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Ibuprofen = Muscle Tears?

Hey guys just had a quick question. I got a little injury on my hand and ankle…nothing big at all…but I am prescribed to take anti-inflammatory pretty much…ibuprofen will help me if I take 400mg a day…spread through the day…so pretty much 200mg mid day, 200mg at night.
I was wondering if taking ibuprofen can damage the muscle though…make it more prone to muscle tears?

I know that certain chemicals in antibiotics can promote a muscle tear (from what I read form Louie Simmons site)
So was just wondering if it was safe for me to still lift heavy n hard while treating those couple injuries with ibuprofen (speed up the process) but yeah definately was prescribed to take it.

***Also once the pain goes away (it isnt constant I have to find it) is it cured because of taking the anti-inflammatory and the inflamation is gone…or did it just mask it and once I get off it’ll creep back up?

Thanks for replies.

not a doctor but been discussed before w/ concerns about impeding protein synthesis. the dr. in my house is sleeping and she’ll kill me if i wake her for your question. bottom line dosage typically needs to be thru the roof to cause issues w/ protein synthesis. Regarding muscle tears ???

short answer: PRN pain meds (as needed) rest for a bit, and at the very least train around the injury, meaning if it’s legs injured focus up top, if it’s shoulders, focus on legs.

I think chronic overuse of NSAIDs is the problem, not simple usage during an actual injury, as it eliminates the natural inflammation process required for muscle building. Plus it can lead to developing stomach ulcers right? I have been told in the past to use NSAIDS during the acute injury phase, which lasts like 2 days, then after that ice and rest.

edit: forget what I said, listen to MODOK, he is way more knowledgeable on this topic

haha damn I am confused.
Let me give some more depth.
My one injury is minor…actually I don’t even feel it is injured at all right now…it went away…doctor told me I probably have a bone bruised in my hand…he said this cause i had NO LOSS of function or strength in my hand…but it was tender to tap it in certain areas…this was from fighting obvisouly…but very little pain right now when I tap it.

But there is some pain when I squeeze the top of my hand together with my other hand.
I"m not too worried bout it…like I said NO LOSS of strength or function. And no numbing pain of any sort, no tingling…nothing…so I was recommend ibuprofen to speed up the recovery and thats that.

2nd injury is more tricky:
It’s my ankle. It’s been hurting for quite a while rgiht now…I remember when I really first felt it hurt when I sparred and missed a kick, used my foot and since I kick hard well it kinda bent my foot.

Anyways I didn’t think anything of it…it was bit sore the next day and to me it was just something minor.
Well it hasnt gone away since and it’s been pretty long now.
I played a pickup game of football yesterday and my ankle is sore right now from all the running and such.
The pain is on the inside of my ankle.

ANYWAYS I really need it to go away…when I wake up in the morning I can’t really put all my weight on my leg cause it kinda hurts n stuff.
Should I go to some doctor who treats these kinda things? What kinda doctor would that be?

I have absolutely no clue what exercises to do for rehab for an ankle…aside from attaching a rubbed band around it like they do on elitefts.
It needs to get fixed though ASAP.
ANY help is greatly appreciated fellas.

I don’t think there is a single study showing exercise-stimulated muscle growth in man being impeded in practice.

Until scientific findings in other circumstances where published which led to an intuitive extrapolation that it would make sense that that might impede such muscle growth, I never once heard of a bb’er or PL’er who had the slightest idea that he had noticed that NSAID’s impaired his gains.

Kind of like how no one ever noticed Nolvadex during a steroid cycle impeding their gains, till a guru pointed out a study showing reduced IGF-1 under entirely different circumstances, and then everybody feared it and even started thinking it was happening, as that guru was very influential.

Till a number of years went by and most everyone forgot, and then those who hadn’t heard about this just happily went right on with no apparent problem.

Interesting timing. I have a little muscle strain I’m working through in my back this past week. I’ve been popping Ibuprofrens and aspirin all week, and even a percocet last night.

Went to my chiro this morning and, as an alternative to typical off-the-shelf NSAID’s, she recommended Bromelian, one of the ingredients usually found in a ‘multi’ digestive enzyme supplement. It’s derived from pineapple.

