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Anti-inflammatories (Ibuprofen) and protein synthesis


jimmybro1

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I have recently injuryed the tendon in both my tumbs making it almost impossible to press even with suicide grip.

Have been seeing the physio and had wrists strapped, ultrasound, and massaging done. Physio suggested to get some anti inflammatories.

I went to the doctor today and got the anti-inflammatories and when I was their asked if it would help my recover faster he couldn't give me a clear answer and from what he said I don't think it does.

After doing a little research on Ibuprofen I have found it decreases protein synthesis. If their is no recovery benifit of taking Ibuprofen why would I if all it does is remove inflammation and doesn't improve recovery.

There is the link to the study http://m.utoledo.edu/hshs/kinesiology/p ... r_msse.pdf

Thoughts?

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Muscle repair and hypertrophy is basically an inflammatory reaction, When you damage the muscle fibers this causes inflammation which signals for their repair and growth. Anti-inflammatories inhibit that process so its best to stay away from them around your training time particularly. Try training around your injury or giving it some rest, you will probably be better off for a bit of a break and eating up as opposed to trying to train through it.

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I agree, limiting your igf response with too much anti inflams.

They were handy when I did my knee tendon, only cause I had to walk on it, and it got fkn inflamed>

Have a read of the following puts it all in perspective, with a few studies to back it up.

http://www.thefactsaboutfitness.com/res ... illers.htm

If its effecting your day to day life perhaps a low dose is all G

Hope you recover fast bru

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Day to day life is fine just can't train with the intensity I won't too :P

Can still train legs and the pulling exercises so it could be worse I guess, but things like picking up plates etc can set if off. Might be worth just strapping up like a boss so got some good compression on it.

Totally agree with the above comments I'm not a fan of taking them either, especially if they aren't going to increase recovery rate!

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I guess the reason for taking it would be so you can push yourself more than without it...unless there's another reason I've missed.

So would guess the slight loss in recovery from the anti-inflammatory response is offset by the extra weight you were able to lift in the workout...I guess

And it doesn't say protein synthesis stops in the presence of IBuprofen...does it?

Do you need inflammation to "trigger" protein synthesis :doh:

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"Because of this information and the conclusions we can draw, it might seem that tissue damage and muscle growth aren’t linked. But it’s a bit more complex than that.

Increased muscle protein synthesis, or building up of new proteins, is what’s required for muscle growth to happen. This is balanced out by muscle protein breakdown. To grow, we have to increase MPS more than MPB (Tipton and Ferrando, 2008).

In practice, we see that both processes of building up and breaking down are strongly linked. When you increase MPS, MPB will tend to increase as well. This increases the overall protein turnover, or the total amount of protein coming in and out of the muscle.

Increased protein turnover with a net increase in MPS rates will result in more proteins building up in the muscle – growth, in other words.

In muscle, this process is linked to physical changes in the sarcomeres. It was once thought that these changes were a result of damage, but it’s been shown that this is actually the beginnings of the growth process. We see that both elevated protein synthesis and tissue remodeling can occur with no markers of inflammation.

Yet, inflammation of the muscle still seems to be integral to the growth process. Even though there’s no direct link as yet between inflammation and increased protein synthesis, there’s a strong correlation.

There are certain proteins in the outer membrane and connective tissues of the muscle fibers that are responsible for transmitting signals deeper into the cell. When the fiber becomes more resistant to damage, it’s thought that it also becomes more resistant to this signaling. When a muscle is “protected” from eccentric damage, it also seems less sensitive to mechanical signals that stimulate growth.

This could be one reason that it’s progressively harder to trigger growth with weight training. The more conditioned a muscle is, the harder it is to make it grow.

That’s one possible link, although it’s still just a correlation. It just happens that resistance to eccentric damage and growth signaling are linked by that one process. It doesn’t mean that the two things are directly connected.

When certain anti-inflammatory drugs are taken, what we see is that protein synthesis rates are very low as compared to groups that didn’t take the drugs (Trappe et al, 2002).

