DOMs and Inflammation

[Jester]

I've been pimping HST to my friends who workout, I've now converted 6 people to "the way" . . .

Anyway, I was re-reading the HST explanation linked from the main page, and what caught my attention were the studies that showed muscle proteins in the blood - microtrauma and mechano/myocyte leakage.

To cut to the chase, it struck me that this could be what causes the inflammation associated with training, especially after the initial workouts from an SD. These proteins don't belong in the blood, and would create some sort of immune response surely...? Just as there's an immune response when you get soft tissue damage...

There's also the link between inflammation, swelling and pain, and I was thinking that this is where DOMs might enter in...why we feel it etc. And because muscle's repair themselves and the leakage of proteins wouldn't be continuous, this is why the inflammation isn't everlasting...


Anyway...just a few thoughts I was throwing around in my head..

 

[Fausto]

Quote[/b] ]I've been pimping HST to my friends who workout, I've now converted 6 people to "the way" . . .

Way to go, mate!

I think you may be on the right track somewhat although I thought it was merely lactic acid from the glycolytic cycle after using glycogen

Dan the man, might give a more thourough answer though!

 

[jvroig]

Hey Fausto,

Quote[/b] ] I thought it was merely lactic acid from the glycolytic cycle after using glycogen

Umm... no, not really.

It was once thought to be lactic acid build-up, but now it is generally more accepted that it is because of tiny tears in the muscle fibers caused by eccentric movements or simply unaccustomed training levels.

However, a 2003 research (Ji-Guo Yu (2003), Re-evaluation of exercise-induced muscle soreness: an immunohistochemical and ultrastructural study, Umeå Univ., ISBN: 91-7305-503-4. ) claims DOMS is not caused by those tiny tears at all, but that DOMS is simply a reinforcement process - the muscle responds to the training by reinforcing itself by adding new sarcomeres (segments in the muscle fibrils). It is this process (the reinforcement) that causes cells to swell and puts pressure on nerves and arteries - and bam, that's the pain and discomfort of DOMS for you. This also explains why additional training doesn't make an existing DOMS worse - the reinforcement process is already in progress, so it hardly makes a difference at all, at worse the process just takes a little longer to finish.

Regards,
-JV

 

[imported_dkm1987]

It's called the remodeling effect, but understand that even Yu mentions

Quote[/b] ]In our study the amorphous widened Zdiscs
might reflect an initial alteration of the Z-disc due to
the unusual strain imposed upon the muscle fibers during
the eccentric exercise and in that sense represent myofibrillar damage.

In conclusion, ultrastructural myofibrillar alterations
do occur after unaccustomed eccentric exercise. However,
by taking into account the protein composition of the
alterations, as estimated by immunohistochemistry and
immunoelectron microscopy, we propose that the alterations
reflect myofibril remodeling rather than myofibril
damage.

This is one reason why I posted some comments on another thread about a difference between damage and trauma and that damage may not be necessary.

In other work by Malm he further looked at the correlation between inflammation and doms and found that the immunohistological changes seen where present in muscle but little difference from control or between either group (those exhibiting DOMS and those that didn't). On the other hand changes seen between groups were higher in the epymysium of those experiencing doms and that these changes in the epymysium where present without any signs of skeletal muscle cell damage.

Not that this changes much where working out is concerned but it does make one rethink the whole damage before hypertrophy idea. Which brings to light earlier work by Malm (2000) and a study I read a while back by Crameri et al on satellite cell activation in which they showed that even though the satllite cell population was proliferated with an acute bout (remember acute bouts cause damage right?) of high intensity exercise (eccentric cycling in Malm's case and eccentric step off with knee extensions in Crameri's) but did not induce differentiation. Now the real interesting thing is

Quote[/b] ]In seven of the eight subjects tested, no evidence of gross myofibre lesions leading to myofibre necrosis was observed during any of the testing days. In those subjects not
showing myofibre lesions, individual fibers did show slight rounding in appearance. No positive staining of CD68+ reactive macrophages was noted within the myofibres.
Additionally, no myofibres were observed which were negative for desmin, negative for dystrophin or positive for fibronectin.

 

[semajes]

So, DKM, if I'm following you, the suggestion is that actual damage may not be necessary to induce "remodeling" in a muscle. Does remodeling necessarily mean growth?

Also, if it is possible for a training stimulus to proliferate satellite cells, but not cause differentiation ... umm, .... what the hell do we do then? Has there been any research (that you are aware of) along these lines? ie. what causes differentiation?

 

[Fausto]

JV

Quote[/b] ]It is this process (the reinforcement) that causes cells to swell and puts pressure on nerves and arteries - and bam, that's the pain and discomfort of DOMS for you.

Well...well...here comes another physiology lecture,

this what I love about this Forum, the learning just never stops.