Apparently, in addition to aiding digestion, it acts as an anti-inflammatory.

This morning is the first I’ve heard of it in that way, so I can’t speak for it’s efficacy. Perhaps Bill or MODOK have some insight to any clinical studies/applications?

[quote]MODOK wrote:
Bill Roberts wrote:
I don’t think there is a single study showing exercise-stimulated muscle growth in man being impeded in practice.

Until scientific findings in other circumstances where published which led to an intuitive extrapolation that it would make sense that that might impede such muscle growth, I never once heard of a bb’er or PL’er who had the slightest idea that he had noticed that NSAID’s impaired his gains.

Kind of like how no one ever noticed Nolvadex during a steroid cycle impeding their gains, till a guru pointed out a study showing reduced IGF-1 under entirely different circumstances, and then everybody feared it and even started thinking it was happening, as that guru was very influential.

Till a number of years went by and everyone forgot, and once again no one noticed any problem in practice.

We discussed this at length a few years ago on here, and there was some very compelling primary literature stating otherwise. I will try to dig it up, but it might take me a little while…I’m at work today.

But it does make sense just from a layman’s perspective, as muscle growth could have some inflammatory-mediated component. At least thats the case the studies have made.[/quote]

I agree that it’s a completely reasonable extrapolation, but not all such things wind up makinhg any difference in practice.

On the studies you may find and which in any case you have already read in the past: One thing to keep in mind that measurement of shortly post-exercise protein synthesis is I think no be-all, end-all in whether a bb’er or powerlifter is going to become bigger and stronger or not.

For example, taking Lee Haney (as he gave a very specific figure) as an example, he averaged 3 lb muscle gain per year in his years as Mr Olympia. And he knew what he was doing.

This is not, IMO, because of an improvement of 0.1 milligram of added protein per kilo per hour shortly after exercise or any other such figure.

Or take supercompensation as an example.

Or the importance of adding additional nuclei to muscle cells so that their homeostasis point for protein synthesis will be higher.

To me, whether a detectable-to-the-user difference has existed in years of experience by a very large number of bb’ers and PL’ers, many of whom have used NSAID’s daily for extended periods of time and also have had extended periods of time of not doing so, says a whole lot more than for example some finding on post-exercise protein-synthesis rate.

(Your link hadn’t appeared yet when I wrote the above)


At the moment I have only skimmed it; will read thoroughly later today.

I haven’t done the calculation but as a thought: If you took the difference in measured amount of synthesis, figured it for whatever number of hours post-exercise you thought appropriate, and multiplied by say 200 training days per year, I expect the number would be quite vast.

So if it were the case that post-exercise protein synthesis rate were the be-all end-all, the difference in gains ought to be something like – oh, I dunno, not having done the calculation yet – maybe 20 lb, maybe 40 lb, maybe more per year.

Clearly it isn’t, and so also clearly, that rate does not tell all.

By “in practice,” I meant a determination showing less muscle gains over an extended period of time – say at least 6 or 8 weeks in subjects capable of gaining signficant amounts in that period – with adminstration of an NSAID vs non-administration. I don’t think that has been shown.

Agreed, as personal opinion an NSAID should not be used for just being a little sore.

I dont have access to reference the study, however, not long ago I read a recent article (2008 publication) which specifically saught to determine whether or not NSAID’s (specifically ibuprofen) diminished muscle growth. The article determined that NSAID’s do not impair muscular repair/synthesis. I have however heard ibuprofen can increase the risk of tendonal rupture… that last part’s just hear-say though so take that as you will…

That’s what I mean I do not want any TENDONAL RUPTURE! lol Modok knows I train heavy n hard…I don’t want to be squatting 405 for 10 and then having my legs blowing out! lol

Also Modok like I said I played pick up football last night at 12am - 1:45am…my ankle is more than just a little sore today.
I’m wondering if there could be something more it’s been like almost a FEW MONTHS it’s been like this.

Should I go see a doctor? If so what kind?
I’ve NEVER iced it tohugh…sohuld I just follow the RICE method for a couple weeks and see where we go from there including using the ibuprofen?
Thanks so much guys, the help here is always tremendous.


