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Healthy adult males should have from one to nine nanograms per mL of GH in their blood.

Anti-Inflammation Supps

TJ

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As some of you guys know being sore is actually inflammation. Cherry juice has actually been shown to increase muscle recovery by 20% (If I recall correctly) due to acting as an anti-inflammatory but I didn't want any liquid carbs. I was looking for supplements that could have similar benefits acting as an anti-inflammatory. I came across this supplement and thought some of you may be interested in it not only for it's benefits in muscle recovery but any inflammatory problem we may come across...even heart disease.

More information:
http://www.t-nation.com/readTopic.do?id=910074

To buy:
http://www.t-nation.com/category.jsp?categoryID=34&pageNo=1&s=navStore

Or, for you organic guys, devil's claw is also a good supplement for inflammatory problems.

Information:
http://altmedicine.about.com/od/herbsupplementguide/a/DevilsClaw.htm

To buy:
http://www.physicianformulas.com/store/Scripts/prodview.asp?idproduct=50&name=Devils-Claw
 

tgunz

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pineapple juice is also an excellent PWO anti inflammatory drink
 

Braaq

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Fish Oil an anti-inflammatory, it is the main reason why I take it.
 

Ironslave

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NSAID's, especially post workout, pretty much negate any chance of building muscle. Healthy? No question. Detrimental for putting on muscle? Also no question.
 

jornT

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I agree with IS that NSAIDS (around training) probably whouldn't be a good idea. Negating any chance of building muscle...I think that's a bit over the top.

But anyway, recent research:

http://www.physorg.com/news126711822.html

Taking daily recommended dosages of ibuprofen and acetaminophen caused a substantially greater increase over placebo in the amount of quadriceps muscle mass and muscle strength gained during three months of regular weight lifting, in a study by physiologists at the Human Performance Laboratory, Ball State University.



This was done in 60-78 years old though, less pain --> better training is a likely explanation




The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance
training.
Appl Physiol Nutr Metab. 2008 Jun;33(3):470-5.

High doses of ibuprofen have been shown to inhibit muscle protein synthesis after a bout of resistance exercise. We determined the effect of a moderate dose of ibuprofen (400 mg.d-1) consumed on a daily basis after resistance training on muscle hypertrophy and strength. Twelve males and 6 females (~24 years of age) trained their right and left biceps on alternate days (6 sets of 4-10 repetitions), 5 d.week-1, for 6 weeks. In a counter-balanced, double-blind design, they were randomized to receive 400 mg.d-1 ibuprofen immediately after training their left or right arm, and a placebo after training the opposite arm the following day. Before- and after-training muscle thickness of both biceps was measured using ultrasound and 1 repetition maximum (1 RM) arm curl strength was determined on both arms. Subjects rated their muscle soreness daily. There were time main effects for muscle thickness and strength (p < 0.01). Ibuprofen consumption had no effect on muscle hypertrophy (muscle thickness of biceps for arm receiving ibuprofen: pre 3.63 +/- 0.14, post 3.92 +/- 0.15 cm; and placebo: pre 3.62 +/- 0.15, post 3.90 +/- 0.15 cm) and strength (1 RM of arm receiving ibuprofen: pre 18.6 +/- 2.8, post 23.4 +/- 3.5 kg; and placebo: pre 18.8 +/- 2.8, post 22.8 +/- 3.4 kg). Muscle soreness was elevated during the first week of training only, but was not different between the ibuprofen and placebo arm. We conclude that a moderate dose of ibuprofen ingested after repeated resistance training sessions does not impair muscle hypertrophy or strength and does not affect ratings of muscle soreness.

Haven't looked into this one.
 

Ironslave

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I agree with IS that NSAIDS (around training) probably whouldn't be a good idea. Negating any chance of building muscle...I think that's a bit over the top.

But anyway, recent research:

http://www.physorg.com/news126711822.html

Taking daily recommended dosages of ibuprofen and acetaminophen caused a substantially greater increase over placebo in the amount of quadriceps muscle mass and muscle strength gained during three months of regular weight lifting, in a study by physiologists at the Human Performance Laboratory, Ball State University.

This was done in 60-78 years old though, less pain --> better training is a likely explanation

negating was maybe a bit over the top, but severely limiting it, definitely. But inflamation is a potent trigger of hypertrophic responses, theres no doubt about that.

Here's some science stuff for JornT, and those interested.

