mass-building supplement for weightlifters and gym-rats alike. Today’s study gets at the crux of this argument, so without much further ado, let’s dissect this paper!

The Study

Study Strengths

Because you have the abstract above (and have the ability to read), I’ll start off by listing the study’s strengths, which to my surprise were a whole bunch. First off, big points to any study which uses healthy, resistance-trained subjects. This eliminates any effects that could be confounded by what are called, “beginner gains.” This study was also a randomized, double-blind, placebo-controlled study, which ensures that both groups are identical (aside from the experimental protocol) and that any biases from both researchers and subjects which might affect the results are eliminated. Body composition was measured using dual-energy x-ray absorptiometry (DXA), otherwise known as the “Gold Standard” for body comp measures. Another awesome feature of this study was the use of muscle biopsies. Not too often do people agree to donate a chunk of their own muscle tissue (nor is it permitted often). Biopsies were taken before strength testing to eliminate any effects that might occur due to exercise. You can’t get more accurate than actually looking at someone’s muscle tissue!

Nutritionally speaking, recommended calorie and protein intakes were well-above adequate (+500kcals/day above baseline needs and 2g/kg BW, respectively), although this was merely recommended and not tightly controlled. Nevertheless, a dietary supplement was given out (290kcals, 24g CHO/45g PRO/1g Fat) in order to reach the additional calorie and protein requirements needed to promote muscle gains. Subjects were also told to avoid foods high in omega-3 fatty acids as well as commonly used NSAIDS which might interfere with the inflammatory response of exercise.

Study Weaknesses

The fact that dietary intake was self-reported this potentially confounds the results, even though 4-day dietary records were used to validate intakes. Another potential weakness of the study was that the placebo group was given a corn-oil supplement which can be converted to AA (from linoleic acid) using various enzymatic pathways in the body. Dietary analysis, however, revealed similar levels of linoleic acid in the diets. This, however, is only as valid as the diet records. All in all, this was a well carried-out study with very few weaknesses.

Results

The researchers found that there were no significant differences between the two groups in terms of body mass, fat free mass, fat mass, percent body fat, 1RM bench press, or 1RM leg press. Pity. However, anaerobic peak power was significantly different between the two groups, with the higher peak power coming from the AA group on days 25 and 50. This comes on the heels of previous research which showed that, 10 days of a soybean derivative – that naturally contains AA – increased time to fatigue in active males during a cycling test at 85% VO2 max [10] as well as in soccer players performing exhaustive, intermittent sprints [11]. Nevertheless, the major finding of this study was that AA supplementation did not lead to greater gains in strength, muscle hypertrophy or body composition when compared to a placebo, which, let’s be honest, is the main goal of most of the readers of this Blog.

Summary & Finals Comments

In the end, it appears that AA supplementation may be more of a waste of money rather than a muscle-building fatty acid (especially when AA supplements range from $50-60 a pop!). However, this is only one study. Obviously more studies need to be done in order to confirm or refute the findings presented here. Given that it’s been 5 years since this study was done, without any corresponding follow-up whatsoever, this tells me that AA supplementation doesn’t appear to be the “next big thing;” at least not now. There may be some potential benefits if you’re an endurance athlete, but right now, it’s still speculative and the results are more relevant to phosphatidylserine (the soybean derivative I mentioned earlier). So next time you hear outrageous claims about arachidonic acid providing awesome muscle and strength gains, just remember that it’s probably based off of speculation rather than sound scientific research.

References

1. Zhou L, Nilsson Å. Sources of eicosanoid precursor fatty acid pools in tissue. J Lipid Res. 2001;42(10):1521-42.

2. Helge JW, Wu BJ, Willer M, Daugaard JR, Storlien LH, Kiens B. Training affects muscle phospholipid fatty acid composition in humans. J Appl Pysiol. 2001;90(2):670-7.

3. Andersson A, Sjödin A, Hedman A, Olsson R, Vessby B. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Am J Physiol Endocrinol Metab. 2000;279(4):E744-51.

4. Vandenburgh HH, Shansky J, Karlisch P, Solerssi RL. Mechanical stimulation of skeletal muscle generates lipid-related second messengers by phospholipase activation. J Cell Physiol. 1993;155(1):63-71.

5. Vandenburgh HH, Shansky J, Solerssi RL, Chromiak J. Mechanical stimulation of skeletal muscle increases prostaglandin F2 alpha production, cyclooxygenase activity, and cell growth by a pertussis toxin sensitive mechanism. J Cell Physiol. 1995;163(2):285-94.

6. Rodemann HP, Goldberg AL. Arachidonic acid, prostaglandin E2, and F2 alpha influence rates of protein turnover in skeletal and cardiac muscle. J Biol Chem. 1982;257(4):1632-8.

7. Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent Fatty Acids 1990;39(2):95-104.

8. Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Am J Physiol Endocrinol Metab. 2002;282:E551-556.  

9. Kelley DS, Taylor PC, Nelson GJ, Mackey BE. Arachidonic acid supplementation enhances synthesis of eicosanoids without suppressing immune functions in young healthy men. Lipids 1998;33:125-130.

10. Kingsley MI, Miller M, Kilduff LP, McEneny J, Benton D. Effects of phosphatidylserine on exercise capacity during cycling in active males. Med Sci Sports Exerc. 2006;38:64-71.

11. Kingsley MI, Wadsworth D, Kilduff LP, McEneny J, Benton D. Effects of phosphatidylserine on oxidative stress following intermittent running. Med Sci Sports Exerc. 2005;37(8):1300-6.