ibuprofen painkillers effect on muscle development

[zepata]

hi i was curious as to whether some over the counter/under the counter drugs have an effect on muscle development or maybe even cause a loss of some muscle.. in particular i was wondering about ibuprofen and even oxycodone, i was given both for a back problem i've been having, i can still lift in other areas, i just was wondering their effects on muscles. Thanks.

[bradley]

Originally posted by zepata
hi i was curious as to whether some over the counter/under the counter drugs have an effect on muscle development or maybe even cause a loss of some muscle.. in particular i was wondering about ibuprofen and even oxycodone, i was given both for a back problem i've been having, i can still lift in other areas, i just was wondering their effects on muscles. Thanks.

***Here are a couple of abstracts relating the effects of NSAIDs on protein syntheisis.

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.


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Skeletal muscle PGF(2)(alpha) and PGE(2) in response to eccentric resistance exercise: influence of ibuprofen acetaminophen.

Trappe TA, Fluckey JD, White F, Lambert CP, Evans WJ.

Nutrition, Metabolism, and Exercise Laboratory, Donald W. Reynolds Center on Aging, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA. trappetodda@uams.edu

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.

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***This review is relating the use of opiates and a decrease in testosterone and LH.

Effects of exogenous and endogenous opiates on the hypothalamic--pituitary--gonadal axis in the male.

Cicero TJ.

Narcotics acutely depress serum testosterone levels in the male. Three mechanisms could be involved: an enhancement of the degradation of testosterone; a direct inhibition of testicular steroidogenesis; or, finally, an inhibition of the hypothalamic-pituitary-luteinizing hormone (LH) axis resulting in a reduction in LH-dependent testicular steroidogenesis. The currently available evidence indicates that narcotics do not affect the catabolism of testosterone by the liver or testicular steroidogenesis. Rather, the data favor a direct action on the hypothalamic--pituitary--LH axis, probably by inhibiting the secretion of LH-releasing hormone (LH-RH) from the hypothalamus. The effects of narcotics on serum LH appear to be mediated via specific opioid receptors, suggesting that a naturally occurring opioid-like substance exists that normally inhibits LH. In support of this conclusion, opiate receptor blockers markedly increase serum LH levels shortly after their subcutaneous administration. In addition, endogenous opioids also seem to participate in testosterone's negative feedback control of the hypothalamic--pituitary--LH axis. Thus, it appears that opiate drugs inhibit the function of the hypothalamic-pituitary-gonadal axis by occupying opiate receptors in the hypothalamus and, moreover, that endogenous opioids exist that normally bind to these receptors and regulate activity in this axis.

[AllUp]

What do you mean? what are you trying to say? what are you telling me? what does it all mean?? -Caveman Lawyer :P

Thx Bradley, I always wanted to know if those Pkillers had an effect on Prot synthesis/Muscle growth. I used to always think to myself "Maybe you shouldnt take anything despite the pain, You could be gimping yourself HC." :D

-AllUp

[zepata]

thanks for response bradley, im assuming that this doesnt include aspirin then? would protein synthesis still be hindered using that? thanks.

[bradley]

Originally posted by zepata
thanks for response bradley, im assuming that this doesnt include aspirin then? would protein synthesis still be hindered using that? thanks.

This would hold true for aspirin, which is a NSAID, due to the effect that aspirin has on prostaglandins.

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Prostaglandin F2 stimulates growth of skeletal muscle cells via an NFATC2-dependent pathway

Valerie Horsley1,2 and Grace K. Pavlath2
1 Graduate Program in Biochemistry, Cell and Developmental Biology
2 Department of Pharmacology, Emory University, Atlanta, GA 30322

Address correspondence to Grace Pavlath, Emory University School of Medicine, Dept. of Pharmacology, Room 5027, O.W. Rollins Research Building, Atlanta, GA 30322. Tel.: (404) 727-3353. Fax: (404) 727-0365. E-mail: gpavlat@emory.edu

Skeletal muscle growth requires multiple steps to form large multinucleated muscle cells. Molecules that stimulate muscle growth may be therapeutic for muscle loss associated with aging, injury, or disease. However, few factors are known to increase muscle cell size. We demonstrate that prostaglandin F2 (PGF2) as well as two analogues augment muscle cell size in vitro. This increased myotube size is not due to PGF2-enhancing cell fusion that initially forms myotubes, but rather to PGF2 recruiting the fusion of cells with preexisting multinucleated cells. This growth is mediated through the PGF2 receptor (FP receptor). As the FP receptor can increase levels of intracellular calcium, the involvement of the calcium-regulated transcription factor nuclear factor of activated T cells (NFAT) in mediating PGF2-enhanced cell growth was examined. We show that NFAT is activated by PGF2, and the isoform NFATC2 is required for PGF2-induced muscle cell growth and nuclear accretion, demonstrating the first intersection between prostaglandin receptor activation and NFAT signaling. Given this novel role for PGF2 in skeletal muscle cell growth, these studies raise caution that extended use of drugs that inhibit PG production, such as nonsteroidal antiinflammatory drugs, may be deleterious for muscle growth.

[BUFF STUFF]

uh oh

you got bradleys reports on yo ass


tuttut



these studies raise caution that extended use of drugs that inhibit PG production, such as nonsteroidal antiinflammatory drugs, may be deleterious for muscle growth.

[DelveyBoy]

i dont know,but my stomach is ****ed after taking ibuprofen