T IS GENERALLY AGREED that successful skeletal muscle regeneration following intense exercise or injury is facilitated by the protein synthesis machinery and the recruitment of myogenic stem (satellite) cells. Upstream activation of these processes, however, is poorly understood. A growing body of evidence suggests cyclooxygenase (COX) activity plays an important role, as COX inhibition via nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to blunt load-mediated muscle protein synthesis rates (13). These drugs markedly inhibit COX-mediated synthesis of prostaglandins (12, 14), which may be necessary to initiate the acute increases in muscle protein synthesis following high-intensity muscle contractions and/or injury. In addition, a role for prostaglandins in cardiac muscle hypertrophy via increased protein synthesis has been established (2, 4, 5). While the aforementioned human skeletal muscle studies (12–14) have focused on metabolic responses to acute mechanical overload, recent evidence in the rat model of chronic mechanical overload (synergist ablation) clearly demonstrates that chronic ibuprofen administration blunts the long-term skeletal muscle hypertrophy adaptation (10). This latter finding raises the question of whether COX inhibitors impair in vivo satellite cell recruitment in addition to their established inhibitory effects on muscle protein synthesis. On the basis of evidence in cultured rodent satellite cells (6), inhibition of satellite cell proliferation, differentiation, and/or fusion might be expected with NSAID treatment in humans in vivo; however, this has yet to be evaluated until recently.

The interesting work of Mackey et al. (3) in the Journal of Applied Physiology is the first to demonstrate an impaired satellite cell response with NSAID treatment in humans following exercise. Trained endurance athletes showed a 27% increase in satellite cell number 8 days after a 36-km run, and this response was completely abolished by indomethacin treatment. While indomethacin is a nonselective COX inhibitor, there is evidence that COX-mediated prostaglandin synthesis during muscle regeneration may be preferentially driven by the COX-2 isoform (1). Treatment with a selective COX-2 inhibitor would therefore be a valuable follow-up to Mackey's work.

Skeletal muscle satellite cells are traditionally thought to serve two major purposes in adult muscle: 1) aiding in repair or regeneration following focal myofiber damage (1), and 2) serving as nuclear donors during extensive myofiber growth that appears to be facilitated by myonuclear addition (9). Apart from the novel results regarding satellite cell inhibition by indomethacin, the work of Mackey et al. (3) presents a number of noteworthy findings. First, satellite cell number increased in response to a single endurance exercise bout. As suggested by the authors, the endurance exercise bout appears to have activated some resident satellite cells from quiescence to reenter the cell cycle, leading to proliferation. A major question is "Why?" This mode of exercise is not typically associated with myofiber hypertrophy—certainly not the degree of hypertrophy that is thought to require myonuclear addition to support growth. Furthermore, activation this early (following a single exercise bout) would not likely be needed for myonuclear addition even if the stimulus were more appropriate for hypertrophy (e.g., resistance exercise) since most myofibers have room for expansion before reaching a theoretical myonuclear domain "ceiling" (8, 9). Thus the increased number of satellite cells in this model probably served an alternate purpose.

One logical explanation would be to support regeneration of damaged myofibers following the extensive run. However, this is not supported by the second major finding in this work. Irrespective of NSAID or placebo treatment during the days following the run, the number of regenerating myofibers was negligible and did not differ from baseline (as indicated by 0–0.52% of myofibers positive for embryonic myosin heavy chain and a small and unchanging percentage of myofibers with centrally located nuclei). This is not surprising since the subjects studied were trained endurance athletes, a novel feature of the study. The young (25 yr) trained runners (peak oxygen consumption ~62 ml O2·kg–1·min–1) were studied while preparing for a 36-km race; thus a fair amount of protection against myofiber damage would be expected. Essentially, these athletes were accustomed to the exercise, which is not typical of most human studies of satellite cell activity. If not to support hypertrophy or damage repair/regeneration, why the (albeit modest) increase in satellite cell number? While this intriguing question cannot be answered by the histological data in Mackey et al. (3), the study certainly points to the possibility of a yet-to-be-defined function of resident skeletal muscle satellite cells.

The satellite cell findings highlighted are based strictly on the cells revealed immunohistochemically by a primary antibody against neural cell adhesion molecule (NCAM). This group and others have used NCAM immunoreactivity to identify a population of cells architecturally positioned beneath the basal lamina that are generally presumed to be skeletal muscle satellite cells. However, the ideal marker of satellite cells is a subject of continued debate. An additional strength of this work is the authors' comparative study of NCAM+ cells vs. fetal antigen-1 (FA1)+ cells. While the majority of NCAM+ cells were also FA1+, a fair number of FA1+ cells were found outside of the merosin-labeled basement membrane. While the authors speculate that these FA+ (NCAM–) cells may represent a precursor cell subpopulation of myogenic lineage, it is entirely possible that nonmyogenic cells were labeled by FA1 in addition to the "classic" skeletal muscle satellite cells.

