http://www.physorg.com/news126711822.html
Ibuprofen or acetaminophen in long-term resistance training increases muscle mass/strength
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.
Anyone have anything to say about this?
The only thing I can say is I hope it's a legitimate thing because it certainly would be nice on those rough days...
Study participants are pretty old...nonetheless interesting. Whats the typical recommended dose for acetaminophen? I was thinking 1-2 grams?
wow
I'd prefer the ibuprofen personally, I actually feel good when I take it, like it makes my mood feel better.
LOX upregulation could be key here,
http://www.mindandmuscle.net/forum/index.php?showtopic=33229
and
http://www.mindandmuscle.net/forum/index.php?showtopic=33229
and
QUOTE
doi:10.1016/j.mce.2006.12.026 How to Cite or Link Using DOI (Opens New Window)
Copyright © 2006 Elsevier Ireland Ltd All rights reserved.
Review
Enzymes involved in arachidonic acid release in adrenal and Leydig cells
P. Malobertia, F. Cornejo Maciela, A.F. Castilloa, R. Castillaa, A. Duartea, M.F. Toledoa, F. Meulia, P. Melea, C. Paza and E.J. PodestáCorresponding Author Contact Information, a, E-mail The Corresponding Author
aDepartment of Biochemistry, School of Medicine, University of Buenos Aires, Paraguay 2155, 5° (C1121ABG), Buenos Aires, Argentina
Available online 5 January 2007.
Abstract
Stimulation of receptors and subsequent signal transduction results in the activation of arachidonic acid (AA) release. Once AA is released from phospholipids or others esters, it may be metabolized via the cycloxygenase or the lipoxygenase pathways. How the cells drive AA to these pathways is not elucidated yet. It is reasonable to speculate that each pathway will have different sources of free AA triggered by different signal transduction pathways. Several reports have shown that AA and its lipoxygenase-catalyzed metabolites play essential roles in the regulation of steroidogenesis by influencing cholesterol transport from the outer to the inner mitochondrial membrane, the rate-limiting step in steroid hormone biosynthesis. Signals that stimulate steroidogenesis also cause the release of AA from phospholipids or other esters by mechanisms that are not fully understood. This review focuses on the enzymes of AA release that impact on steroidogenesis.
Copyright © 2006 Elsevier Ireland Ltd All rights reserved.
Review
Enzymes involved in arachidonic acid release in adrenal and Leydig cells
P. Malobertia, F. Cornejo Maciela, A.F. Castilloa, R. Castillaa, A. Duartea, M.F. Toledoa, F. Meulia, P. Melea, C. Paza and E.J. PodestáCorresponding Author Contact Information, a, E-mail The Corresponding Author
aDepartment of Biochemistry, School of Medicine, University of Buenos Aires, Paraguay 2155, 5° (C1121ABG), Buenos Aires, Argentina
Available online 5 January 2007.
Abstract
Stimulation of receptors and subsequent signal transduction results in the activation of arachidonic acid (AA) release. Once AA is released from phospholipids or others esters, it may be metabolized via the cycloxygenase or the lipoxygenase pathways. How the cells drive AA to these pathways is not elucidated yet. It is reasonable to speculate that each pathway will have different sources of free AA triggered by different signal transduction pathways. Several reports have shown that AA and its lipoxygenase-catalyzed metabolites play essential roles in the regulation of steroidogenesis by influencing cholesterol transport from the outer to the inner mitochondrial membrane, the rate-limiting step in steroid hormone biosynthesis. Signals that stimulate steroidogenesis also cause the release of AA from phospholipids or other esters by mechanisms that are not fully understood. This review focuses on the enzymes of AA release that impact on steroidogenesis.
how about
Inflammatory gene changes associated with the repeated bout effect.
Hubal MJ, Chen TC, Thompson PD, Clarkson PM.
