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Rhabdo question
Posted: 11 January 2012 07:12 AM   [ Ignore ]
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Today’s WOD scaling by GardDawg included the warning about Rhabdo induced with jumping pull ups.

“So after making a big deal about not subbing jumping pull ups for pull ups they show up in a WOD.  Remember jumping pull ups have no eccentric component to them.  Here is a fairly good vid.  See how they don’t lower themselves under control.  http://media.crossfit.com/cf-video/CrossFit_CFTOFS-JPUworkout.wmv

This is serious folks.  There is no eccentric component.  We had a forum member who ignored this.  A 23 year old active female, who did 43 jumping pull ups a a sub for pull ups in Cindy.  43.  43 jumping pull ups in 20 minutes. 43.  She spent a week in the hospital with Rhabdo.  Pay attention.  Watch the vid.  Don’t mess yourself up.”

Am I interpreting the above correctly that the jumping pull up when done correctly is not supposed to lower under control?  The video shows that. 

What causes the excess muscle breakdown associated with the exercise of jumping to do the pull up then lowering under control?

Thanks for any feedback. A brief search turned up more warnings but I couldn’t find much explanation.

John

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Posted: 11 January 2012 07:20 AM   [ Ignore ]   [ # 1 ]
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Nevermind.  Should have started with Crossfit Journal.


From CrossFit Journal June 2011
Rhabdomyolysis Revisited by Will Wright MD

It is known that eccentric or “negative” muscle contractions
are more often associated with exertional rhabdomyolysis.
Eccentric movements are particularly stressful for muscles
because the muscle cells are lengthening while trying to
contract. This “stretching” increases muscle tension and
predisposes the muscle cell to injury. Eccentric contractions
are a component of many movements, such as
jumping pull-ups, the deceleration or lowering phase of
lifts, push-ups and running downhill—to mention a few.
In fact, after review of the known cases of rhabdomyolysis
in the CrossFit community, these movements were often
part of the workouts that preceded the condition.”

I understand it now.  As the muscle shifts from trying to lengthen while also having to maintain the clamped or hold function the cells get confused effectively trying to burn ATP but also releasing myoglobin as it thinks it is relaxing.  This is similar to a combustion engine injecting the fuel during both the push and the pull stroke on the piston so it fires with double intensity on the fire explosion side but never cleans out functionally through normal exhaust.

good article-one of the free ones.

J

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Posted: 11 January 2012 07:32 AM   [ Ignore ]   [ # 2 ]
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JohnStJohn - 11 January 2012 07:20 AM

I understand it now.  As the muscle shifts from trying to lengthen while also having to maintain the clamped or hold function the cells get confused effectively trying to burn ATP but also releasing myoglobin as it thinks it is relaxing.  This is similar to a combustion engine injecting the fuel during both the push and the pull stroke on the piston so it fires with double intensity on the fire explosion side but never cleans out functionally through normal exhaust.

J

The muscle isn’t confused and the release of myoglobin is never a “planned” event in any muscle (its release from cardiac cells is diagnostic of a heart attack).  Muscle cells are being ripped open; hence the “lysis” in the name.  This is severe muscle damage with added adverse outcome of impaired kidney function (presumed to be due to oxidized myoglobin or the heme component).

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Posted: 11 January 2012 02:23 PM   [ Ignore ]   [ # 3 ]
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JDG - 11 January 2012 07:32 AM
JohnStJohn - 11 January 2012 07:20 AM

I understand it now.  As the muscle shifts from trying to lengthen while also having to maintain the clamped or hold function the cells get confused effectively trying to burn ATP but also releasing myoglobin as it thinks it is relaxing.  This is similar to a combustion engine injecting the fuel during both the push and the pull stroke on the piston so it fires with double intensity on the fire explosion side but never cleans out functionally through normal exhaust.

J

The muscle isn’t confused and the release of myoglobin is never a “planned” event in any muscle (its release from cardiac cells is diagnostic of a heart attack).  Muscle cells are being ripped open; hence the “lysis” in the name.  This is severe muscle damage with added adverse outcome of impaired kidney function (presumed to be due to oxidized myoglobin or the heme component).

I simplified a great deal in my analysis but the muscle cell has to have a “confusion” for the continued dependence on ATP and the myoglobinuria.  If this were just muscle damage then the typical anaerobic glycolisis pathway with LDH catalyzing reaction of NADH by pyruvate to give NAD and lactate which becomes lactic acid under hypoxic low pH conditions.  The question I was trying to simply answer is why does the muscle which under normal hell stress of a WOD follow the pathway of classic homolactic fermentation, while some secondary pathway that isn’t in regular biochem class where a person doing non-aerobic fatigue contraction of a muscle group under a load that is not unwieldly (42 jumps with lowering under load) cause a damage to the tissue that a massive movement like a clean or snatch does not. 

