Perhaps you need a review of muscle fibre types. The soreness you feel is simply from micro trauma to the muscle fibres themselves. When the fibre(s) heal they come back a little stronger. That is the same in any muscle fibre regardless of type. The muscles in the human body simply adapt to what stress you put on them. In endurance athletes it's the red fibres or slow twitch fibres. In strength athletes it's primarily the fast twitch or white muscle fibres that are working. The different fibre types just carry out certain functions better than the other. The white or fast twitch fibres are more likely to hypertrophy than the red or slow twitch fibres. As they improve efficiency there is an increase in mitichondria and cappilery supply thus increasing oxygen utilization and muscular endurance. The results are just a little different. Improved overall strength and power versus increased endurance capacity. The rest of the changes are in our respiratory and cardiovascular systems. Don't foget the heart is a muscle as well. That's the simple explanation. There is plenty of information on the web about the topic so do a search. This article is pretty good and easy to understand.
http://www.isokinetics.net/...musclefibertypes.htm

I'm aware of this but wonder about the reparation of slow twitch fibres when suffering micro trauma after an endurance workout. Fast twitch fibers repair themselves and hypertrophy results. Slow twitch fibers repair themselves and there is little if any hypertrophy. How is the muscle stronger and more fatigue resistant than before? Are the repaired fibers themselves of a stronger make up without being larger? Perhaps the fiber itself is able to create more myofilaments, in a way become denser, to allow greater contratile strength and endurance?

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Well, your body adapts in ways to make the same workout less destructive to your muscles. For example, oxygen delivery to those muscles improves, so if you were relying on 10% of your energy from anaerobic pathways for a 7:00min/mile pace on Monday, maybe you'll only need to get 9% of your energy from anaerobic pathways for 7:00min/mile pace on Friday. Less anaerobic work = less muscle acidosis = less tissue damage.
Another example, mitochondrial density increases with endurance training, so again, there is less reliance on anaerobic pathways, and less tissue damage occurs.

So this raises the obvious question... what about if I rely 10% on anaerobic pathways for 7:00 pace on Monday, and then use 10% anaerobic pathways again on Friday, only this time it results in 6:55 pace? Well... I can't help you there. I don't know enough about biochemistry off the top of my head to provide you with a convincing argument as to why one of those workouts would cause more soreness than the other.

Why are you assuming that Monday/Friday's workout lasted 2-3minutes?

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Why are you assuming that Monday/Friday's workout lasted 2-3minutes?
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Huh? I don't think I made that assumption. I'm not sure how you read that into my post. Maybe I didn't word something clearly, or you just interpreted it in a different way than I intended.

Also, one more thing on neuromuscular efficiency - as you train more with a certain activity, your nervous system will become more efficient at recruiting muscle fibers to engage in that activity. So say on Monday you run 7:00min/mile, only recruiting (X)% of the available muscle fibers that could be engaged in that activity. Then, on Friday, your body has made adaptations, and you can recruit (X+1)% of the available muscle fibers. This results in less loading on each individual fiber for a given pace, and hence, may reduce soreness.

he's saying that's the duration of an effort that would rely 10% on "anaerobic" pathways

Firstly, thanks for the feedback, especially Doug. Doug said: "Less anaerobic work = less muscle acidosis = less tissue damage". Coming back to the tissue damage and reparation itself. I'm wondering if, once we have the slow twitch fibers themselves, that's it - we can improve the biochemistry and efficiency of their function (increasing fatigue resistance) but the fibers remain much the same; they get sore, they repair.

My thinking started from the perspective of marathon training. It seems from my experience, those runs over 30k are aimed mostly at fatigue resistance of muscles. I was curious as to the physiological processes behind increasing fatigue resistance. Another question would be comparing the training effect of a harder 20k vs an easier 32k run. The legs could easily be the equivalent soreness if the intensities were well managed. One might make an argument that the training affect was equal as well, including development of fatigue resistance.

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Anaerobic metabolism per se has little, if anything, to do with post-exercise muscle soreness.

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Steve

http://www.PeaksCoachingGroup.com

Fast twitch fibers repair themselves and hypertrophy results. Slow twitch fibers repair themselves and there is little if any hypertrophy.
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Wait a minute here who is to say that no hypertrophy occurs in slow twitch fibres? I think a great deal of people on here would argue with that. Are you saying that your legs look no different now than say 5,6, 10 years ago etc.. whenever it was you started swim, bike, run but mostly bike, run in this instance?