…interesting read on the subject.

To Rasturai: Btw, it is not that I am ignoring your problem while diverting attention to a side issue, it is that injury treatment is not something I have any expertise in. The other advice you are getting is much better based than anything I could say on it.

On the muscle growth matter: Unfortunately I’ve yet to give a thorough, proper read to it. It does appear to me that it is saying that placebo showed a better increase in 24 hour post-exercise protein synthesis rate of 0.027% (with considerable imprecision to the value), and I believe the percentage is of the mass of biopsied muscle tissue that was analyzed.

So, if post-exercise protein synthesis rate were the be-all end-all determination of long-term hypertrophy, that would be 0.65% per 24 hours, and if let’s say one trains 200 times per year and that figure remained constant relative to the starting muscle weight, the total extra protein synthesized in one year, compared to if ibuprofen were used, from those 200 bouts would amount to 120% of that muscle weight.

That would be just the DIFFERENCE resulting from this measured increased rate.

So if this really told the story, if an ibuprofen user gets some given result in changed muscle mass, a non-user ought to be doing something like 100 lb of muscle better per year thanks to his non-use.

But clearly that’s not the case.

And so while the post-exercise protein synthesis rate is an interesting fact, it doesn’t have the cumulative effect, or remotely like the cumulative effect, than it would have if it were the real long term cause of hypertrophy.

I’m convinced that long-term hypertrophy is not the result of cumulative tiny changes in cells. Rather a cell undergoes a signifant change, or it may “plump,” so to speak, but the degree of cumulative plumping is limited.

Why? Because better results have been seen with it.

Is muscle inflammation necessary for muscle growth? If so, wouldn’t inhibiting it chemically preclude maximizing muscle growth?

They would if they were coming from the same individual.

There are several things going on:

First, in exercise science. Generally speaking, it is demanding on resources to do a sufficiently long term study with a sufficient number of subjects for really conclusive results on effect of one given thing, such as using ibuprofen or not, that likely (we can I think conclude from real world experience) has no profound effect.

(If the expected effect were very large then the study could be more modest and still expect to find it if it exists.)

Many people must be involved, and there are problems such as compliance. People are pains in the ass, basically.

And then after you do this, and get it published, you are going to be criticized for not showing the mechanism.

WTF? You did all this hard work and now you are getting criticized.

On the other hand, it’s easy and fast to have administer a single exercise bout and then run some analyses on biopsies, and it looks way scientific. (And it is, in terms of answering a very specific biochemical question, but not necessarily at all towards answering a practical question.)

Boom, you’ve got a paper out there in a fraction of the time with a fraction of the effort. And you will not be criticized.

More broadly speaking, there is IMO an enormous fundamental problem in science and even moreso in medicine in how results are interpreted.

To a horribly frequent extent, one thing is measured – let’s say whole-body impedance or body density or sum of skinfolds – and the claim is made that another thing was measured, e.g. bodyfat.

And to someone not familiar with the field, they actually think bodyfat was measured. But no, what was measured was impedance, body density, or sum of skinfolds.

Properly when one is stating the findings, the basic or main entries should be those. Having as a clearly derived estimation that these figures are estimated to correspond with such and such amount of bodyfat is fine. But don’t, in your main tables or reports of results, say that the bodyfat amount WAS this or that.

This is so extremely widespread and insidious a problem that when something, because it is readily doable (such as measuring rate of protein synthesis), is very widely done, it becomes treated as the be-all and end-all even by scientists working in the field. Regardless of lack of proof that it is, or even obvious demonstration that it is not.

So anyway that is the first part of why there is so much emphasis in the literature on measurements like that, and much less on measured practical outcomes.

It is NOT that I’m opposed to these being measured. Not at all. All such data adds to understanding. Indeed it is a very interesting question I think as to why post-exercise protein synthesis can be so much lower in the protocol used here, yet weightlifters who use it don’t see anything like a corresponding amount of less protein anabolism or greater catabolism over time. Very interesting, and we wouldn’t know the question even existed if not for data like this.

