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I remember related research coming out probably 20 years ago. A good friend of mine from martial arts had a lot of joint issues and we were talking about it after practice. He was a nurse and then eventually a PA. If I recall, I think we concluded that the timing of use was critical. But the best timing was not the best for anti inflammation. You want inflammation to spark recovery but not so much that you have lasting joint pain and swelling.
Personally I used it in combo with naproxen. I used it the morning of training, training in the evening, and about an hour or so after training. It gave relief and I never really saw an issue with tissue growth especially if using AAS. My joints are pretty shit now but what can we expect from heavy lifting for 40 years and 45 grappling on the mat.
My feeling is that AAS made the joint worse probably more than ibuprofen. My joints were always worse after a cycle. -
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Not any better from my understanding. It's also an NSAID. The article states it used ibuprofen in the study merely bcoz it is the most popular/abused NSAID. Point being, inflammation IS needed for utmost growth. But hey you're the guru on all this stuff haha - do you know different?Comment
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I use Nap because it makes my shoulders feel better. I would assume 99% of all pro athletes including bodybuilders use NSAID's at some point in their career's in the real world. Also one study is not science, it's horseshit until it's been duplicated over and over again with the same results by other researchers at different institutions.
ADMIN/OWNER@Peak-MuscleComment
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Here's another one...
Ibuprofen treatment blunts early translational signalling responses in human skeletal muscle following resistance exercise
James F. Markworth , Luke Daniel Vella , Vandré Casagrande Figueiredo , David Cameron-Smith
Journal of Applied PhysiologyPublished 15 May 2014Vol. no. DOI: 10.1152/japplphysiol.01299.2013
ABSTRACT
Cyclooxygenase (COX-1 and 2) pathway derived prostaglandins (PGs) have been implicated in adaptive muscle responses to exercise, but the role of PGs in contraction-induced muscle signalling has not been determined. We investigated the effect of inhibition of COX-1 and 2 activities with the NSAID ibuprofen on human muscle signalling responses to resistance exercise. Subjects orally ingested 1200 mg ibuprofen (or placebo control) in three 400 mg doses administered ~30 min prior to, ~6 h and ~12 h following a bout of unaccustomed resistance exercise (80% 1 RM). Muscle biopsies were obtained at rest (PRE), immediately post (0 h), 3 h post, and at 24 h of recovery. In the placebo group, phosphorylation of ERK1/2 (Thr202/Tyr204), RSK (Ser380), mitogen-activated kinase 1 (Mnk1, Thr197/202), and p70S6Kinase (p70S6K, Thr421/Ser424) increased at both 0 h & 3 h post-exercise, with delayed elevation of p-p70S6K (Thr389) and p-S6 (Ser235/S36 and Ser240/244) at 3 h post. Only p-ERK (Thr202/Tyr204) remained significantly elevated in the 24 h post-exercise biopsy. Ibuprofen treatment prevented sustained elevation of MEK-ERK signalling at 3 h (p-ERK1/2, p-RSK, p-Mnk1, p70S6K Thr421/Ser424) and 24 h (p-ERK1/2) post-exercise and this was associated with supressed phosphorylation of rpS6 (Ser235/236 and Ser240/244). Early contraction induced p-Akt (Ser473) and p-p70S6K (Thr389) were not influenced by ibuprofen , but p-p70S6K (Thr389) remained elevated 24 h post-exercise only in those receiving ibuprofen treatment. Early muscle signalling responses to resistance exercise are, in part, ibuprofen sensitive, suggesting that PGs are important signalling molecules during early post-exercise recovery.Comment
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Here's an interesting one...
Am J Physiol Regul Integr Comp Physiol. 2007 Jun;292(6):R2241-8. Epub 2007 Feb 22.Click here to read Links
Resistance exercise and cyclooxygenase (COX) expression in human skeletal muscle: implications for COX-inhibiting drugs and protein synthesis.
Weinheimer EM, Jemiolo B, Carroll CC, Harber MP, Haus JM, Burd NA, LeMoine JK, Trappe SW, Trappe TA.
Human Performance Laboratory, Ball State University, Muncie, IN 47306, USA.
We have shown that ibuprofen and acetaminophen block cyclooxygenase (COX) synthesis of prostaglandin PGF(2alpha) and the muscle protein synthesis increase following resistance exercise. Confusingly, these two drugs are purported to work through different mechanisms, with acetaminophen apparently unable to block COX and ibuprofen able to nonspecifically block COX-1 and COX-2. A recently discovered intron-retaining COX, now known to have three variants, has been shown to be sensitive to both drugs. We measured the expression patterns and levels of the intron 1-retaining COX-1 variants (-1b1, -1b2, and -1b3), COX-1, and COX-2 at rest and following resistance exercise to help elucidate the COX through which PGF(2alpha), ibuprofen, and acetaminophen regulate muscle protein synthesis. Skeletal muscle biopsy samples were taken from 16 individuals (8M, 8F) before, 4, and 24 h after a bout of resistance exercise and analyzed using real-time RT-PCR. Relatively few individuals expressed the intron 1-retaining COX-1b variants (COX-1b1, -1b2, and -1b3) at any time point, and when expressed, these variants were in very low abundance. COX-1 was the most abundant COX mRNA before exercise and remained unchanged (P > 0.05) following exercise. COX-2 was not expressed before exercise, but increased significantly (P < 0.05) at 4 and 24 h after exercise. The inconsistent and low levels of expression of the intron 1-retaining COX-1 variants suggest that these variants are not likely responsible for the inhibition of PGF(2alpha) production and skeletal muscle protein synthesis after resistance exercise by ibuprofen and acetaminophen. Skeletal muscle-specific inhibition of COX-1 or COX-2 by these drugs should be considered.Comment
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ANother one...
Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E551-6.Click here to read Links
Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis.
Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ.
Donald W. Reynolds Center on Aging, Department of Geriatrics, University of Arkansas for Medical Sciences, and the Central Arkansas Veterans HealthCare System, Little Rock, Arkansas 72205, USA. trappetodda@uams.edu
We examined the effect of two commonly consumed over-the-counter analgesics, ibuprofen and acetaminophen, on muscle protein synthesis and soreness after high-intensity eccentric resistance exercise. Twenty-four males (25 +/- 3 yr, 180 +/- 6 cm, 81 +/- 6 kg, and 17 +/- 8% body fat) were assigned to one of three groups that received either the maximal over-the-counter dose of ibuprofen (IBU; 1,200 mg/day), acetaminophen (ACET; 4,000 mg/day), or a placebo (PLA) after 10-14 sets of 10 eccentric repetitions at 120% of concentric one-repetition maximum with the knee extensors. Postexercise (24 h) skeletal muscle fractional synthesis rate (FSR) was increased 76 +/- 19% (P < 0.05) in PLA (0.058 +/- 0.012%/h) and was unchanged (P > 0.05) in IBU (35 +/- 21%; 0.021 +/- 0.014%/h) and ACET (22 +/- 23%; 0.010 +/- 0.019%/h). Neither drug had any influence on whole body protein breakdown, as measured by rate of phenylalanine appearance, on serum creatine kinase, or on rating of perceived muscle soreness compared with PLA. These results suggest that over-the-counter doses of both ibuprofen and acetaminophen suppress the protein synthesis response in skeletal muscle after eccentric resistance exercise. Thus these two analgesics may work through a common mechanism to influence protein metabolism in skeletal muscle.Comment
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Good reads BMJ thanks. Didn't know tylenol did the same damn.Comment
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Thank you for this. I was not aware. Good stuff.The older I get the better I used to be.Comment
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