The fact that the increased (NCAM+) satellite cell number was blunted with NSAID treatment, even in the absence of visible myofiber necrosis or detectable increases in regeneration, suggests COX-mediated prostaglandin synthesis may be initiated simply by exercise or, as the authors point out, indomethacin may have influenced the function of other pathways independent of COX/prostaglandin that caused the inhibition. These alternate pathways have received limited attention relative to studies of COX-dependent effects; however, their investigation in exercise models is warranted, particularly since individual NSAIDs have varying influences on cell cycle regulators and transcription factors (11). Overall, the thought-provoking work of Mackey et al. (3) should stimulate further in vitro and in vivo investigations to enhance our understanding of these myogenic cells and the negative influence(s) of specific NSAIDs. Several questions remain regarding the underlying mechanisms of individual drugs, but these human data are an important addition to the mounting evidence that NSAIDs in general may extinguish the fire sparking skeletal muscle adaptations to exercise.

REFERENCES

1. Bondesen BA, Mills ST, Kegley KM, Pavlath GK. The COX-2 pathway is essential during early stages of skeletal muscle regeneration. Am J Physiol Cell Physiol 287: C475–C483, 2004.[Abstract/Free Full Text]
2. Frias MA, Rebsamen MC, Gerber-Wicht C, Lang U. Prostaglandin E2 activates Stat3 in neonatal rat ventricular cardiomyocytes: a role in cardiac hypertrophy. Cardiovasc Res 73: 57–65, 2007.[Abstract/Free Full Text]
3. Mackey AL, Kjaer M, Dandanell Jørgensen S, Mikkelsen KH, Holm L, Døssing S, Kadi F, Koskinen SO, Jensen CH, Schrøder HD, Langberg H. The influence of anti-inflammatory medication on exercise-induced myogenic precursor cell responses in humans. J Appl Physiol In press; doi:10.1152/japplphysiol.00157.2007.
4. Mendez M, LaPointe MC. Trophic effects of the cyclooxygenase-2 product prostaglandin E2 in cardiac myocytes. Hypertension 39: 382–388, 2002.[Abstract/Free Full Text]
5. Mendez M, LaPointe MC. PGE2-induced hypertrophy of cardiac myocytes involves EP4 receptor-dependent activation of p42/44 MAPK and EGFR transactivation. Am J Physiol Heart Circ Physiol 288: H2111–H2117, 2005.[Abstract/Free Full Text]
6. Mendias CL, Tatsumi R, Allen RE. Role of cyclooxygenase-1 and -2 in satellite cell proliferation, differentiation, and fusion. Muscle Nerve 30: 497–500, 2004.[CrossRef][ISI][Medline]
8. O'Connor RS, Pavlath GK. Point: Satellite cell addition is obligatory for skeletal muscle hypertrophy. J Appl Physiol In press; doi:10.1152/ japplphysiol.00101.2007.
9. Petrella JK, Kim JS, Cross JM, Kosek DJ, Bamman MM. Efficacy of myonuclear addition may explain differential myofiber growth among resistance-trained young and older men and women. Am J Physiol Endocrinol Metab 291: E937–E946, 2006.[Abstract/Free Full Text]
10. Soltow QA, Betters JL, Sellman JE, Lira VA, Long JH, Criswell DS. Ibuprofen inhibits skeletal muscle hypertrophy in rats. Med Sci Sports Exerc 38: 840–846, 2006.
11. Tegeder I, Pfeilschifter J, Geisslinger G. Cyclooxygenase-independent actions of cyclooxygenase inhibitors. FASEB J 15: 2057–2072, 2001.[Abstract/Free Full Text]
12. Trappe TA, Fluckey JD, White F, Lambert CP, Evans WJ. Skeletal muscle PGF2{alpha} and PGE2 in response to eccentric resistance exercise: influence of ibuprofen acetaminophen. J Clin Endocrinol Metab 86: 5067–5070, 2001.[Abstract/Free Full Text]
13. Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Am J Physiol Endocrinol Metab 282: E551–E556, 2002.[Abstract/Free Full Text]
14. Weinheimer EM, Jemiolo B, Carroll CC, Harber MP, Haus JM, Burd NA, Lemoine JK, Trappe SW, Trappe TA. Resistance exercise and cyclooxygenase (COX) expression in human skeletal muscle: implications for COX-inhibiting drugs and protein synthesis. Am J Physiol Regul Integr Comp Physiol 292: R2241–R2248, 2007.[Abstract/Free Full Text]
 

jornT

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I'm wondering why nobody posted something like:

ZOMG, what about fish oil!!!??!?!11!!
 

Braaq

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I'm wondering why nobody posted something like:

ZOMG, what about fish oil!!!??!?!11!!