Specifically we see this in a type of drug called non-steroidal anti-inflammatory drugs, or NSAIDS. This includes things like ibuprofen, naproxen, and acetaminophen.

Researchers have traced this to the COX-2 enzyme, which is involved in some steps of the inflammation process. It seems that when COX-2 is blocked by drugs, protein synthesis and resulting growth is impaired.

Taking drugs that block COX-2 seems to compromise muscle. However, there’s some recent research that calls this into question, at least with lower doses. Krentz et al (2008) showed that 400mg of ibuprofen per day had no negative effects during the six weeks of the study.

The research by Trappe et al used maximum over the counter doses, so this could be a dose-response matter.

Obviously we’ve got a little conflict here. Some of this research is telling us that we don’t need muscle damage and inflammation for growth to occur; but we also observe that blocking some steps in the inflammation process can affect protein synthesis.

What are the possible explanations for this?

The time course of the changes is one possible avenue. Inflammation takes awhile to kick in, and is probably responsible for the longer-term changes in MPS rates. This is different from the processes that govern the immediate post-exercise changes.

Since protein synthesis rates in the muscle increase for upwards of 24 to 48 hours after an exercise session, it’s possible that inhibiting the inflammation effects would become more relevant over time even if there’s no problems immediately after the workout.

The process of long-term muscle growth requires satellite cells, which are immature muscle fibers found around muscle tissue. Under certain conditions, satellite cells are triggered to increase in number and become more like full-grown muscle fibers.

When an existing muscle fiber is damaged, these developing satellite cells will contribute their nuclei to those damaged fibers. The more nuclei that a muscle fiber has, the more protein synthesis it can support, and the bigger it gets.

Inflammation is strongly linked to the processes that activate satellite cells, and this is where COX-2 most likely contributes.

One of the biggest activators of satellite cells is a group of growth factors called prostaglandins. Specifically prostaglandin E2 (PGE2) has shown that it not only triggers satellite cell activity, but contributes to protein synthesis in existing fibers. Obviously, PGE2 is something you want around after a workout.

It just happens that COX-2 is what regulates the synthesis of prostaglandins, and thus it’s linked to this long-term growth process. When you block the actions of COX-2, you wind up blocking that long-term process (Trappe et al, 2001).

Now, I’m not so worried about the effects of painkillers blocking growth; that’s not the point. The point is to show that inflammation does play a role of some sort – it’s just that the role isn’t what most people assume it is.

This is backed up somewhat by the fact that eccentric exercise doesn’t seem to impact protein synthesis rates any more than other kinds of weight training (Phillips et al, 1997; Moore et al, 2005; Cuthbertson et al, 2006), but it does seem to correlate with greater muscle growth and protein turnover in some cases (Nedergaard et al, 2007).

Increases in muscle size without any noticeable increases in post-exercise MPS rates is hard to explain, unless you account for the contribution of satellite cells.

However, I have to stress again – DOMS itself is not a by-product of muscle fiber inflammation. Being sore does not mean that your muscles are undergoing growth. They might be undergoing repair, but these are not the same things.

I’m going tag-heavy here because emphasis is important."

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^ Long article but the bold highlights the jist of it.

Inflammation seems to be key to muscle growth, makes sense I guess if you're not straining your muscles enough their is no reason for adaption.

Moral of the story be sure your sore after a workout!

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cool man good read.

got a question around the topic...

They must have got their subjects up to an inflamed state in order to conclude that inflammation causes protein synthesis vs supressing that inflamed state with Ibuprofen. And they say that the DOMS aren't an indication of inflammation, that's cool.

It would be hugely helpful if they could tell us when they know their subjects muscles are inflamed so that we can aspire to that same state every single time :pfft:

I mean, I'm just doing it on hit and miss but they must be really good at reaching it.

