Lactic Acid Update

Balance

Since you advise me to change to this thread here I am.

Did i wake up from a nightmare ?

Someone is doing serious questions and doubts about the effectiveness of the lactate threshold theories ? I can´t believe…

And all the threshold followers what they are doing? They simply try to adjust their own past fix threshold concepts to a new emergent new fashion physiologist concepts.

Yesterday (as to say) it was the lactate threshold a kind of salvation and the effective way to improve aerobic condition. Today, it comes someone that doesn´t know nothing relevant about training technique really - Noakes and /or Richard Gibbens – to dismiss all threshold gurus, How is this possible?

Now that´s the intersting part I always mention. Physiologists they don´t agree one with each other. Let them disagree. Yesterday the training was been like it was and today the training that´s the same. The only thing that changes that are physiology knowledge.

ZuZu says : 2) learning to identify physical feedback that signals such laboring is imminent. It so happens that exceeding the lactate threshold is a prelude to the onset of struggling (whether it is the cause of struggling or not). Since blood lactate measurements are now relatively easy to obtain (and can be correlated with heart rate and, in a more subjective sense, with perceived exertion), why not use the lactate threshold as an objective marker for effort intensity?

Correct. Simply what Noakes and others they say recently, Thomas Rowland said since a long ago:

" Since lactic acid is a by-product of anaerobic metabolism, peak levels of blood lactate after short, high intensity exercise have been used as a means of estimating anaerobic fitness. The validity of this approach has been highly suspect because muscle cell lactate is not necessarily in equilibrium with that in the extracellular fluids, and also because blood lactate levels are an expression of clearance and elimination rates as much as muscle production.

Consequently, blood lactate concentrations cannot be assumed to reflect concentrations of muscle lactate.

Paterson and Cunningham used postexercise lactate levels as indicators of "anaerobic capacity" in 10-15 year-old children. In a earlier study the same treadmill protocol, the test-retest coefficient for postexercise lactate levels was only r= .53, with wide intraindividual variability. Measurements of lactate levels during exercise testing of children has therefore not been embraced as a useful means of evaluating anaerobic fitness; lactate values have been used largely to estimate submaximal anaerobic threshold and to identify maximal testing efforts.

Several considerations are important if one uses lactate levels during

exercise testing of children. These have been reviewed by Armstrong and Welsman. Peak blood lactates levels are reached 1-2 min. after a maximal progressive test in children , as compared to 5-7 min. postexercise in adults. Lactate levels may vary according to mode of exercise, test protocol, site of blood sampling, and lactate essay methodology. These factors must be considered when one makes comparisons of lactate levels obtained in different studies"

(I don´t quote more because I don´t want violate copyrights)

Of course that we may still use lactate meters – despite they aren´t accurate but if all “threshold theories” as promoting aerobic condition that goes out as no useful and that goes to the recycle bin.

ZUZu also says that: “Someday the entire notion that there is a "lactate threshold" may be debated or even discarded, but how you feel during that stage of effort between "in control" and "in trouble" will always serve as an effective training barometer.

Rigt ZuZu. But in between the lactate threshold and and running in trouble to the exhaustion you don´t know no useful intensity plateaux that are useful as training formats? I do. If i´m in complete disagreement what Richard Gibbens says (all-out training) I also knows that are effective ways to improve the aerobic condition out of the anaerobic threshold method without get “into trouble”.

One more item to be discussed. Are you sure that dehydration doesn´t affect latic metric tests? Then read what the Russians physiologist they say:

“The dehydration of the athlete during the physical exercise (when the blood samples are collect) determines a false increase of the lactate concentration, that will have to be corrected by the determination of the water deficit calculated for the concomitant determination of the hematocrit.”

I really think that you all, you want to follow the last hype theory, but you may wait. Training for the distance needs well sustain and test concepts, not fashion theories, or the last tests done with rats.

Humor me wrote:

Richard_ wrote: "...recent research has shown that even at high intensities there is no shortage of oxygen to working muscles."

Really? Then why would anyone dream of using EPO? They've got a needle fetish?