What is wrong with fish oil? In terms of building muscle and weight training, fish oil can be a beneficial supplement.
Many independent studies have shown that a diet supplement of fish oils (eicosapentaenoic acid and docosahexaenoic acid) can result in a significant reduction in morning stiffness and the number of painful joints in rheumatoid arthritis (RA) patients by markedly reducing interleukin-1beta production.
Some RA patients using fish oil supplementation may be able to discontinue NSAIDs without experiencing a flare-up of their disease, according researchers at the Albany Medical College.
For instance, Rheumatoid arthritis is believed to involve an overactivity of certain inflammatory agents derived from arachidonic acid. the main components of fish oils (Eicosapentaenoic acid EPA and docosahexaenoic acid DHA), are known to inhibit the formation of these inflammatory agents. Research has shown that fish oil supplementation is beneficial in alleviating the symptoms of rheumatoid arthritis some other inflammatory diseases.
Long-term supplementation with fish oils can significantly benefit rheumatoid arthritis patients and may lessen their need for NSAID’s and other RA medications.
 

Duality

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What is wrong with fish oil? In terms of building muscle and weight training, fish oil can be a beneficial supplement.
Many independent studies have shown that a diet supplement of fish oils (eicosapentaenoic acid and docosahexaenoic acid) can result in a significant reduction in morning stiffness and the number of painful joints in rheumatoid arthritis (RA) patients by markedly reducing interleukin-1beta production.
Some RA patients using fish oil supplementation may be able to discontinue NSAIDs without experiencing a flare-up of their disease, according researchers at the Albany Medical College.
For instance, Rheumatoid arthritis is believed to involve an overactivity of certain inflammatory agents derived from arachidonic acid. the main components of fish oils (Eicosapentaenoic acid EPA and docosahexaenoic acid DHA), are known to inhibit the formation of these inflammatory agents. Research has shown that fish oil supplementation is beneficial in alleviating the symptoms of rheumatoid arthritis some other inflammatory diseases.
Long-term supplementation with fish oils can significantly benefit rheumatoid arthritis patients and may lessen their need for NSAID’s and other RA medications.


booo mr copy and paste


i experienced a very painful experience in my junior year of highschool that may help. i had always taken 2-3 fish oil softgels daily since i can even remember playing sports or lifting. buy one day my mom didn't buy more when we ran out, so i stopped taking them. didn't think much of it. about 2 weeks later i began experiencing intense (INTENSE) pain in my left elbow. this was so bad it would wake me up at night. it then popped up in the right and i was seriously hating life. i inadvertanly started taking fish oil again once we got more and within another 1.5 weeks, the pain just dissapated. i came to the realization that absolutely had to be the fish oil because i did nothing different besides that. i haven't stopped taking it since and....no pain :xyxthumbs:

seriously it is great stuff fish oil. i would def try it to fix your joint woes before going the glucosamine route.
 

Braaq

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booo mr copy and paste


i experienced a very painful experience in my junior year of highschool that may help. i had always taken 2-3 fish oil softgels daily since i can even remember playing sports or lifting. buy one day my mom didn't buy more when we ran out, so i stopped taking them. didn't think much of it. about 2 weeks later i began experiencing intense (INTENSE) pain in my left elbow. this was so bad it would wake me up at night. it then popped up in the right and i was seriously hating life. i inadvertanly started taking fish oil again once we got more and within another 1.5 weeks, the pain just dissapated. i came to the realization that absolutely had to be the fish oil because i did nothing different besides that. i haven't stopped taking it since and....no pain :xyxthumbs:

seriously it is great stuff fish oil. i would def try it to fix your joint woes before going the glucosamine route.

:dunnodude: I copy and pasted some names, don't have all of em memorized but not the whole thing :no: noob
 

jornT

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What is wrong with fish oil? In terms of building muscle and weight training, fish oil can be a beneficial supplement.
Many independent studies have shown that a diet supplement of fish oils (eicosapentaenoic acid and docosahexaenoic acid) can result in a significant reduction in morning stiffness and the number of painful joints in rheumatoid arthritis (RA) patients by markedly reducing interleukin-1beta production.
Some RA patients using fish oil supplementation may be able to discontinue NSAIDs without experiencing a flare-up of their disease, according researchers at the Albany Medical College.
For instance, Rheumatoid arthritis is believed to involve an overactivity of certain inflammatory agents derived from arachidonic acid. the main components of fish oils (Eicosapentaenoic acid EPA and docosahexaenoic acid DHA), are known to inhibit the formation of these inflammatory agents. Research has shown that fish oil supplementation is beneficial in alleviating the symptoms of rheumatoid arthritis some other inflammatory diseases.
Long-term supplementation with fish oils can significantly benefit rheumatoid arthritis patients and may lessen their need for NSAID’s and other RA medications.

You completly missed the point.
 

Ironslave

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I should have used better judgement with my original post. Yes, fish oils and anti inflams are great for RA and general health (to an extent).

But anti-inflams post workout for a bodybuilder are a poor idea. Do they decrease muscle soreness? Sure, but muscle soreness is in large part a result of the inflammation and sensitizing nociceptors to pain stimulation. This response is a trigger for muscle hypertrophy.
 
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