Something is causing these cells to behave differently under this anaerobic condition where they are tyring to relax but also held in a contracting condition to force an overload in that fermentation of the anaerobic pathway for pyruvate.

typically muscle cells avoid suicide by exhausting ATP supply and this is usually because at low pH as oxygen drops and glycolytic production fo protons increases the PH falls to 6.4 in the muslce tissue in seconds.  This typically reduces PFK (the phosphofructokinase enzyme) falls in activity at low pH which slows glycolysis.  I wonder if the load while trying to contract somehow prevents the cells in the muscle fibers from experiencing this high power output since the jump prevents as much fatigue from occurring and the muscles are fooled into believing they are not doing the work yet they still are.  then the cells exhaust ATP supply and undergo an apoptosis.

But my analogy was a lot simpler if not quite correct.

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Posted: 11 January 2012 02:52 PM   [ Ignore ]   [ # 4 ]
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JohnStJohn - 11 January 2012 02:23 PM
JDG - 11 January 2012 07:32 AM
JohnStJohn - 11 January 2012 07:20 AM

I understand it now.  As the muscle shifts from trying to lengthen while also having to maintain the clamped or hold function the cells get confused effectively trying to burn ATP but also releasing myoglobin as it thinks it is relaxing.  This is similar to a combustion engine injecting the fuel during both the push and the pull stroke on the piston so it fires with double intensity on the fire explosion side but never cleans out functionally through normal exhaust.

J

The muscle isn’t confused and the release of myoglobin is never a “planned” event in any muscle (its release from cardiac cells is diagnostic of a heart attack).  Muscle cells are being ripped open; hence the “lysis” in the name.  This is severe muscle damage with added adverse outcome of impaired kidney function (presumed to be due to oxidized myoglobin or the heme component).

I simplified a great deal in my analysis but the muscle cell has to have a “confusion” for the continued dependence on ATP and the myoglobinuria.  If this were just muscle damage then the typical anaerobic glycolisis pathway with LDH catalyzing reaction of NADH by pyruvate to give NAD and lactate which becomes lactic acid under hypoxic low pH conditions.  The question I was trying to simply answer is why does the muscle which under normal hell stress of a WOD follow the pathway of classic homolactic fermentation, while some secondary pathway that isn’t in regular biochem class where a person doing non-aerobic fatigue contraction of a muscle group under a load that is not unwieldly (42 jumps with lowering under load) cause a damage to the tissue that a massive movement like a clean or snatch does not. 

Something is causing these cells to behave differently under this anaerobic condition where they are tyring to relax but also held in a contracting condition to force an overload in that fermentation of the anaerobic pathway for pyruvate.

typically muscle cells avoid suicide by exhausting ATP supply and this is usually because at low pH as oxygen drops and glycolytic production fo protons increases the PH falls to 6.4 in the muslce tissue in seconds.  This typically reduces PFK (the phosphofructokinase enzyme) falls in activity at low pH which slows glycolysis.  I wonder if the load while trying to contract somehow prevents the cells in the muscle fibers from experiencing this high power output since the jump prevents as much fatigue from occurring and the muscles are fooled into believing they are not doing the work yet they still are.  then the cells exhaust ATP supply and undergo an apoptosis.

But my analogy was a lot simpler if not quite correct.

“the continued dependence on ATP and the myoglobinuria” How are these two connected? 

“lactic acid under hypoxic low pH conditions” Lacate never becomes lactic acid, check your pKa values (3.86).  pH never reaches this level, even in muscle tissue. 

The muscle cells are not undergoing any regulated form of lysis.  They are trying to contract, and that contractile force is NOT able to overcome the eccentric loading.  The sarcomeres (that take all the load and provide all the force) are attached to the cell membrane and to the extracellular matrix; when the myosin fibers give out under the strain - well, the cells are ripped open.  The number one reason for presentation of Rhabdo is blunt force trauma - no muscle contraction necessary, just busted cells.  If the muscles cannot support the continued eccentric load on a contractile movement, there’s tissue damage.  Enough damage and you get swelling and pain.  Even more damage (+ confounding factors, hydration status, medication, metabolic disorder) and you get Rhabdo (or perhaps a compartment syndrome).  Are we arguing the same point, or is your view of Rhabdo dramatically different?  Perhaps there’s a discussion disconnect?