Any chance they shared their training methods as well...

thanks

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In order to determine if there is inflammation they measure serum markers of skeletal muscle damage such as creatine kinase and tumor necrosis factor alpha (TNF-alpha). Obviously you can't go and measure this after a gym session every day but the type of exercise that causes this type of tissue inflammation is heavy eccentric loading. So anything with an accentuated eccentric portion of the lift will cause muscle inflammation if it is done in adequate volume. The standard protocol in these studies is around 6-8 working sets above 60% in the 6-12 rep range. This is quite a broad protocol open to interpretation but it just shows that a huge amount of volume isn't necessary to see the types of responses that the researchers are getting.

The thing is, muscle growth can occur in the absence of specific markers of tissue inflammation. Muscle fiber tension in the form of concentric only lifts like the dead lift, cleans, snatches etc elicits protein synthesis and muscular hypertrophy without causing much in the way of inflammation. Because of this its easier to train with higher volume/more times a week with these types of exercise.

It would be interesting to see a study comparing eccentric loading and concentric only loading to see if NSAIDs had the same effect on both types of training. It would be my guess that both types of training would be significantly effected but eccentric training more so than concentric only.

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NSAIDs inhibit the production of prostaglandins which are part of the protein synthesis process. Thats been pretty well documented. However, where injuries prevent training because of pain & inflammation, it seems reasonable to use minimal doses to assist the workout. Most NSAIDs are only a few hrs active in the body & DOMs associated with muscle breakdown & subsequent repair, can & does go on into the next day normally. So its reasonable to assume that prostaglandins recover & normal PS occurs albut being delayed for a few hours. That's why most people don't notice too much effect IMO. The one to avoid though is the corticosteroid prednisone which is very catabolic to muscle

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NSAIDs inhibit the production of prostaglandins which are part of the protein synthesis process. Thats been pretty well documented. However, where injuries prevent training because of pain & inflammation, it seems reasonable to use minimal doses to assist the workout. Most NSAIDs are only a few hrs active in the body & DOMs associated with muscle breakdown & subsequent repair, can & does go on into the next day normally. So its reasonable to assume that prostaglandins recover & normal PS occurs albut being delayed for a few hours. That's why most people don't notice too much effect IMO. The one to avoid though is the corticosteroid prednisone which is very catabolic to muscle

I've just decided to take some time off and let it recover rather than mask the pain.

I know someone who had a corticosteroid injection in his elbow and was back in the gym the next day throwing around weights like nothing had happened.

Not sure if he had any muscle loss from the inject he might be on anaoblics as well though, he said the injection lasted him a year then needed to have it done again. But isn't it just masking the pain, so the injury is going to get worse over time and eventually become permanently injured?

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NSAIDs inhibit the production of prostaglandins which are part of the protein synthesis process. Thats been pretty well documented. However, where injuries prevent training because of pain & inflammation, it seems reasonable to use minimal doses to assist the workout. Most NSAIDs are only a few hrs active in the body & DOMs associated with muscle breakdown & subsequent repair, can & does go on into the next day normally. So its reasonable to assume that prostaglandins recover & normal PS occurs albut being delayed for a few hours. That's why most people don't notice too much effect IMO. The one to avoid though is the corticosteroid prednisone which is very catabolic to muscle

I've just decided to take some time off and let it recover rather than mask the pain.

I know someone who had a corticosteroid injection in his elbow and was back in the gym the next day throwing around weights like nothing had happened.

Not sure if he had any muscle loss from the inject he might be on anaoblics as well though, he said the injection lasted him a year then needed to have it done again. But isn't it just masking the pain, so the injury is going to get worse over time and eventually become permanently injured?

depends on the injury. If its bursitis then it can be very useful. Muscle tears can help relieve the inflammation & get movement back into the site. Tendon or ligaments are only short lived or minimal effect as these often need surgery to repair.

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Fell in to temptation in the weekend pain in my wrist become incredible!

Took one 200 mg pill and a few hours later I felt drunk and my legs had inflated like balloons! Called the doctor and they suggested discontinuing (obviously!)

On the herbals now! Natures Kiss Anti-Flamme ! Seems to work, but definitely not as effective as Ibuprofen

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