Genetic Medicine, Children's National Medical Center, Washington, District of Columbia, United States; Exercise Science, University of Massachusetts, 110 Totman, Amherst, Massachusetts, 01003, United States.
This study proposed that attenuated expression of inflammatory factors is an underlying mechanism driving the repeated bout effect (rapid adaptation to eccentric exercise). We investigated changes in mRNA levels and protein localization of inflammatory genes following two bouts of muscle lengthening exercise. Seven male subjects performed 2 bouts of lower body exercise (separated by 4 wks) in which one leg (ECC) performed 300 eccentric/concentric actions, and the contralateral leg (CON) performed 300 concentric actions only. Vastus lateralis biopsies were collected at 6h, and strength was assessed at baseline, and 0, 3 and 5d post-exercise. mRNA levels were measured via semi-quantitative RT-PCR for the following genes: CYR61, HSP40, HSP70, IL1R1, TCF8, ZFP36, CEBPD, and MCP-1. Muscle functional adaptation was demonstrated via attenuated strength loss (16% less; p=0.04) at 5d post-bout 2 as compared to bout 1 in the ECC leg. mRNA expression of three of the eight genes tested was significantly elevated in ECC from bout 1 to bout 2: ZFP36 (+3.9-fold), CEBPD (+2.3-fold) and MCP-1 (+2.6-fold), while all eight mRNA levels were unaffected by bout in the CON leg. Immunohistochemistry further localized the protein of one of the elevated factors (MCP-1) within the tissue. MCP-1 co-localized with resident macrophage and satellite cell populations, suggesting that alterations in cytokine signaling between these cell populations may play a role in muscle adaptation to exercise. Contrary to our hypothesis, several inflammatory genes were transcriptionally upregulated (rather than attenuated) after a repeated exercise bout, potentially indicating a role for these genes in the adaptation process. Key words: muscle damage, adaptation, MCP-1.
Inflammatory gene changes associated with the repeated bout effect.
Hubal MJ, Chen TC, Thompson PD, Clarkson PM.
Genetic Medicine, Children's National Medical Center, Washington, District of Columbia, United States; Exercise Science, University of Massachusetts, 110 Totman, Amherst, Massachusetts, 01003, United States.
This study proposed that attenuated expression of inflammatory factors is an underlying mechanism driving the repeated bout effect (rapid adaptation to eccentric exercise). We investigated changes in mRNA levels and protein localization of inflammatory genes following two bouts of muscle lengthening exercise. Seven male subjects performed 2 bouts of lower body exercise (separated by 4 wks) in which one leg (ECC) performed 300 eccentric/concentric actions, and the contralateral leg (CON) performed 300 concentric actions only. Vastus lateralis biopsies were collected at 6h, and strength was assessed at baseline, and 0, 3 and 5d post-exercise. mRNA levels were measured via semi-quantitative RT-PCR for the following genes: CYR61, HSP40, HSP70, IL1R1, TCF8, ZFP36, CEBPD, and MCP-1. Muscle functional adaptation was demonstrated via attenuated strength loss (16% less; p=0.04) at 5d post-bout 2 as compared to bout 1 in the ECC leg. mRNA expression of three of the eight genes tested was significantly elevated in ECC from bout 1 to bout 2: ZFP36 (+3.9-fold), CEBPD (+2.3-fold) and MCP-1 (+2.6-fold), while all eight mRNA levels were unaffected by bout in the CON leg. Immunohistochemistry further localized the protein of one of the elevated factors (MCP-1) within the tissue. MCP-1 co-localized with resident macrophage and satellite cell populations, suggesting that alterations in cytokine signaling between these cell populations may play a role in muscle adaptation to exercise. Contrary to our hypothesis, several inflammatory genes were transcriptionally upregulated (rather than attenuated) after a repeated exercise bout, potentially indicating a role for these genes in the adaptation process. Key words: muscle damage, adaptation, MCP-1.
