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  1. #1
    Eazy20's Avatar
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    Effects of prescription narcotics and muscle growth

    Hey guys, I get prescribed 7.5mg Percocets for chronic pain in my leg from a bad break of my tib/fib a couple years back. I don't take them regularly, maybe a couple of times a week when I really need them. I was just curious if there are any studies that correlate narcotic use and hindering muscle growth?

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    Ive got a study somewhere related to pain killers limiting the rise in protein synthesis which in turn will affect muscle growth and repair.

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    Hydrocodone and oxycodone are both known for lowering testosterone as a side effect. I have a vicodin perscription for my post concussion syndrome migranes but I try to take as little as possible since i'm currently on PCT

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    Quote Originally Posted by marcus300;561***9
    Ive got a study somewhere related to pain killers limiting the rise in protein synthesis which in turn will affect muscle growth and repair.
    Were the doses on the study that of which would be considered abuse? Or typical dosaging? Like I said, I only take them when I really need them. If I averaged it out I would say it would be even less than a couple of times a week. I'm the type of person that grits my teeth until I can't take it anymore before resorting to pain killers. I was just curious if having to pop one every once in awhile was hurting my gains.

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    Quote Originally Posted by scotty51312 View Post
    Hydrocodone and oxycodone are both known for lowering testosterone as a side effect. I have a vicodin perscription for my post concussion syndrome migranes but I try to take as little as possible since i'm currently on PCT
    I read somewhere that it wasn't the actual script drug, but the acetaminophen that does this, but even still it had to be a fairly high amount. I know vicodin tends to have a relatively large amount of acetaminophen in it...I think my script only has about 300mg/pill...When I was on vicodin it was something like 500mg/pill of acetaminophen

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    I believe this article will answer all of your questions, so knock yourself out:

    http://www.thefactsaboutfitness.com/...ainkillers.htm

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  8. #8
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    Some interesting reading material here, even though they used vicoprofen (hydrocodone/ibuprofen) The concept is the same there are studies showing all opiods are catabolic in nature

    Cytokine, growth factor, and hormonal responses following eccentric exercise-induced muscle damage: Influence of hydrocodone bitartrate and ibuprofen administration
    James Stoppani, University of Connecticut


    Abstract
    Exercise-induced muscle damage is associated with inflammatory and regenerative phases that are modulated by the interaction between inflammatory cytokines (namely IL-1β, IL-6, TNF-α), growth factors (IGF-I, IGFBP-1, IGFBP-3), and anabolic hormones (GH, testosterone ). Administration of NSAID and opioids is a common practice following muscular injury. While this practice is believed to be an adjunct to the healing process it may be detrimental to muscle regeneration through alterations in the inflammatory and endocrine responses. Therefore, the purpose of this investigation was twofold: (1) to observe the responses of circulating IL-1β, IL-6, TNF-α, IGF-I, IGFBP-1, IGFBP-3, GH, and testosterone following eccentric exercise-induced muscle damage (EX), and (2) to investigate the effects of ibuprofen and vicoprofen on these circulating factors following EX. Forty-two male subjects performed 100 eccentric contractions (10 sets of 10 repetitions) of the dominant quadriceps muscle group using 120% of their 1RM on an isotonic leg extension machine. Blood samples were measured immediately before (Pre), midway through (Mid), immediately following (IP), 15min, 30min, 1h, 2h, 4h, 6h, 24h, 48h, 72h, 96h, and 120h following EX. Subjects were randomly placed in either group: (a) placebo, (b) vicoprofen, or (c) ibuprofen, in a double blind manner. Following EX, significant increases were observed for circulating concentrations of GH (266%, at IP, p < .003), IGFBP-1 (40% at 24 h, p < .0002), and IL-6 (78% at 6 h, p < .0000) as compared to resting values. The vicoprofen group demonstrated significantly higher and lower concentrations of IGFBP-1 and testosterone, respectively, by day 5 as compared to the placebo group (IGFBP-1, p < .03; testosterone, p < .04) and the ibuprofen group (IGFBP-1, p < .05; testosterone, p < .05). The most significant finding from this study was the increased serum IGFBP-1 concentration 24 hours after EX. These data suggest that the primary response following exercise-induced muscle damage is catabolic in nature. While this response appears to be detrimental to the myoregenerative process, it may be required for complete muscle fiber regeneration. The drug intervention data indicated that vicoprofen administration induced a catabolic state during the 5d recovery period from EX. These results suggest that opioids; may interfere with normal muscle regeneration following exercise-induced muscle damage through alterations in the endocrine and inflammatory responses.





    Heres another even though the opiods were spinal i dont' believe the adminsration really matters

    Clinical note
    Altered sexual function and decreased testosterone in patients receiving intraspinal opioids
    Purchase
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    References and further reading may be available for this article. To view references and further reading you must purchase this article.