There certainly is a decrease in muscle oxygenation (as shown by near infrared spectroscopy measurements). Recent research has demonstrated that muscle deoxygenation is by no means complete when fatigue sets in during submaximal aerobic exercise. However, it is interesting to note that cerebral oxygenation levels decrease sharply in the seconds before exercise ceases. As such, the brain may set the limits to performance and it is possible, although anecdotal, that a cerebral oxygenation threshold might exist.

balance,

I will try to get the reference to you before the end of the weekend (the wife has a "honey-do" list for me this weekend :) ).

In the meantime, here is some info to consider. First, it has only been assumed that an oxygen debt exists in working muscles. It has never been proven, despite numerous attempts by researchers to do so. Any exercise physiology textbook should confirm that oxygen debt has always been assumed, never proven.

And as I alluded to, more recent research has shown that there is no shortage of oxygen to working muscles. So instead of confirming the assumption that there is a limited supply of oxygen to muscles the research shows the exact opposite.

Obviously, there is some upper limit to how much oxygen our bodies can produce (a VO2max). However, that doesn't mean that a person is able to exercise at a rate that elicits VO2max. 70% of tested subjects do not show a VO2max when tested. Instead exercise terminates due to other factors, not limited oxygen. Based on this, many exercise physiologists now regularly use the term VO2peak instead of VO2max and any exercise physiology textbook should note the usage of both the term VO2peak and why it is used in lieu of VO2max.

So if oxygen supply is not the limiting factor in maximal work, then what is? Based on mitochondrial research some have suggested the limit is mitochondrial enzyme density - i.e. there is enough oxygen avaiable but the mitochondria can't process it fast enough to meet the energy needs of the working muscles.

Noakes et al has suggested the limit is found in the central governor.

My personal bias is that the central governor is the correct answer.

This brings up the question as to why VO2peak increases with performance? Why do you need to suck more air as you run faster? The answer is that muscle fiber activation drives oxygen consumption. Activate more fibers and you will consume more oxygen. Faster running requires more fibers to be activated, which results in more oxygen being consumed. Verifying this belief are studies on VO2peak achieved during running on either a flat treadmill or an inclined treadmill. Both muscle fiber activation and VO2peak are higher in the same subject when running uphill on the inclined treadmill as compared to running on a level treadmill. If the subject was truly at VO2max while running on a flat treadmill, then running uphill shouldn't have resulted in a higher oxygen consumption for the same subject.

Is anyone else bothered by the small number of references supplied with the articles on the powerrunning.com site? I just read the "Do High Lactate Concentrations Actually Improve Performance" article there. There were only two references and both studies (on rats) included one of the same authors. Of course, both studies came to much the same conclusion. What a surprise!

Also, there are several mentions of "modern research", "newer research", or "many scientists" without providing references. Maybe this research actually exists, but I certainly cannot tell without accurate references.

Richard,

you say that: "Why do you need to suck more air as you run faster? The answer is that muscle fiber activation drives oxygen consumption. Activate more fibers and you will consume more oxygen. Faster running requires more fibers to be activated, which results in more oxygen being consumed. Verifying this belief are studies on VO2peak achieved during running on either a flat treadmill or an inclined treadmill. Both muscle fiber activation and VO2peak are higher in the same subject when running uphill on the inclined treadmill as compared to running on a level treadmill. If the subject was truly at VO2max while running on a flat treadmill, then running uphill shouldn't have resulted in a higher oxygen consumption for the same subject."

Why would fiber activation require you to breath harder if oxygen debts in the mucle do not exist? The information you provide here seems contradictory to what you said earlier.

Also, there are tools we can use to measure oxygen deficits. Mountain climbers use them. They are called pulse Oximeters. Of course these measure the percentage of haemoglobin (Hb) which is saturated with oxygen in the blood, not what is going on in the muscle. Mountain climbers are more woried about passing out than they are about performace of course. I don't know if this is relevant, but I thought I would mention it anyway.

about a year ago kevin beck completely tore his "theories" to shreds on one of the runners world forums. Dissected and destroyed them. but it did not stop richard. facts? who needs em?

if you want to see how obtuse this fool is, read the thread yourself:

http://forums.runnersworld.com/thread.jspa?threadID=198234&tstart=0

Antonio,

I have worried about dehydration effecting my lactate tests. This is why I try to ensure that the athlete is well hydrated before the test, and that they continue to consume liquids during the tests. Of course there is a method to prevent dehydration from effecting your tests. This requires you take blood hemoglobin measurements before and after the test to see how much your blood volume has decreased. This is designed only for testing the anaerobic threshold, which I do not really test for. I only really need a good estimation, which I can get from the tests I administer.

