Nutrition & Supps
Anti-Inflammatory = Anti-Hypertrophy?
Non-steroidal anti-inflammatory drugs provide quick relief from muscle aches and pains. But could unwanted side effects lie in store?
By Scott Stevenson, PhD, LAc
Rusted and weathered, you’ve been banging away at the heavy iron for months without a break. Take a break now and progress stalls. Your knees are aching and your bum shoulder is up to its old tricks, but your training cycle doesn’t call for it, so you keep plugging away. Even with ever-worsening muscle soreness, you’re still getting stronger. So, you “man up,” and dig into that bottle of aspirin you keep in your gym bag in hopes of keeping the muscle-building train rollin’ on its tracks.
Or are you just fooling yourself? Deep down, some part of you is wondering, “No pain, no gain, right?” Well, that little voice is asking an awfully good question as it turns out.
Aspirin has been used as a pain killer, fever reducer and non-steroidal anti-inflammatory (NSAID) for centuries in its natural form within white willow bark . It’s main action is inhibiting a particular class of enzyme (cyclooxygenase or COX) and reducing prostaglandin molecules that, among other things, mediate inflammation and pain [2, 3].
The best understood class of prostaglandins come from omega-6 fatty acid arachidonic acid and are typically inflammatory in nature, [3, 4]. Thus, taking an NSAID reduces inflammatory prostaglandin synthesis throughout the entire body, “hitting it where it hurts,” as well as everywhere else prostaglandins are made. Because of this, NSAIDs can cause gastric upset and even risk gastrointestinal bleeding . Because of this, “coxib” drugs were invented to target the COX-2 form of the enzyme (e.g., Celebrex and Vioxx), but reducing the gastrointestinal risks resulted in new cardiovascular side effects . (Prescription-only Celebrex is now the lone COX-2-specific NSAID on the U.S. market for this reason.)
At this point, you might be thinking, “Yeah, OK, but I’ve got an iron gut and good cholesterol, so if it let’s me keep training, is there really that much of an issue if I use an NSAID?” Well, if you like to train purely for the sake of training, muscular gains notwithstanding, this may be a moot issue for you. However, if your gut-wrenching workouts are intended as a trigger for new muscle growth, keep reading.
You see, weight training damages  and inflames  skeletal muscle, which in turn leads to larger fibers. The reconstruction includes a host of intracellular events that are tied to increasing muscle protein synthesis . Basically, taking an NSAID like aspirin after a heavy training bout and can end up derailing that precious muscle-building process [8-14].
Of Mice and Men
In various “long-haul” studies of mice and rats, NSAIDs do indeed impair muscle growth [15-17], and in particular, it’s the inhibition of the COX-2 isoform that’s the culprit [15-21]. However, the opposite is true in people: Celebrex (COX-2 specific) reduces muscle soreness, but does not reduce post-exercise muscle protein turnover  or damage , unlike your typical drug store NSAIDs [11, 12]. But the story is not that simple. A recent study found that taking good old acetaminophen or ibuprofen, daily over 3 months of weight training, actually increased muscle growth and strength gains in untrained older folks . Confused? I don’t blame you. So, what gives?
How Much is Enough?
The confusion could be due to a couple things. By reducing pain and soreness, NSAIDs might let you train harder  and thus make better gains. On the other hand, in some circumstances, NSAIDs could adjust inflammation downward to optimize an otherwise excessive training protocol . Heck, despite how good it may feel (in a masochistic sort of way), one study found that easing into training and avoiding muscle soreness and damage doesn’t slow strength or muscle gains at all , suggesting that crippling muscle pain isn’t mandatory for successful strength training.
Risks and Rewards
So, weight training is obviously pro-inflammatory (and promoting muscle growth), and over the counter NSAIDs oppose this. In some cases, NSAIDs might even be helpful to prevent overstimulation and overtraining. Anecdotally (and I don’t recommend this by the way), I’ve talked to powerlifters and bodybuilders (of the older and crazier variety mostly) who would take NSAIDs so they could train harder and longer, but still “get away with it.” More time under the bar, with less debilitating joint and muscle pain translates, they believe, into greater strength gains.