I stand on the middle on this one. Common wisdom leads me to believe that as anti-inflammatory medication they may affect anabolism to some degree. I also remember an article that mentioned NSAIDs impair ability to recover from muscle injuries (really?) and actually negatively affect muscle strength.
On the other hand, in the real world, I see plenty of athletes every day taking NSAID at will and having absolutely no problems with strength or muscle mass.
On the other hand, in the real world, I see plenty of athletes every day taking NSAID at will and having absolutely no problems with strength or muscle mass.
At his place, LyleMcD has thrown out the idea that maybe the old folks just have too much inflammation in the first place, thus lowering it is good.
It is important to note that acetaminophen has an entirely different method of action than ibuprofen. In fact, acetaminophen isnt even an NSAID. Mostly its a pro-cannabinoid drug.
One (partial) explanation may be the fact NSAIDs inhibit aromatase to some degree. Though I sincerely doubt that explains the bulk of this...
QUOTE
An earlier study from the laboratory, measuring muscle metabolism (or more precisely, muscle protein synthesis, the mechanism through which new protein is added to muscle), had looked at changes over a 24 hour period. This “acute” study found that both ibuprofen and acetaminophen had a negative impact, by blocking a specific enzyme cyclooxygenase, commonly referred to as COX.
But that study looked at only one day. Over three months, says Dr. Trappe, the chronic consumption of ibuprofen or acetaminophen during resistance training appears to have induced intramuscular changes that enhance the metabolic response to resistance exercise, allowing the body to add substantially more new protein to muscle.
But that study looked at only one day. Over three months, says Dr. Trappe, the chronic consumption of ibuprofen or acetaminophen during resistance training appears to have induced intramuscular changes that enhance the metabolic response to resistance exercise, allowing the body to add substantially more new protein to muscle.
Perhaps this is the case where the bodies adaptation to the substance overshoots the inhibition. Think of how drugs like Triacana work. It's a thyroid drug that will temporarily increase thyroid, but within days will suppress thyroid and is used medically for the purpsoe of thyroid suppression. Or 6-oxo. It's an anti-estrogen, but the body adapts to it by increasing testosterone to such an extent that estrogen is unaffected.
experimentation time. I wonder why no mention of immune sides was mentioned. after straight days on nsaids I start getting a sore throat or tooth infection
Wouldnt those doses screw with your liver enough over time to not be worth the extra bump in muscle?
I am less interested in it for actually taking the doses they used, and more that it means low-dose nsaid can be used for other reasons and not fuck with progress at the gym.
QUOTE (Kellyb @ Apr 7 2008, 05:21 PM) 
Perhaps this is the case where the bodies adaptation to the substance overshoots the inhibition. Think of how drugs like Triacana work. It's a thyroid drug that will temporarily increase thyroid, but within days will suppress thyroid and is used medically for the purpsoe of thyroid suppression. Or 6-oxo. It's an anti-estrogen, but the body adapts to it by increasing testosterone to such an extent that estrogen is unaffected.
I think this is unlikely. The ibuprofen/aceto groups still should have been weaker than the placebo group.
Muscle mass increase seems to have at least two different pathways. So, perhaps blocking one path was causing the other path to be expressed more??
I want to know the specifics of exercise protocol that was used, as well as additional details related to measurements of muscle mass.
I want to know the specifics of exercise protocol that was used, as well as additional details related to measurements of muscle mass.
QUOTE (eclypz @ Apr 6 2008, 11:36 PM)
I'd prefer the ibuprofen personally, I actually feel good when I take it, like it makes my mood feel better.
Yeah me too!
This "study" bothered me and I doubt we'll ever see it make it to peer reviewed journal. Then again, I have seen worse.
QUOTE (Deserusan)
I'd like to see the actual study including exercise protocol, caloric intake, etc. What concerns me about "reports" like this is that they aren't peer reviewed or accepted for publications. It created a buzz in the medical community and probably support from OTC pharma hence the reason it was released in a sensationalistic manner.