Richard_ wrote:

recent research has shown that even at high intensities there is no shortage of oxygen to working muscles.

Then try holding your breath during a 10K.

LetsRun.com Pissing Contest Scoreboard 17:25 UTC

Antonio: Pisses on the mark

Richard_: Pisses on his foot

jtupper: "Why the hell do I need to take a piss to prove anything?"

ESPN wrote:

Richard_ wrote:

recent research has shown that even at high intensities there is no shortage of oxygen to working muscles.

Then try holding your breath during a 10K.

ESPN is right, in essence. While you can't hold your breath for a 10km, there is no shortage of O2 to working muscles, even during a highly anaerobic event, like an 800m. There's always O2 available. The RATE of O2 availability is the limiting factor.

jtupper-ware,

What are you talking about? If there is oxygen there then it is there. Rate has nothing to do with it. Lack of mitochondria may mean you can not produce energy no matter how much oxygen you have sure, but I don't think this has anything to do with rate. VO2max is a measure over time so this is a rate. Is this what you mean? Maybe I am just misunderstanding you.

balance wrote:

Also, there are tools we can use to measure oxygen deficits. Mountain climbers use them. They are called pulse Oximeters. Of course these measure the percentage of haemoglobin (Hb) which is saturated with oxygen in the blood, not what is going on in the muscle. Mountain climbers are more woried about passing out than they are about performace of course. I don't know if this is relevant, but I thought I would mention it anyway.

Here's what we know about exercise:

when you START to exercise, your ventilation rate goes up - i.e. - you take more, and bigger breaths. this initial rise is NOT due to any function of oxygen use by the muscles, but is thought to be caused by neural activity from receptors that sense MOTION, not consumption of oxygen.

As for what stimulates ventilation later on in exercise, it is difficult to see - here's what the data tells us: there is an increase in the pressure of carbon dioxide carried by the venous system - the PCO2. This makes sense - your working muscles are giving off more CO2 than normal. However, from what we know of the venous system, there are no PCO2 sensors there, thus they can't be a stimulus for ventilation.

There are sensors on the arterial side that sense PCO2 and PO2. However, over the course of exercise, there is virtually no change in arterial PO2 (actually increases slightly) and virtually no change in arterial PCO2 (actually declines slightly). The lung is more than effective in "blowing off" the excess CO2 and taking in oxygen.

So now we need to consider the muscles themselves. The ability of O2 to be taken from/stick to the Hemoglobin is determined by the inherent binding properties of hemoglobin itself in relation to the partial pressure of O2 - the oxygen binding curve. This is why the mountain climbers use pulse oximeters - since they are at high altitudes with low pressures, the amount of O2 that can be held by hemoglobin is much less. Thus, pulse oximeters used by moutain climbers don't measure "oxygen deficits" - but rather the amount of oxygen being held. [As a technical note, pulse oximeters measure the COLOR of hemoglobin, which is a function of oxygen binding (more O2 bound = more red); however, CO can make the color more red, so pulse oximeters aren't always true measures of O2 in the blood]

In any case, pulse oximeters for someone exercising would show that there is more than enough oxygen in the arterial side - the arterial PO2 remains constant.

I am very interested in this discussion, it is most enlightening. I think I will delay my run for an hour or two to consider the information on this thread.

Wait a minute, I just thought of something. We may all be talking about different things here. Are Richard and jtupper-ware just trying to say that there is always oxygen available in the muscles (or around the muscles, in the blood in this case), but that VO2max is the limiting factor. Because that is what I have been trying to say. In this case we may be able to breath in and absorb just as much oxygen into the blood as any world record holder can, but we do not have the VO2max to be able to utilize the oxygen that is available. A lack of mitochondria is basically what is preventing this from happening. Of course red blood cell concentration plays a part in this too, which is why people take EPO. If you had all the mitochondria you needed but did not have enough red blood cells to carry the oxygen to the cells, the red blood cells would be the limiting factor, not the mitochondria. I guess both can be true, depending on the athlete. One runner could have enough oxygen available, just not enough mitochondria to use it. The other runner could have enough mitochondria, but not enough red blood cells to carry oxygen to it. In the later case an oxygen debt would exist in the muscles. The development of injecting EPO into people originally came about because some people have genetic illnesses that inhibit enough oxygen from getting to their muscles. These patients have oxygen debts to be sure; at least they do if they don't inject EPO into their bodies.