So you saying the pressure on nerves and arteries causes the pain, does lactate have sweet buggerall to do with it? I though that being acid it would naturally cause inflamation and thus the burning, painful sensation! Well, what can I say, science is science, right

Dan

Quote[/b] ]On the other hand changes seen between groups were higher in the epymysium of those experiencing doms and that these changes in the epymysium where present without any signs of skeletal muscle cell damage.

Not that this changes much where working out is concerned but it does make one rethink the whole damage before hypertrophy idea

Now you really got me what's the take on musculo-skeletal damage then? Of no use? I think I need some basic physio here before I tackle this one.

Forgive me for sounding daft, but I merely play along with bacteria and fungi, never get too far into the whole biochemistry thing, basically because there is no need for it as we are not doing research but it is nevertheless a fascinating subject!

So...I am all ears!

 

[imported_dkm1987]

Quote[/b] (semajes @ Oct. 06 2005,6:33)]So, DKM, if I'm following you, the suggestion is that actual damage may not be necessary to induce "remodeling" in a muscle.  Does remodeling necessarily mean growth?
Also, if it is possible for a training stimulus to proliferate satellite cells, but not cause differentiation ... umm, .... what the hell do we do then?  Has there been any research (that you are aware of) along these lines? ie. what causes differentiation?

First off let's clarify some things.

Trauma is needed, but it's the extent that I question. Do I feel that actual damage(tearing and or necrosis) is needed? No I don't. I may not be right either though. Strain is very much needed in my opinion. Strain on any living cell causes changes. To understand this look at Integrin signaling.

There's a lot of things that cause differentiation and quite a bit of research on it. The study I cited above by Crameri suggests that one acute bout doesn't do it and successive bouts are needed. So as Bryan has said repeatedly, even though acute bouts cause immediate changes, a chronic application is what is needed. This falls in line with all the MPS studies, the molecular signaling work, and others that look at hypertrophy.

Fausto, first let me say again, one must first define levels of damage. If you define damage as any structural change albeit with or without actual necrosis then I would say yes. If you say damage is only a necrotic event then I would say no.

Another post I made a while back is when looking at testosterone use and satellite cells, sat cells can be caused to differentitate without any work at all in the presence of test. This says that what must occur is a signal telling the satellite cells to differentiate, this signal can be induced many ways, IE Load, Work, Hormones.

In my opinion only, as I stated in the thread about local vs. systemic, you can't take one aspect from the other and expect to see much of a change. But it any case a chronic application seems to be needed.

 

[semajes]

Thanks, DKM. Very helpful. Now the only question remaining is about remodeling. Is remodeling the same as growth, or is it just repair (and home improvement) work that doesn't necessarily lead to an increase in size?

 

[imported_dkm1987]

When reading Yu's work done earlier he showed a significant number of fibers in biopsies taken 2–8 days after exercise that showed myofiber lesions. He supposed that when dividing the area of these fibers into two groups; areas of myofibers lacking staining for titin, nebulin, and alpha-actinin but positive for desmin and actin, and myofibrillar areas strongly stained for desmin and actin and revealing sarcomeres containing alpha-actinin, titin, and nebulin. That the focal lack of titin,nebulin, and alpha-actinin clearly supports the hypothesis of muscle injury being caused by eccentric exercise, whereas those positively stained for desmin and actin reflect increased protein synthesis.

 

[thehamma]

Quote[/b] ]Now the only question remaining is about remodeling. Is remodeling the same as growth, or is it just repair (and home improvement) work that doesn't necessarily lead to an increase in size?

Quote[/b] ]When reading Yu's work done earlier he showed a significant number of fibers in biopsies taken 2–8 days after exercise that showed myofiber lesions. He supposed that when dividing the area of these fibers into two groups; areas of myofibers lacking staining for titin, nebulin, and alpha-actinin but positive for desmin and actin, and myofibrillar areas strongly stained for desmin and actin and revealing sarcomeres containing alpha-actinin, titin, and nebulin. That the focal lack of titin,nebulin, and alpha-actinin clearly supports the hypothesis of muscle injury being caused by eccentric exercise, whereas those positively stained for desmin and actin reflect increased protein synthesis.

??????????????
Does anyone understand this? If you do I'd like someone to explain it to me on a more practical level.

thanks
thehamma

 

[semajes]

Well, certainly increased protein synthesis is what we're after, and muscle injury, damage, or trauma seems to be associated with kicking off the cascade of events leading to growth, so ... if this is all associated with "remodeling", wouldn't that mean that DOMS is, in fact, pretty highly correlated with the stimulation of hypertrophy?

 

[imported_dkm1987]

No, because DOMS can be elicited without the remodeling effect, and the remodeling can occur without DOMS.

It is correlated with unaccustomed muscle activity but this can happen with or without subsequent trauma, signal cascades, hypertrophy.


thehamma,
I'll simplify a bit for you. When looking at what happened via staining techniques YU found 2 things, 1. Eccentrics caused a situation where the fiber's weren't damaged but did start a change in their structure. 2. This structure change could be correlated to increased Protein Synthesis.