I played hockey growing up for many years as a kid which gave me a good base of leg strength and muscle structure. I also ran through high school then stopped. I then lifted weights for a few years before gettting back to endurance sports. My legs and ass have definately shrunk a little since stopping weight lifting (I can't stand weight training anymore) but are still very muscular. Slow twitch fibres still hypertrophy but there cross section is not as large as fast twitch fibres and certainly hypertrophy at a much smaller rate and total cross section maxes out faster than fast twitch fibres. Otherwise the majority of adaptive changes that occur in the muscle cells that give us improved endurance capacity or fatique resistance is due to increased mytochondria and capillery supply.

Sorry, I wasn't clear. I was speaking of experienced athletes who have maxed out slow twitch hypertrophy. Thanks for your input and clarification.

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http://www.triathloncoach.ca

Anaerobic metabolism per se has little, if anything, to do with post-exercise muscle soreness.
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Please explain. I'm no biochemist, but it seems to make sense that if muscle acidosis is occurring due to an excess of free protons, then tissue damage is occurring. Please correct me if I'm wrong, because I want to know the truth of the matter. I'm smart enough to know that I don't necessarily know very much.

For Paolo - in regards to my "10% anaerobic pathways" comment... There's no point in exercise where you're relying 100% on aerobic pathways or 100% on anaerobic pathways. When you're just cruising at an easy pace, you're getting X% of your energy from aerobic pathways, Y% from anaerobic pathways, and Z% from creatine-related pathways. As you increase intensity, your reliance on anaerobic systems increases. Its not like substrate level phosphorylation (anaerobic energy production) without an accompanying Krebs cycle just "switches on" when you hit your LT. Your LT is just when energy production from anaerobic systems becomes so predominant that your body can't buffer the excess protons being produced as a by-product of substrate level phosphorylation.
Hope this helps clear up my previous post.

Well, if you're looking at muscle soreness being generally associated with muscle injury (there is some debate as to how closely they are related), then the evidence is fairly clear that, in vivo, physiological anaerobiosis, or physiological acidosis (in other words anaerobic metabolism and/or acidosis in situations one would experience during exercise) do not cause muscle injury, and hence muscle soreness to any great extent. The critical element to most, if not all, muscle injury models is eccentric/lengthening muscle actions (E/L), which, again, in and of themselves don't cause much injury. The initial minor injury elicited by E/L is minor, but sufficient to initiate a cascade of events leading to a secondary, and more substantial injury. The secondary injury is primarily a result of the inflammatory response instigated by the initial lesser mechanical injury. The adaptation the OP cites

"For example, I do a 2 hour run and my quads are sore. I then recover and the next time I do the 2 hour run my quads are less sore or not at all."

is well acknowledged in the scientific world (if you believe that sciency stuff) and attributed to some adaptive response that appears to attenuate the inflammatory response, hence reducing the secondary injury. It certainly wouldn't have anything to do with anaerobic metabolism since, for a 2 hr run, the contribution from anaerobiosis is essentially nill. Anyway, the nature of the adaptive response is still unclear, but happens within a couple weeks after the initial novel exercise, and lasts for quite a while. It doesn't depend on aerobic adaptations (e.g. mitochondrial/capillary density) whatsoever.

Props to you for stating that you know enough to know you don't know much. Most of us are in that boat, but far to few are willing to admit it.

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Steve

http://www.PeaksCoachingGroup.com

Ok, good point about the 2 hour run having little contribution from acidosis. I should have thought that through a little more clearly before making my first post. If acidosis does play a role, it seems like it would be most likely to occur when doing work at tempo intensity and above (which you actually may be near for a 2 hour run, depending on how hard you want to go). My point about the mitochondrial density had to do with that fact that as your mitochondrial density increases, you can stay more aerobic for a given speed, and hence less acidosis occurs at that speed.

I'm not trying to be difficult, it just seems counter-intuitive to me that acidosis would play no role in muscle soreness, so... I'm gonna spend a little time reading journal articles to get more educated on it. I'll probably just end up reaching the same conclusions that you already have, but maybe I'll find out something new.

What acidosis?

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In Reply To

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so... I'm gonna spend a little time reading journal articles to get more educated on it. I'll probably just end up reaching the same conclusions that you already have, but maybe I'll find out something new.

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My advice to you is to start with a basic exercise physiology text.

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I've always like this abstract (from a Paulo approved University of New Mexico paper at that!)

The widespread belief that intense exercise causes the production of “lactic
acid” that contributes to acidosis is erroneous. In the breakdown of a glucose
molecule to 2 pyruvate molecules, three reactions release a total of four
protons, and one reaction consumes two protons. The conversion of 2
pyruvate to 2 lactate by lactate dehydrogenase (LDH) also consumes two
protons. Thus lactate production retards rather than contributes to acidosis.
Proton release also occurs during ATP hydrolysis. In the transition to a higher
exercise intensity, the rate of ATP hydrolysis is not matched by the transport of
protons, inorganic phosphate and ADP into the mitochondria. Consequently,
there is an increasing dependence on ATP supplied by glycolysis. Under these
conditions, there is a greater rate of cytosolic proton release from glycolysis
and ATP hydrolysis, the cell buffering capacity is eventually exceeded, and
acidosis develops. Lactate production increases due to the favorable
bioenergetics for the LDH reaction. Lactate production is therefore a
consequence rather than a cause of cellular conditions that cause acidosis.
Researchers, clinicians, and sports coaches need to recognize the true causes
of acidosis so that more valid approaches can be developed to diminish the
detrimental effects of acidosis on their subject/patient/client populations.

