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09-05-2017, 11:01 AM | #1 |
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Effects of Prostaglandins and COX Inhibiting Drugs on Skeletal Muscle
Effects of Prostaglandins and COX Inhibiting Drugs on Skeletal Muscle Adaptations to Exercise.
Article · Literature Review · March 2013 with 58 Reads DOI: 10.1152/japplphysiol.00061.2013 · Source: PubMed Todd A Trappe 1st Todd A Trappe Sophia Liu at Ball State University 2nd Sophia Liu 11.81 · Ball State University Abstract It has been ~40 years since the discovery that prostaglandins are produced by exercising skeletal muscle, and since the discovery that inhibition of prostaglandin synthesis is the mechanism of action of what are now known as cyclooxygenase (COX)-inhibiting drugs. Since that time, it has been established that prostaglandins are made during and after aerobic and resistance exercise and have a potent paracrine/autocrine effect on muscle metabolism. Consequently, it has also been determined that orally consumed doses of COX-inhibitors can profoundly influence muscle prostaglandin synthesis, muscle protein metabolism, and numerous other cellular processes that regulate muscle adaptations to exercise loading. Although data from acute human exercise studies, as well as animal and cell culture data would predict regular consumption of a COX-inhibitor during exercise training would dampen the typical muscle adaptations, the chronic data do not support this conjecture. From the studies in young and older individuals lasting from 1.5-4 months, no interfering effects of COX-inhibitors on muscle adaptations to resistance exercise training have been noted. In fact, in older individuals a substantial enhancement of muscle mass and strength has been observed. The collective findings of the prostaglandin/COX pathway regulation of skeletal muscle responses and adaptations to exercise are compelling. Considering the discoveries in other areas of COX regulation of health and disease there is certainly an interesting future of investigation in this re-emerging area, especially as it pertains to older individuals and the condition of sarcopenia, as well as exercise training and performance of individuals of all ages.
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09-05-2017, 11:06 AM | #2 |
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Prostaglandin and myokine involvement in the cyclooxygenase-inhibiting drug enhancement of skeletal muscle adaptations to resistance exercise in older adults
Article · December 2012 with 40 Reads DOI: 10.1152/ajpregu.00245.2012 · Source: PubMed Todd A Trappe 1st Todd A Trappe Robert Standley at Florida Hospital Translational Research Institute for Metabolism and Diabetes 2nd Robert Standley 22.72 · Florida Hospital Translational Research Institute for Metabolism and Diabetes Bozena Jemiolo at Ball State University 3rd Bozena Jemiolo 35.61 · Ball State University Scott W Trappe Last Scott W Trappe Abstract Twelve weeks of resistance training (3d/wk) combined with daily consumption of the cyclooxygenase-inhibiting drugs acetaminophen (4.0g/d; n=11, 64±1y) or ibuprofen (1.2g/d; n=13, 64±1y) unexpectedly promoted muscle mass and strength gains 25-50% above placebo (n=12, 67±2y). To investigate the mechanism of this adaptation, muscle biopsies obtained before and ~72h following the last training bout were analyzed for mRNA levels of prostaglandin (PG)/COX pathway enzymes and receptors (arachidonic acid synthesis: cPLA(2) and sPLA(2); PGF(2α) synthesis: PGF(2α) synthase and PGE(2) to PGF(2α) reductase; PGE(2) synthesis: PGE(2) synthase-1, -2, and -3; PGF(2α) receptor and PGE(2) receptor-4), cytokines and myokines involved in skeletal muscle adaptation (TNF-α, IL-1β, IL-6, IL-8, IL-10), and regulators of muscle growth (myogenin, MRF4, myostatin) and atrophy (FOXO3A, atrogin-1, MuRF-1, IKKβ). Training increased (P<0.05) cPLA(2), PGF(2α) synthase, PGE(2) to PGF(2α) reductase, PGE(2) receptor-4, TNF-α, IL-1β, IL-8, and IKKβ. However, the PGF(2α) receptor was up-regulated (P<0.05) only in the drug groups and the placebo group up-regulation (P<0.05) of IL-6, IL-10, and MuRF-1 was eliminated in both drug groups. These results highlight prostaglandin and myokine involvement in the adaptive response to exercise in older individuals and suggest two mechanisms underlying the enhanced muscle mass gains in the drug groups: 1) The drug-induced PGF(2α) receptor up-regulation helped offset the drug suppression of PGF(2α)-stimulated protein synthesis after each exercise bout, and enhanced skeletal muscle sensitivity to this stimulation. 2) The drug-induced suppression of intramuscular PGE(2) production increased net muscle protein balance after each exercise bout through a reduction in PGE(2)-induced IL-6 and MuRF-1, both promoters of muscle loss.
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09-06-2017, 09:07 AM | #3 |
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so all in all what do these two studies mean ......Tylenol or ibuprphen eat up muscle or no ?
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09-06-2017, 09:22 AM | #4 |
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According to these studies, no. In fact older athletes may actually gain muscle. In this area studies conflict. Myself I use the anti-inflammatory drugs as I need them and never noticed any loss of muscle. lol, every huge guy I know also use them when needed.
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09-07-2017, 12:13 AM | #5 |
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Well there you have it. Just like the egg - they used to be good for you, then they became bad for you, now good for you again haha. What a joke. Fuck all these contradicting studies. I've ate my share of ibuprofen, tylenol, vicodins & percocet and I'd say I got pretty damn big doing so. I'll stick with my theory regarding damn near everything - USE, don't abuse - and you'll be alright.
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