Aside from the gastrointestinal side effects mentioned above, know also that reducing acute muscle damage with an NSAID (flurbiprofen in particular ) may actually impair muscle function weeks later. Additionally, long-term (3 mo.) daily use of acetaminophen may substantially affect how your tendons adapt to training .
If you’re not quite sure what to do with your aching joints and beat up muscles while waiting for a scientific breakthrough on this matter, it may just be the right time to listen to that little nagging voice in your head, take a break from the heavy training, and heal up a bit.
Scott W. Stevenson, PhD, LAc, is an online bodybuilding coach, exercise physiologist, and licensed acupuncturist residing in Tucson, AZ. He can be reached via www.ScottStevensonPhD.com.
1. P. Rao and E. E. Knaus. Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques, 2008. 11(2): p. 81s.
2. S. Winzeler and B. D. Rosenstein. Aaohn J, 1998. 46(5): p. 253.
3. S. H. Ferreira. British journal of clinical pharmacology, 1980. 10 Suppl 2: p. 237S.
4. P. C. Calder. The American journal of clinical nutrition, 2006. 83(6 Suppl): p. 1505S.
5. R. Tamblyn, et al. Annals of internal medicine, 1997. 127(6): p. 429.
6. H. Kuipers. Int.J Sports Med, 1994. 15: p. 132.
7. T. A. Jarvinen, et al. The American journal of sports medicine, 2005. 33(5): p. 745.
8. B. J. Schoenfeld. Journal of strength and conditioning research / National Strength & Conditioning Association, 2012. 26(5): p. 1441.
9. T. A. Trappe, et al. The Journal of clinical endocrinology and metabolism, 2001. 86(10): p. 5067.
10. J. F. Markworth and D. Cameron-Smith. American journal of physiology. Cell physiology, 2011. 300(3): p. C671.
11. U. R. Mikkelsen, et al. Journal of applied physiology, 2009. 107(5): p. 1600.
12. A. L. Mackey, et al. Journal of applied physiology, 2007. 103(2): p. 425.
13. T. A. Trappe, et al. American journal of physiology. Endocrinology and metabolism, 2002. 282(3): p. E551.
14. H. P. Rodemann and A. L. Goldberg. The Journal of biological chemistry, 1982. 257(4): p. 1632.
15. B. A. Bondesen, et al. American journal of physiology. Cell physiology, 2006. 290(6): p. C1651.
16. Q. A. Soltow, et al. Medicine and science in sports and exercise, 2006. 38(5): p. 840.
17. M. L. Novak, et al. American journal of physiology. Regulatory, integrative and comparative physiology, 2009. 296(4): p. R1132.
18. C. L. Mendias, et al. Muscle & nerve, 2004. 30(4): p. 497.
19. J. S. Otis, et al. Experimental cell research, 2005. 310(2): p. 417.
20. W. Shen, et al. Journal of applied physiology, 2006. 101(4): p. 1215.
21. N. A. Burd, et al. American journal of physiology. Endocrinology and metabolism, 2010. 298(2): p. E354.
22. G. Paulsen, et al. Scandinavian journal of medicine & science in sports, 2010. 20(1): p. e195.
23. T. A. Trappe, et al. American journal of physiology. Regulatory, integrative and comparative physiology, 2011. 300(3): p. R655.
24. M. K. Sohn, et al. Muscle & nerve, 2000. 23(8): p. 1219.
25. D. Slivka, et al. American journal of physiology. Regulatory, integrative and comparative physiology, 2008. 295(1): p. R273.
26. K. L. Flann, et al. The Journal of experimental biology, 2011. 214(Pt 4): p. 674.
27. D. K. Mishra, et al. The Journal of bone and joint surgery. American volume, 1995. 77(10): p. 1510.
28. C. C. Carroll, et al. Journal of applied physiology, 2011. 111(2): p. 508.