To keep things from being too run-on, next point is next post :slight_smile:

Next, as to how we actually do things:

Having leads – that is to say, things that suggest promise – from scientific measurements or findings is very useful. It suggests that there is reason to try some given approach.

For example, Dr Lowery and I would say an all-star cast had a recent paper comparing different nutrition protocols. Measurement of muscle glycogen was a key thing being evaluated.

Now does it have to be the case that getting the most glycogen loading MUST be the best for hypertrophy over the long term or a matter of weeks? No, I think it would be totally unwarranted to assume that that would HAVE to be the case.

But it’s an interesting finding and their discovering that very heavy loading of glucose pre-workout was by no means wasted but was delivered to muscle, helps give some backup to a practical observation that for example I’d made on that subject (but was told I was insane :wink:

Not that my having made that observation was part of the development of Coach Thibaudeau’s protocol: I had never communicated it to him. I mention it because I expect there were other practical observations.

So here we have this lead that maybe we can go heavier on carbs pre-workout and in the time not that far back from the workout than had previously been thought.

That thought might also have come without anything from a scientific study, but certainly in many cases the study would be the source of a useful lead.

Next thing is to see whether we can find it to work in practice, to the best of our ability to tell (which if I can say so, I think has had a good track record of not producing garbage that doesn’t work.)

If it does, then to me, the practical result is more important than the finding.

If for example it is instead found that something quite different, that for example doesn’t give the increase in muscle glycogen, gives better results yet, then as for myself I wouldn’t fret about that: I would value the practical results more.

For one thing, because it never was proven that increasing glycogen the most at the approximate time of workout is the be-all and end-all. Therefore we don’t know that a protocol that doesn’t do that, but instead does something else – oh who knows what, say fatty acid loading, just to be silly – might not be better yet.

The truth about whether it is better or not would be in the practical results, not in whether it was predicted to be by the glycogen model.

Last part of all this follows next.

The last thing: Why do writers bring out all these points such as insulin increase or post-exercise protein synthesis rate and so on when explaining a new product?

Well first, the individual writer may be no different than many of the scientists in actually thinking that whatever parameter is being discussed does actually show being better. I very much would expect that is the case much or probably most of the time.

It is one of the ways that I am eccentric that I keep track of what actually is being measured, what is the proof that the thing being measured must actually correspond with the thing of interest, and so forth. As mentioned, it is completely typical for, for example, a doctor who ordered an HIV test back in the day when the test did not directly measure HIV but rather antibodies to HIV, to tell a patient that they tested positive and “have HIV.”

(I personally know a case where a woman was told this, who did not have HIV but only antibodies to the antigen used in the test, which can be acquired by exposure to other things. These days the test is for HIV DNA so it is fair enough to call it a test for HIV. But the old test was not, it was a test for HIV antibodies, yet doctors widely did not understand what was being tested. Just as an example of how far wrong one can go by not knowing what is being tested and what its existence actually proves or does not prove.)

Not just to the average writer but for I would say even the very, very good ones, they don’t stop and worry about whether the thing measured, for example post-exercise protein synthesis rate, really proves hypertrophy will be better. It just makes sense to them and the scientists seem to think so, so it’s taken as a matter of course.

Secondly, there’s the problem of oversimplification caused by deciding to mention something that most probably is really important, but simply leaving it at that rather than adding caveats about how it alone is not sufficient, and it alone is only one part of what is being accomplished. For example this happened with the I, Bodybuilder video and article and some concluding from it that the big breakthrough and the way Anaconda worked was spiking insulin, that if you knew how much insulin was spiked then you knew how effective something was, etc.

If you have someone who goes on and on like me, that sort of thing will automatically be taken care of in most cases, but if you have someone writing some suitably tight prose and having only a normal degree of attention to such things rather than a really peculiar degree, it very frequently won’t be.

Lastly, why bring up these mechanisms at all if we don’t know for a fact that the difference achieved in some biochemical analysis must mean the method gives better practical results?

Well first, the writer may well genuinely think or expect it does, as explained above. And in many cases there is good reason to think it important. For example, there’s good reason to think that insulin is important to hypertrophy.