Is all this back and forth all about nit picking the details, and not being clear that we are referring to VO2max being the limiting factor in performance, and that we don't always have oxygen debts per say in the blood, but at the cellular level in the muscles we may never get to use it.

I think this is what we are talking about here, in which case, I think Richard and jtupper-ware just need to be clearer about what they are talking about. This is something that everyone already knows. Once you try to give it a new name or speak about it arbitrarily no one knows what you are talking about. Then you can go and give it a new name and call it a new theory when all the while it is the same theory just disguised to confuse everyone from the truth. Or perhaps you just don't know better.

balance,

"Why would fiber activation require you to breath harder if oxygen debts in the mucle do not exist?"

When a muscle fiber is inactive it requires little energy to sustain itself. For example, if you are sitting on your couch watching tv, you are not actively contracting many muscle fibers and your energy needs are small - you need only produce enough energy to sustain life and operate the remote.

However, if you get up from the couch and start running you engage a larger volume of muscle, muscle that is being used to propel you. These active muscle fibers' energy needs are now higher than they were when they were inactive sitting on the couch. To meet the energy needs of these fibers, the mitochondria must produce more energy. This calls for more oxygen.

Your body does not constantly intake all the oxygen it is capable of intaking at all times. Your heart rate and respiration vary depending on the level of activity of your body. While sitting your respiratory system is working at an idle. As your activity increases the respiratory system increases its output to meet the increasing demand. The muscles and mitochondria are signalling the brain to increase oxygen delivery. The brain speeds up respiration and heart rate, thus delivering more oxygen to the working muscles.

When a muscle fiber fires, it is an all or none contraction. The fiber fires as fast as it is capable and with all the strength it can produce. At a walking pace you only need a small number of fibers firing to sustain your pace. To go faster you must either fire the working fibers more frequently or recruit more fibers or both. Having to increase firing rate and # of active fibers doesn't mean that the working fibers were at their limit of oxygen consumption, it only means they were not capable of producing additional power to reach and sustain your increasingly faster pace. These newly recruited fibers were at rest and are now being called upon to work. Their energy needs increase and more oxygen is requested from the cardiovascular systems for these fibers. Thus, the faster your pace the more energy you burn and the more oxygen you need to produce that energy.

At some point you are working as hard as you are capable of working and your oxygen consumption has peaked. The question is did you reach the limit of your body's ability to absord, transport, and utilize oxygen? Or did your muscles reach their working limit due to some other reason and now that they are at their limit oxygen consumption peaks? If you could get your muscles to work faster or if you could recruit more muscle fibers would oxygen consumption also increase or would it either plateau or drop?

At VO2max the theory has been that you have reached the limit of your cardiovascular system, that oxygen absorption, transport, and delivery has plateaued, but that your muscles can continue to work even harder. But by working even harder your muscles' energy needs can not be met via aerobic metabolism and anaerobic metabolism plays an increasing larger role in providing the energy needed by the working muscles. The by-products of anaerobic metabolism (lactate and/or H+) were believed to cause fatigue, resulting in a mandatory decrease in pace.

If you were truly at your VO2max then activating more fibers should not increase oxygen consumption, since by definition you are at your bodies max ability to absord, transport, and deliver oxygen to those working muscles.

To test this I have you run on a flat treadmill in a maximum test and measure your VO2peak. After you have recovered sufficiently I have you repeat the test but have you run on an incline (which from previous studies I know causes a greater activation of muscle fibers). Again you run to your maximum ability and I test your VO2peak. If your reached VO2max while running on a level surface, you should not use more oxygen when running uphill even though more muscle fiber is activated. If your VO2peak increases when running uphill it simply means your muscles are using more oxygen while running uphill than when running on a level surface, indicating that additional oxygen was available when running on a level surface but was not used by your muscles for whatever reason.