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Posted: 11 January 2012 03:03 PM   [ Ignore ]   [ # 5 ]
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I think I always want to know the physical chemistry of the mechanism because my background is physical chemistry and biochemistry.  But my exercise physiology understanding is limited only to what I am guessing.  Why exactly does that movement produce busted cells while other massive loads do not?  If this is simply damage, why does this type of load from a jumping pull up.  Wouldn’t there be a hyopthesis that could be validated to show that this contractile force is resulting in a lysis?  If you’re positive I’m OK with it but I’m asking a question and I am trying to fit this to a biochemical mechanism.  If it is simply a blunt force trauma due to loading by jumping and maintaining the contraction then you are correct.

It just surprised me because the loads seemed disconnected for these movements compared to what the muscles can produce and I was curious if there could be a factor not yet understood related to the underlying biochemistry.

My lab works primarily in oncology and apoptosis events so I was simply putting forward a theory.

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Posted: 11 January 2012 03:53 PM   [ Ignore ]   [ # 6 ]
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It isn’t always the load, for instance jumping air squats have also been shown to induce Rhabdo.  Think about load, volume, over what time interval, with underused muscle groups, and other exacerbating factors; it’s a large equation with lots of variables.  In the end, the medical issues are what define Rhabdo.  Some muscle cells are bound to lyse under load, and be replaced.  But when the amount of lysis and (several references currently suggest) resulting myoglobin or heme caused kidney injury, that’s when it become clinically relevant.
I don’t believe any study has definitively shown HOW the muscle cell is ruptured on a molecular level, but it does not appear to be the result of a biochemical process gone haywire.
I have a CFKMagazine article on Rhabdo and the contractile damage from a couple years ago, if you PM me an email address, I’d be happy to send it to you.
I don’t claim to have the complete mechanism on this condition, and the literature is less than complete on the topic as well…

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Posted: 11 January 2012 05:51 PM   [ Ignore ]   [ # 7 ]
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Hey, I have that articles from CF journal which were part of my first post.  I recognize the effect is the point to the CF community.  Since my lab focuses on cell death and there are some relatively simple smooth and skeletal muscle cell animal models I can employ.  I was posing most of my questions to hear myself think which I unfortunately do at parties making me a very boring person to hang with. 

One Polish article I found relates differences in cardiac muscle tissue after an arrest to show that the death has an apoptosis pathway and the pathway is actually proposed as a rhabdo event.  The cells kept working under a metabolic load that kept filling them faster than the waste could be removed and programmed cell death occurred.  I was curious since the animal model could be performed for say rat hind leg (not sure how I would get the rat to stress and contract the muscle but it’s an interesting IRB application and question for the grad students).  Muscle cells are not typically what we work with as they are just not as exciting as cancer but this is a curious question and that gets research geeks salivating.

But I won’t ever contradict the exercise physiologists or trainers on the proper form or dangers of the condition.

Thanks for chatting with me! 

J

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Posted: 11 January 2012 07:23 PM   [ Ignore ]   [ # 8 ]
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MI-induced cardiac cell death may very well induce a biochemical pathway leading to apoptosis (or necroptosis?); really, metabolic waste products, and not the hypoxia-induced cascade perhaps with HIF1alpha as the culprit?  Smooth and skeletal muscles are different animals but maybe future research will put these events closer together on the continuum…  I would think this cardiac cascade is different than exercise-induced rhabdo, or even just clinical rhabdo… But both cell types are under a demand to keep contracting (one mental, one physio-electrical) and both are under less than optimal conditions (one lacking O2, and the other with potentially limiting metabolites for energy) for continued function.  Now you have me thinking aloud wink

I think of rhabdo as exactly what it means, any syndrome that extends from the lysis of muscle cells (regardless of mechanism or cause).  I would accept that the cause of “rhabdo” could span the entire spectrum from blunt force trauma/torn muscles and programmed cell death with aspects of your hydration status and kidney function to medication intake and genetic make-up being crucial as well.  With exercise-induced rhabdo (EIR), I would fall on the side of muscle-cell rupture (by force rather than design) and allow for all additional confounding factors.  Because EIR is “usually” coupled with localized inflammation (not usually a hallmark of apoptosis, correct?), and is “usually” quite acute in terms of the accumulation of myoglobin in the blood and urine I think of it as being more similar to the blunt trauma event.  This mechanism also jives with the loaded eccentric movements being a major cause of EIR.  All circumstantial, I know…  Until you get that grant! wink

I’m not sure my CFKMag article is in the CFJ site yet, they are not done porting them over.  And as for how they induce rhabdo in lab animals- forced decline running (downhill) is used as is electrostim on a fixed limb.