NSAID's which are indiscriminant to either the COX I or COX II pathway can cause numerous pathogolies related to the GI tract, kidneys, and the circulatory system. Even the "next gen" COX-2 selective inhibitors were shown to double the risk of heart attacks. Saying these help build muscle when they most likely gave these to untrained elderly who most likely have elevated inflammatory markers due to age alone is terribly disgusting. Talk about a "doctored" study.
Don't get me wrong, there is a time and place for OTC NSAID's like Advil and Tylenol. However, those who are taking them chronically are fools and the people responsible for publishing this article should have their heads examined or at least their medical licenses revoked. You'll notice that no relevant clinical safety markers were addressed in this press release. I'd love to see how their kidney's were functioning or if they did before and after endoscopy to check for any uclers that may have developed.
What's sad is the FDA lets claims like this go unchecked but a supplement manufacturer can't say fish oil will help in certain areas of clinically diagnosed depression despite hundreds of studies to supporting this non-prescription approach to treatment. They seem more concerned with corporate profitability than truly what is best for the American people. Anyone remember Vioxx or Fen-Phen? Those worked out well until over 150,000 product liability cases were filed and the list keeps growing. The next "study" we'll see published is that cigarettes are great for weight loss. It's true and they really are, especially when they give you cancer or when you are on a calorie restricted diet while on a ventilator.
NSAID's which are indiscriminant to either the COX I or COX II pathway can cause numerous pathogolies related to the GI tract, kidneys, and the circulatory system. Even the "next gen" COX-2 selective inhibitors were shown to double the risk of heart attacks. Saying these help build muscle when they most likely gave these to untrained elderly who most likely have elevated inflammatory markers due to age alone is terribly disgusting. Talk about a "doctored" study.
Don't get me wrong, there is a time and place for OTC NSAID's like Advil and Tylenol. However, those who are taking them chronically are fools and the people responsible for publishing this article should have their heads examined or at least their medical licenses revoked. You'll notice that no relevant clinical safety markers were addressed in this press release. I'd love to see how their kidney's were functioning or if they did before and after endoscopy to check for any uclers that may have developed.
What's sad is the FDA lets claims like this go unchecked but a supplement manufacturer can't say fish oil will help in certain areas of clinically diagnosed depression despite hundreds of studies to supporting this non-prescription approach to treatment. They seem more concerned with corporate profitability than truly what is best for the American people. Anyone remember Vioxx or Fen-Phen? Those worked out well until over 150,000 product liability cases were filed and the list keeps growing. The next "study" we'll see published is that cigarettes are great for weight loss. It's true and they really are, especially when they give you cancer or when you are on a calorie restricted diet while on a ventilator.
QUOTE (Deserusan @ Apr 9 2008, 01:58 AM)
This "study" bothered me and I doubt we'll ever see it make it to peer reviewed journal. Then again, I have seen worse.
you're just jealous.
TYLENOL IS NOT AN NSAID
QUOTE (eclypz @ Apr 9 2008, 11:22 AM)
you're just jealous.
I prefer opiates for pain. NSAID's are weak sauce when you think about how fun it is to drool.
QUOTE (Mr.Kite @ Apr 9 2008, 11:27 PM)
TYLENOL IS NOT AN NSAID
You are right and I wrote that little piece in haste. Still acetaminophen is one of the leading causes of acute liver failure and has been tied to renal cancer, etc. I saw that there are over 56,000 ER visits each year from it's abuse and over 100 people die annually from it.
Thought about this more ...
Is it possible that ibuprofen is lowering overall inflammatory response, which allows the body to use more energy for muscle accrual?
If that were the case, it should not matter when the volunteers took ibuprofen.
Is it possible that ibuprofen is lowering overall inflammatory response, which allows the body to use more energy for muscle accrual?
If that were the case, it should not matter when the volunteers took ibuprofen.
I suspect you guys are overthinking this. The study participants were elderly, all over 60.