And second, the article winds up being short and unsatisfying if it consists of one sentence: “We tried it and found it to work better in practice.”

People like reasons for why it makes sense that it ought to be better, and that’s entirely reaosnable. I like reasons for why something plausibly ought to be better, as well.

But unlike many, despite being a published scientist with some I think quite decent science done very rigorously, myself I don’t care if there is no evidence why something works or doesn’t work.

For example, one of the endurance athletes we work with had a very interesting finding, involving very high dose of a given herb, that worked very well for him – remarkably well – and also for at least one other (I don’t recall) that he recommended it to. I was asked to find whatever evidence there might be for why it might work. And also to see if there were any known reasons why there should be concern on the dosage.

The herb is well known and there are many studies on it, though none for that application. There isn’t a shred of known information about how it works that makes a lick of sense to me as to how it could help an endurance athlete’s performance.

But if worked well for a broader number of endurance athletes than just the 2 or 3 that had tried it, the only reason it would matter to me in the slightest that we could find no mechanism for why, is that I’d like to learn it. But I wouldn’t doubt its performance from that: only its performance in practice would have me doing that.

Or, quicker example: While I do know a mechanism that may explain why Proviron is a lousy muscle anabolic, either let’s say I didn’t, or grant that I do. Either way, the reason for my not recommending that people base their muscle-building cycles on it is not because of knowing a mechanism for why it might not work, but because practice shows it not to work.

Regardless that studies in rats say that it is an effective anabolic, more potent than testosterone.

I know that was very lengthy but I think there is a lot of depth and importance to your question.

PS: In all that, though hopefully covering the broader general question, there could have been more thorough yet reasonably short treatment of the exact questio, but there was only one line.

To which I replied they would be, if from the same person.

(And meaning, if that person presented the claimed critical importance on the basis not on practical results, but on measured post-exercise protein synthesis, while also saying those didn’t prove a case with regard to the ibuprofen.)

With regard to being critically important in practice or not:

Back when the standard procedure was to train on an empty stomach or maybe a light meal 2 hours or so before the workout, or a fairly low calorie MRP maybe an hour before the workout, and have no during-workout nutrition, while burning many hundreds of calories during the workout, when that was the case results WERE better in practice to have this high nutrient intake afterwards. The muscles were starving (figuratively speaking) by that point. Even just looking at calories, the calories consumed since the last intake were nothing like the amount burned in the following hours.

If it were presented that a resulting measured difference in post-exercise protein synthesis proved being better for hypertrophy, I’d disagree that that proved it. I would want to know what happened in practice. However I would imagine that many, including very good writers, would feel that this did show it, or was at least good evidence towards this being a good thing to do. All else being equal, myself I would consider it evidence to be hopeful.

Now, since then we have found that when pre and during workout nutrition is as presently suggested, then high post-workout intake is not needed in practice.

So how imporant it is in practice is not an absolute, but depends on what came before.

Bill, this kind of what I was hinting at in my post concerning the 20g. protein post-workout dosage study on www.ergo-log.com: namely, that while post-workout FSR may be important it is not necessarily the whole story. Anabolism in the larger context of daily (and longer) flux may very well play a more critical role overall.

On your point about anabolism not taking place through constant small increases in muscle protein accumulation, I concur. Rather, real world experience (with I believe some justification from various fields of study) suggests something like a “punctuated equlibrium” model. For example, in evolutionary science many scientists believe that evolution did not take place through constant slow changes over eons of time, but, rather, in short highly concentrated bursts of rapid change punctuated by long periods of relative equilibrium. It seems, broadly speaking, that nature is “designed” to allow for only short bursts of departure from equlibrium, rather than constant low-grade departure (of course, this is not the case in many pathological states).

At any rate, just a quick question (as I don’t mean to hijack here): do you think there is reason to consume my 50g. dose of Vitargo & 5g. creatine with my PRE-workout scoop of Surge Recovery (or my beginning -of-workout HC, or my during-workout scoop of Surge Recovery), rather than use it post-workout with my hydrolyzed casein? That is, is the consumption of higher levels of carbs more beneficial pre or during workout than post-workout? Do you see any problem with the use of creatine PRE-workout?