    Judith A. Pake PhD, a, Richard D. Penn MDa and Will G. Ryan MDb

    a Department of Neurosurgery, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA

    b Department of Endocrinology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA

    Accepted 16 September 1993. Available online 28 April 2004.

    Abstract
    Altered sexual function has been reported in individuals addicted to opioids or on methadone maintenance, yet little literature is available regarding the effect of intraspinal opioids on libido or sex hormone levels. We evaluated sexual function and plasma sex hormone levels in six men treated with chronic intraspinal opioids. All patients had some reduction in libido and four patients had difficulty obtaining or maintaining an erection. These changes were noted within 1 month of beginning intraspinal opioid therapy. Serum testosterone levels ranged from 26 to 367 ng/dL (normal, 350–1500 ng/dL); the mean serum level was 197.7 ng/dL (SD = 119.8). Serum testosterone levels and other sex hormones, including follicle-stimulating hormone, luteinizing hormone, sex-hormone-binding globulin, and prolactin, should be measured prior to and at various points during intraspinal opioid therapy. Patients should be queried regarding sexual function and should be cautioned regarding the possibility of these adverse effects prior to initiating spinal opioids. Supplemental testosterone should be considered to treat this dysfunction.
    Last edited by scotty51312; 04-26-2011 at 01:35 PM.

  9. #9
    Eazy20's Avatar
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    Quote Originally Posted by Turkish Juicer View Post
    I believe this article will answer all of your questions, so knock yourself out:

    http://www.thefactsaboutfitness.com/...ainkillers.htm
    Perfect. Just as I read. It's the NSAIDs and not the actual script that hinders muscle growth, and even still it's at fairly high doses taken regularly. So what I take shouldn't be hurting me; at least nothing close to substantial anyway

  10. #10
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    Its the opiods as well. but knock yourself out

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    Quote Originally Posted by scotty51312 View Post
    Its the opiods as well. but knock yourself out
    My main issue with the study you posted was that doses were not mentioned...For all I know they could be taking a much higher dose than I take not to mention my use is on a need-only basis it is FAR from a regular protocol. I mean I have no doubt that to some degree or another it will hinder, but I'm figuring that at how I take the medication, it's affecting me very minimally.

  12. #12
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    Not trying to disuade you when the pain gets bad enough I take them as well, i think the key is doing it only when needed. Lots of people with chronic pain take them to avoid pain before they even feel it. I'll research this subject more out of my own curiosity and see if i can find any dose related studies or med logs

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    Quote Originally Posted by marcus300 View Post
    Great read Marcus, thanks.

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    Quote Originally Posted by scotty51312 View Post
    Not trying to disuade you when the pain gets bad enough I take them as well, i think the key is doing it only when needed. Lots of people with chronic pain take them to avoid pain before they even feel it. I'll research this subject more out of my own curiosity and see if i can find any dose related studies or med logs
    Exactly what I do. There are some weeks I won't hit legs just so I don't have to take the damn meds...I hate taking pain pills, but there comes a time every once in awhile where I just can't grit my teeth anymore and have to give in.

  15. #15
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    Just found this if anyone is interested:

    We determined the dose-dependent effects of central mu-opioid receptor stimulation on rates of tissue protein synthesis. Chronically catheterized conscious rats received an intracerebroventricular injection of [D-Ala2, N-Me-Phe4,Gly5-ol]enkephalin (DAGO, 0.5, 2, or 8 nmol/rat) or water (5 microliters) 45 min before determination of protein synthesis by the flooding dose technique. DAGO produced a significant decrease in tissue protein synthesis in liver (57%), spleen (54%), gut mucosa (36%), gut serosa (23%), kidney (48%), gastrocnemius (33%), and plantaris muscle (27%), but it did not alter rates of protein synthesis in the brain, heart, and soleus muscle. DAGO produced an acute dose-dependent respiratory depression 30 min after intracerebroventricular injection; this depression resulted in acidosis, hypoxia, and hypercapnia (pH 7.19 +/- 0.04, arterial partial O2, pressure 44.2 +/- 3.4 Torr, arterial O2 saturation 65.3 +/- 5.5%, and PCO2 66.3 +/- 4.4 Torr). Intracerebroventricular DAGO increased circulating levels of catecholamines, corticosterone, and growth hormone but did not alter those of insulin and insulin-like growth factor I. Significant positive correlations between protein synthesis and pH were observed in the tissues studied (i.e., liver protein synthesis vs. pH, P < 0.0001, r = 0.902; gastrocnemius protein synthesis vs. pH, P < 0.0001, r = 0.830). Our results indicate that mu-receptor stimulation inhibits tissue protein synthesis, and this effect appears to be secondary to respiratory depression and the resulting acidosis and/or hypoxia. Furthermore, our findings suggest differential sensitivity in tissue response to alterations in pH, hypoxia, and stress hormone elevation.

    So, it would appear that opiods do effect protein synthesis due to the respiratory depression and acidosis and/or hypoxia they cause.

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