I think the likely MOA here is that they could more comfortably lift more weight and so whatever inhibitory effect the drugs have on protein synthesis was overshadowed by the improved ability to add progressive overload.
I think the likely MOA here is that they could more comfortably lift more weight and so whatever inhibitory effect the drugs have on protein synthesis was overshadowed by the improved ability to add progressive overload.
QUOTE (Benson @ Apr 11 2008, 02:09 AM)
I suspect you guys are overthinking this. The study participants were elderly, all over 60.
I think the likely MOA here is that they could more comfortably lift more weight and so whatever inhibitory effect the drugs have on protein synthesis was overshadowed by the improved ability to add progressive overload.
I think the likely MOA here is that they could more comfortably lift more weight and so whatever inhibitory effect the drugs have on protein synthesis was overshadowed by the improved ability to add progressive overload.
i suspect the same. also, one of the negative studies (i don't know how many there are, but it was posted in the thread on lyle's board) used an entire day's recommended maximum dosage immediately after exercise. this latest study dose not use one huge timed dose. rather, the participants were taking the products as directed on the bottle. that spreads the dosage out over a much longer period and maybe even implies that they took it as needed, not the maximum every day.
QUOTE (Proton Soup @ Apr 11 2008, 11:13 AM)
i suspect the same. also, one of the negative studies (i don't know how many there are, but it was posted in the thread on lyle's board) used an entire day's recommended maximum dosage immediately after exercise. this latest study dose not use one huge timed dose. rather, the participants were taking the products as directed on the bottle. that spreads the dosage out over a much longer period and maybe even implies that they took it as needed, not the maximum every day.
+1
It'd be nice to see a study done on younger people.
I suspect the elder people were also more inflamed, had higher levels of inflammation markers etc.
But consider this. There are a lot of people in their thirties that are walking around inflamed and probably aren't aware of it. With the food, stress, lifestyles of a lot of people there's probably a great deal of inflammation that could be remedied with a half-dose of ibuprofen in the afternoon for instance.
I suspect the elder people were also more inflamed, had higher levels of inflammation markers etc.
But consider this. There are a lot of people in their thirties that are walking around inflamed and probably aren't aware of it. With the food, stress, lifestyles of a lot of people there's probably a great deal of inflammation that could be remedied with a half-dose of ibuprofen in the afternoon for instance.
QUOTE (Proton Soup @ Apr 11 2008, 02:13 PM)
i suspect the same. also, one of the negative studies (i don't know how many there are, but it was posted in the thread on lyle's board) used an entire day's recommended maximum dosage immediately after exercise. this latest study dose not use one huge timed dose. rather, the participants were taking the products as directed on the bottle. that spreads the dosage out over a much longer period and maybe even implies that they took it as needed, not the maximum every day.
Doesn't what you just posted goes AGAINST Benson's explanation?
QUOTE (virtualcyber @ Apr 13 2008, 05:19 AM)
Doesn't what you just posted goes AGAINST Benson's explanation?
how so?
QUOTE (Proton Soup @ Apr 13 2008, 02:20 PM)
how so?
What Benson said was that ibu/aceto allowed the participant to exercise better, due to comfort provided by ibu/aceto. If that were true, then, using one huge timed dose close to the time of exercise should have worked much better than spreading ibu/aceto over the day. I thought (?) what you described was the opposite of that ...
If we could just see the loading schemes / actual work volume completed by each group, that would answer a lot.