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Fatigue is biochemical, not biomechanical.
- Andrew Coggan, PhD

Muscle acidosis does occur. Cellular pH drops due to the production of protons. That is the definition of pH - the concentration of "free" protons in a solution. Muscle acidosis is not because of lactic acid, I am well aware of that. At no point in any of my posts did I blame lactic acid for acidosis. Acidosis is due to free protons being released as a result of substrate level phosphorylation.

Now, you can disagree that acidosis is a cause of soreness, and you may be right. I thought it was a contributing factor, but now it seems that I really don't know. That's why I'm going to read up some journal articles.

I don't know what you have against me, but you need to stop your crusade to prove that you're smarter than everyone. Please read my posts next time. If you disagree, at least disagree with what I wrote, not what you seem to think I wrote. I never blamed lactic acid for anything.

I did. You got pretty basic stuff wrong, it's not like all this is controversial stuff. I have to admit that I was only slightly amused with you, but now that you're playing the victim it's getting more fun. Don't forget to thank Dr Roof for that abstract.

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Arrggh! You obviously did not read my posts, even after I reminded you to. The posted abstract did absolutely nothing to disagree/disprove with my previous posts. I never said LA was a cause of acidosis. I specifically mentioned that acidosis was caused by proton release. This thread is now degrading into silliness, and this discussion is obviously going nowhere. There's really nothing more to discuss. To the OP - sorry its degraded to this point.

from PubMed, an article written by J M Condreuse... The article is written in French, but the abstract was provided in English, and it addresses the causes of DOMS:

"Muscle intolerance to exercise may result from different processes. Diagnosis involves confirming first the source of pain, then potential pathological myalgia. Delayed-onset muscle soreness (DOMS), commonly referred as tiredness, occurs frequently in sport. DOMS usually develops 12-48 h after intensive and/or unusual eccentric muscle action. Symptoms usually involve the quadriceps muscle group but may also affect the hamstring and triceps surae groups. The muscles are sensitive to palpation, contraction and passive stretch. Acidosis, muscle spasm and microlesions in both connective and muscle tissues may explain the symptoms. However, inflammation appears to be the most common explanation. Interestingly, there is strong evidence that the progression of the exercise-induced muscle injury proceeds no further in the absence of inflammation. Even though unpleasant, DOMS should not be considered as an indicator of muscle damage but, rather, a sign of the regenerative process, which is well known to contribute to the increased muscle mass. DOMS can be associated with decreased proprioception and range of motion, as well as maximal force and activation. DOMS disappears 2-10 days before complete functional recovery. This painless period is ripe for additional joint injuries. Similarly, if some treatments are well known to attenuate DOMS, none has been demonstrated to accelerate either structural or functional recovery."

What's the "take home message" here? DOMS is likely due to inflammation, but acidosis may play a role, as I stated in a previous post. As in most things in life, it appears that this is not a black and white issue. There's a large grey area, and several factors play differening roles of various significance.
I make absolutely no claims of knowing everything, but I'm not completely ignorant, either.

Ever since defending a thesis on Thursday, I can't bear to read journals / ex phys stuff... how long does thesis-defense-recovery take ;-)

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maybe she's born with it, maybe it's chlorine
If you're injured and need some sympathy, PM me and I'm very happy to write back.
disclaimer: PhD not MD

you once again show a little bit of knowledge is dangerous. this is not what "LT" is at all. quit whining about people like paulo correcting you when you are, in fact, incorrect. instead, go back and learn some physiology.

There was a very good lecture on muscle soreness at the 2007 ACSM meeting by Priscilla Clarkson. (It was actually the Joseph B. Wolffe Memorial Lecture). It is very easy to understand if you have just a little background (i.e. what you'd get from spending a couple of hours with Astrand's text and a little time on PubMed).

You can order a recording from here.

It would be a very high-yield way to spend $12. I'm not sure if they make the video available.

Phil

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Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!

"how long does thesis-defense-recovery take ;-"

It all depends on the individual, but if 10% of your mental energy used in defending your UG thesis came from anaerobic pathways, you will only need 9% for your masters, so you won't be as sore afterwards.

I have an abstract which elaborates on this, but it is written in Swahili.