Thanks for the discussion!

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Posted: 12 January 2012 07:02 AM   [ Ignore ]   [ # 9 ]
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Anytime on the discussion.  I’ll probably skip the grant.  I think what sticks out at me the most is that the two most correlated exertions (not statistical, just anecdotal but I don’t know any literature in this area) seem to be GHD and negative which both seem to force a contractile and relax under load. 

That just sticks out to me.  I have kids who are sprinters and I see fatigue in them and their track mates in different teams and seasons that undergo very big inflammation, soreness and I do not know if there is a crossover from inflammation to a myoglobin level that is a clinical rhabdo (I’m not even clinically relevant enough to know if there is a clinical marker for rhabdo).  My curiosity is simply curiosity and the simple answer could be the athletes just rupture a lot of muscle tissue and cells and the dump is too much to process.  Since most literature on apoptosis in muscle tissue lends itself toward the smooth muscle cells as cardiac, arterial and venous diseases make up the bulk of health problems and exercise induced rhabdo is not a critical problem with “walking vigoriously for 20 minutes a day” I’m guessing that the project would be limited to a side study in a lab with the time which I might be able to put together with a summer med student. 

The brainstorm would be how to induce the event with the eccentric loading.  Your wonder aloud “But both cell types are under a demand to keep contracting (one mental, one physio-electrical) and both are under less than optimal conditions (one lacking O2, and the other with potentially limiting metabolites for energy) for continued function.” is the key question I was curious about with the question to be answered being “Does eccentric loading in skeletal muscle tissue induce (insert your percentage) of muscle cell rupture during the loading” and build the hypothesis around that.  If we could isolate say a fresh gastoc muscle group from the hindquarter and load it under electrostim, biopsy, histo and go nuts with the markers in the tissue for metabolites then the resulting answer would at least give some direction to when the rupture event would occur being part of trauma from the actual event or through a programmed cell death later.

I was assuming you were Will Wright from above but there must be some other articles in the journal.  What do you do?  I’m an associate professor in biomedical engineering and dermatology and my labs focus on cell death in melanoma and dermatology related cancer.

J

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Posted: 12 January 2012 07:02 AM   [ Ignore ]   [ # 10 ]
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Posted: 12 January 2012 08:59 AM   [ Ignore ]   [ # 11 ]
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No, I’m not Will… Jon Gary from the CFK HQ staff.
I am a PI at a biotech company; graduate & post-doc work in biochemistry and molecular biology.  No plumage, as TP suggests…

Clinical marker for rhabdo is generally CK (and/or a urine test for myo), I forget the threshold; maybe 100k (or X-fold over baseline)?  Its really arbitrary when you think about, everyone gets some muscle rupture at some point in their life.  Only when the rupture is too large, or the kidney function is limited in some way will the person be affected and go to the ER for “rhabdo.”  So one person with slight kidney dysfunction or is dehydrated may present with rhabdo while in a “normal” individual those elements are cleared from the blood rapidly and are just fine (apart for some soreness for a couple days).  You’d really need a huge trial assaying blood (full panel: CK, myo, TnI, CKMB, K+, Na+, Ca++, pCO2, pO2, ect.) from, say an entire gym, just after exercise, 1hr, 12hr and 24hr later over the course of multiple WODs to really get a good idea for what happens.  Most of the literature I’ve seen has been with cycle ergometer-based exercise (because its measurable and repeatable) - not really relevant to what we do!

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Posted: 12 January 2012 10:20 AM   [ Ignore ]   [ # 12 ]
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Should the eccentric phase of a deadlift be done quickly to avoid muscle damage? Interesting thread

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Posted: 12 January 2012 10:41 AM   [ Ignore ]   [ # 13 ]
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I’ve never heard of any issues with DL and rhabdo, but maybe some of those high-rep, lower load WODs would be something to respect, similar to heavy KB swings.

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Posted: 12 January 2012 12:11 PM   [ Ignore ]   [ # 14 ]
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JDG - 12 January 2012 08:59 AM

No, I’m not Will… Jon Gary from the CFK HQ staff.
I am a PI at a biotech company; graduate & post-doc work in biochemistry and molecular biology.  No plumage, as TP suggests…

No plumage either; keep hoping for a call in October at 2 am from Stockholm but I usually don’t wait up.

I definitely wouldn’t consider a clinical trial on this one.  That would definitely require some NIH grant and a lot of justification.

But the lab study would be fairly simple.  I’ll send you my contact info.

J

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Posted: 12 January 2012 01:52 PM   [ Ignore ]   [ # 15 ]
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