Words of wisdom; Don't worry about DOMS, if you get it fine, if you don't fine. Remodeling can happen in either case, growth can happen in either case.

 

[faz]

Quote[/b] (semajes @ Oct. 08 2005,3:43)]Well, certainly increased protein synthesis is what we're after, and muscle injury, damage, or trauma seems to be associated with kicking off the cascade of events leading to growth, so ... if this is all associated with "remodeling", wouldn't that mean that DOMS is, in fact, pretty highly correlated with the stimulation of hypertrophy?

this sounds a bit like vince basile

 

[NWlifter]

DOMS and remodling also have to be thought of in light of MPS vs MPD. One could induce both but still see zero net accumulation of protein. Put yourself on a 3 month SD, eat 800 Kcalories then perform a set of eccentrics. You'll kick off the remodeling process, induce DOMS and see zero growth.

The process of DOMS and remodeling is tricky to measure externally. All of us have certain muscles that have grown but rarely, or even never experience tenderness. I myself can perform a ton of sets, eccentrics, you name it, and my delts never get sore. My pecs can get very sore from a set or two of benches.

Here is a quote that I always post and most are probably tired of seeing it

But it's a great explanation of the DOMS part. The Yu stuff with remodeling processes are a great 'inside look' at 'what' might be going on.

Quote[/b] ]From Neuromechanics of Human Movement, by Roger M. Enoka

The sensation of tenderness appears to be triggered by the loss of cellular calcium homeostasis (Clarkson, Cyrnes, McCarmick, Turcotte, & White, 1986; Friden & Lieber, 1997' Jackson, Jones, & Edwards, 1984) due to the activity-induced disruption of sarcomeres. A high intracellular calcium concentration activates proteolytic and lipolytic systems that initiate the degradation of cellular structures (Armstrong, 1990). Because this inflamatory process has a time course smilar to that of the heightened tenderness (Lieber, Schimtz, et al., 1994) and thre is an appropriate activation of the immune system (Malm, Lenkel, & Sjodin, 1999), the sensation of soreness is usually attributed to the inflammatory response.

 

[semajes]

Easy now FAZ. Don't make me come out there.

 

[semajes]

Sorry, I thought that the discussion of the remodeling effect came up only in regards to the discussion of DOMS. Thus, I thought the two were always linked. My mistake.

Doesn't protein synthesis mean an increase in protein structure or muscle? DKM said, the "structure change could be correlated to increased protein synthesis." Also, though, it was said that the remodeling effect could take place without any growth at all. Sorry if I'm being a pain in a$$, I just wanna get my terminology straight, and follow this logically.

 

[imported_dkm1987]

Quote[/b] (semajes @ Oct. 08 2005,5:06)]Doesn't protein synthesis mean an increase in protein structure or muscle?  

Protein structures YES, Muscle NO and YES. There are many proteins in the body, there are many proteins in a muscle. Not all correspond to increased fiber size. For example MIXED muscle Protein Synthesis looks at all proteins in the muscle, the top three are Sarcoplasmic, Myofibrillar and Collagen. Even within myofibrillar there are contractile and non contractile (sometimes called Series Elastic Elements) proteins.

 

[NWlifter]

And to further add, a workout increases synthesis AND degradation. The only way we add muscle is if the synthesis levels are higher than the degradation levels. In a fasting catabolic state, a workout can make ya smaller!

 

[semajes]

Gotcha. Thanks again, DKM.

NWlifter, with regards to what you were saying (I never really thought of this before), does this mean that it is possible that particularly "intense" (pardon the terminology -- I don't know what else to call it) workouts while dieting might be detrimental? In other words, if I am lifting heavy weights, with a lot of volume, while under a caloric deficit, might I be losing the muscle that I am working so hard to retain?

That ... is a troubling thought. Say it ain't so.

 

[imported_dkm1987]

Yes, it's quite possible. One thing I recommend to anyone who ever asks about dieting is to not reduce protein intake. This does show some help in staving off muscle wasting during restricted diets. Besides the PSMF stuff out there one study that particulary sticks in my mind is where they looked at MHC protein synthesis/degradation during restricted protein diets even though they ate isoenergenically. In the study they used .75g/lb vs .32g/lb. All subjects ate around 1800Kcals. Those who ate the reduced protein had lower incidence of synthesis and higher incidence of MHC isoform shifts to a slower isoform than those who ate.75g/lb.

Now heres the catch 22, neither of these groups were exercising. Studies looking at exercise alone on FSR/FBR show pretty conclusively that as one becomes more trained FSR decreases but so does breakdown, so perhaps using the restricted protein with exercise would have provided differing results and been different between groups of untrained vs. trained. If Aaron reads this I'm sure he could comment more on that.