Does this answer your question?

sometimes I get tired

balance,

I'm using the term VO2max in the classical definition - the ability of the cardiovascular system to absord, transport, and deliver oxygen to the tissues of the body.

Saying there isn't sufficient mitochondrial enzymes to process the available oxygen is not the same thing as saying there is an insufficient supply of oxygen to work with.

I am arguing that the classic definition of VO2max is inaccurate.

I do accept that it is possible that the mitochondria are incapable of meeting the energy needs of working muscles via aerobic metabolism. That the limit for aerobic metabolsim is found withing the mitochondria and not the cardiovascular system.

It is a different discussion as to what whether the by-products of anaerobic metabolism cause fatigue or are simply correlated with fatigue.

Does this clear things up as far as what I mean?

Richard,

I believe your VO2max tests on the treadmill might be flawed. Everyone knows that oxygen consumption goes up when you recruit more muscle fibers. We call this upping the intensity. It can be argued that all tests which try to measure VO2max are flawed, and since this is the case you can not use it to give any credibility to your theory. The only thing we can gain from a VO2max test is that we can measure improvements or declines in fitness. Any measure we obtain from the test really doesn't tell us anything. It is not like a high measure is going to tell us that we can run a world record or anything.

A 200 meter sprinter can measure a higher VO2max during a VO2max test than a marathoner. Perhaps it is because they can recruit more muscle fibers, maybe not. The sprinter can't last as long the test as the marathoner, but their VO2max measured over a span of time can be greater. We only need the 200 meter runner to last 1 minute at their peak oxygen consumption to obtain an adequate reading.

You also state that "At some point you are working as hard as you are capable of working and your oxygen consumption has peaked. The question is did you reach the limit of your body's ability to absorb, transport, and utilize oxygen? Or did your muscles reach their working limit due to some other reason and now that they are at their limit oxygen consumption peaks?"

If your muscles reached there working limit then running up a hill would not make them work harder. I still don't see your point.

And, I might point out that recruiting more muscle fibers would increase the amount of oxygen utilized because mitochondria are in the muscles and they aren't going to do there job until they are called upon. Mitocondria use the oxygen, yes? I am not sure you have thought your entire theory all the way through.

Just my two bits on the subject:

I think Richard has taken the Central Governor theory a bit too far. I think he has taken the "why" and tried to change the "how" of distance running. There have been numerous theories of why fatigue occurs, why runners increase performance, why we are limited in our performance over the last century. What hasn't changed much since Lydiard is the "how". As scientists we have to realize there is a lot that we don't know and don't understand. There is a reason why successful distance runners over the last 50+ years have trained in near the same way. If training 4 days a week was successful every elite runner would be doing so. Sadly, there has NEVER been a study that studied the long term effects of training (1 year +). Significant changes in performance take years to develop. This is why physiologists and others in the field disagree so much. All of our studies on training are somewhat faulty because the time period is too short. What we have to do as scientists and students of exercise science is to realize there is NOTHING we can conclude from our studies that is going to seriously affect how runners train. What we can do is try to explain WHY things happen instead of trying to change the HOW.

We know that successful distance runners run high mileage at times, they push their systems to the limit 2-3 times a week, they put in very long runs. That is the "how", so what about the "why"? Why do runners put in high mileage and run long runs? Why do runners run intervals? Why do runners run the ever holy tempo run? A lot of it has to do with specificity. If your goal is run a 15:30 5k then you better spend a lot of time running :75 quarter pace. If your goal is to run a 2:30 marathon then you better spend a lot of time running 5:45 mile pace as well as put in long runs up to 2:30 in duration. Why has the tempo run become the holy grail? Because it more specifically reproduces what you need to do in a race than short interval work or easy running. You're running at a hard, even pace for a number of miles. No, you're not running all-out, but there's only so much you can accomplish with 400 repeats or mile repeats. This goes back to Lydiard. If all you do are intervals then during your race your body will expect a rest. So, why should marathon runners even bother running short, fast intervals like 400s or 800s or even mile repeats or possibly even short races like 3k-10k? Because intervals and shorter races push the body systems to the limit and if you want to increase performance you have to push the limit forward. You're not going to be able to do that on 4 days a week.