Ibuprofen and acetaminophen promote muscle hypertrophy and strength gains during resistance exercise in the elderly
Chad C Carroll, Jared M Dickinson, Jennifer K LeMoine, Jacob M Haus, Eileen M Weinheimer, Christopher J Hollon and Todd A Trappe
Human Performance Laboratory, Ball State University, Muncie, IN
ABSTRACT
This study examined the influence of chronic consumption of ibuprofen or acetaminophen during 12 weeks of knee-extensor resistance training (3d/wk, 70% 1RM) in the elderly. Thirty-six individuals were randomly assigned to one of three groups and consumed the drugs in double-blind placebo-controlled fashion: Placebo (67±2 y; 8M, 4F), Ibuprofen (64±1 y; 9M, 4F; 1.2g/d), or Acetaminophen (64±1 y; 7M, 4F; 4g/d). Resistance training alone (Placebo) increased (p<0.05) quadriceps muscle volume (M only: 8±2%; M+F: 9±1%) and muscle strength (M only: 20±3%; M+F: 23±2%). Compared to Placebo, muscle volume increases were greater in the Ibuprofen (M only: 11±2%, p<0.05; M+F: 11±2%, p=0.06) and Acetaminophen (M only: 13±1%, p<0.05; M+F: 13±1%, p=0.06) groups. Muscle strength increases were also greater than Placebo in the Ibuprofen (M only: 29±4%, p<0.05; M+F: 30±3%, p=0.06) and Acetaminophen (M only: 26±3%, p<0.05; M+F: 28±3%, p=0.06) groups. These results suggest that chronic consumption of ibuprofen or acetaminophen during resistance training induces intramuscular changes that enhance the metabolic response to resistance exercise, which promotes additional muscle hypertrophy and strength gains during resistance training in the elderly.
NIH R01 AG020532 (TT), APS Postdoctoral Initiative Award (CC)
Chad C Carroll, Jared M Dickinson, Jennifer K LeMoine, Jacob M Haus, Eileen M Weinheimer, Christopher J Hollon and Todd A Trappe
Human Performance Laboratory, Ball State University, Muncie, IN
ABSTRACT
This study examined the influence of chronic consumption of ibuprofen or acetaminophen during 12 weeks of knee-extensor resistance training (3d/wk, 70% 1RM) in the elderly. Thirty-six individuals were randomly assigned to one of three groups and consumed the drugs in double-blind placebo-controlled fashion: Placebo (67±2 y; 8M, 4F), Ibuprofen (64±1 y; 9M, 4F; 1.2g/d), or Acetaminophen (64±1 y; 7M, 4F; 4g/d). Resistance training alone (Placebo) increased (p<0.05) quadriceps muscle volume (M only: 8±2%; M+F: 9±1%) and muscle strength (M only: 20±3%; M+F: 23±2%). Compared to Placebo, muscle volume increases were greater in the Ibuprofen (M only: 11±2%, p<0.05; M+F: 11±2%, p=0.06) and Acetaminophen (M only: 13±1%, p<0.05; M+F: 13±1%, p=0.06) groups. Muscle strength increases were also greater than Placebo in the Ibuprofen (M only: 29±4%, p<0.05; M+F: 30±3%, p=0.06) and Acetaminophen (M only: 26±3%, p<0.05; M+F: 28±3%, p=0.06) groups. These results suggest that chronic consumption of ibuprofen or acetaminophen during resistance training induces intramuscular changes that enhance the metabolic response to resistance exercise, which promotes additional muscle hypertrophy and strength gains during resistance training in the elderly.
NIH R01 AG020532 (TT), APS Postdoctoral Initiative Award (CC)
QUOTE (virtualcyber @ Apr 13 2008, 12:41 PM)
What Benson said was that ibu/aceto allowed the participant to exercise better, due to comfort provided by ibu/aceto. If that were true, then, using one huge timed dose close to the time of exercise should have worked much better than spreading ibu/aceto over the day. I thought (?) what you described was the opposite of that ...
here's the reason for the new study, one acute large dose taken after the exercise sets blocks protein synthesis.
QUOTE
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.
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.
QUOTE (Proton Soup @ Apr 13 2008, 10:28 PM)
here's the reason for the new study, one acute large dose taken after the exercise sets blocks protein synthesis.
Gotcha.
I suppose the best strategy is not to take ibu/aceto around exercise, but take it during other times.
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