Definiton of Aerobic and Anaerobic, lets get up to date here.

dingle wrote:

wellnow wrote:

Oxygen delivery is ALWAYS sufficient during lactate production. It is another myth that lactate is produced because of low oxygen delivery.

If you want to explain this, you are going to have to learn to read what other people write and not make these incorrect characterizations. I said that at high levels of exertion, the production of energy (ATP) is limited by oxygen delivery because lactate oxidation (break down of lactate into ATP) is limited by oxygen delivery.

Are you saying that production of ATP is never limited by oxygen delivery?

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No, I am saying that lactate can be, and is produced when there is a plentiful supply of oxygen.

Old textbooks stated that lactate was produced when oxygen supplies was limited, and thus the misleading term "anaerobic glycolysis" came about.

In some ways I can see the point that wellnow is making. A few weeks ago I had my VO2 tested in a lab and seeing the O2 and CO2 numbers helped clarify things for me. The last few minutes of the test, when I was working really hard I described as being "anaerobic." The exercise physiologist was quick to point out that I was not in fact "anaerobic" and that this is a misnomer. He showed me that during those last few minutes I was actually using MORE oxygen than I had during any other point in the test. By definition, this would be a contradiction since anaerobic means without oxygen. The reason I was hurting so badly was the accumulation of lactate. Now I realize that a VO2 test is not the same as a 5k, but I think that the principles are the same.

I also see the point wellnow is trying to make. I still want to know if anaerobic production of ATP produces lactate, why is it a mistake to use the word anaerobic? I don't speak about what happens at the end of a 5K race, or in a VO2max test, but I'm thinking more in the context of interval training. What shall I call the interval sessions which trigger so much anaerobic production of ATP, that subsequently accumulates lactate faster than our body can process it? I say it is still appropriate to call them anaerobic intervals, because it is precisely the anaerobic production of ATP that is the key attribute. For someone else to say, wait a minute, don't you know that lactate is being used as an aerobic fuel? True or not true, it's just beside the main point that the whole goal of the training session is triggering lactate accumulation with the anaerobic production of ATP. I say it is appropriate to call this anaerobic, because it is more anaerobic than tempo runs, or easy runs, or recovery runs.Is my use of the term anaerobic wrong, incorrect, or confusing, in this training context of interval sessions?

I know what wellnow is trying to say because we've been exchanging e-mails privately as well! But here is my question on this topic (and wellnow is more than welcome to jump in here); I also thought it's misleading to describe "anaerobic" as "without oxygen". In fact, I personally described "anaerobic" as "without ENOUGH oxygen". So, Mr. "Yes and No", when you were gasping air and when you were in fact using MORE oxygen, was your body REQUIRING even MORE oxygen than your body was actually using? In other words, were you getting into OXYGEN DEBT?I'm glad I caught this.

I keep seeing this thread popping up but this is the first time I looked at it, but my quick and dirty explanation is this. It is a supply and demand problem.

ATP is needed for a few key things including the muscle contraction/relaxation cycle itself, maintain the sodium/potassium pump, etc. With high intensity exercise, high levels of ATP are needed, so the demand is high. I don't like to think of lack of oxygen as the limiting factor per se, but rather ability of the mitochondria to utilize what is avaialble.

In the cytoplasm, glycolysis takes place, and oxygen is not part of this. Pyruvate is produced and may or may not be converted to lactate. (We won't get caught up differentiating lactate vs. lactic acid.) The pyruvate can then enter the mitochondria and go into the Krebs cycle for great numbers of ATP to be produced, and I think somebody described this previously in the thread. It may also be converted into lactate, which has a number of fates, with metabolism and transport.

Not sure if anybody mentioned it, but one of the key things here is that lactate helps keep aerobic metabolism going. When glucose is broken down to pyruvate, NAD is converted to NADH. This balance between and availability of NAD and NADH is critical. When pyruvate is converted to lactate, the opposite happens, NADH goes back to NAD. So, at high rates of glycolysis, conversion of pyruvate to lactate helps maintain this balance. So lactate isn't a bad thing. See Robergs' articles if you want more information from the scientific end of things - he goes into a lot more biochemistry (pKa's, etc.)

I've run out of time to type now, but can come back to this later and join the discussion if anybody wants more info.

These are some good questions and I will try my best to answer. The reason it is innacurate to be called anaerobic whether it is an interval, a race or a stress test is because it is actually more aerobic than anaerobic. Your athletes are using a greater amount of oxygen (and accumulating a greater amount of lactate) when they are running really hard in an interval session than when they are doing an easy run or even a tempo run. All of the huffing and puffing is to get rid of the high levels of CO2 to utilize or clear the lactate. The confusing part about this and the reason the terms aerobic and anaerobic are inaccurate is that the body is never 100% aerobic or 100% anaerobic. Even sitting here reading this message there are still anaerobic pathways being utilized. So maybe the best way to describe your workouts would be to call them 3k, 5k, 10k or marathon pace.

No one has said that the energy pathway is "100%" aerobic or anaerobic at any time.

Isn't it fair to say that the amount of energy derived from anaerobic pathways is greater at 3K pace than at marathon pace -- to use the system you suggest? The aerobic system is nearly maxed out, so it's supplemented by anaerobic production, right?

You are mostly right, apart from "The reason I was hurting so badly was the accumulation of lactate"

It's the accumulation of hydrogen ions, aka H+, aka, protons, which cause the acidity and hence the pain in your muscles.

This accumulation of H+ will occur towards the end of any race, even if the lactate accumulation is low, such as in a marathon.

The formation of lactate actually reduces proton accumulation by accepting the protons (which come mostly from anerobic metabolsim) into its molecular structure.

What happens to the protons after that is a very complicated problem for physiologists to consider.

However, regardless of pace, all races from 100m upwards cause H+ accumulation and thus pain.

So naturally Hydrogen ion concentration has always shared the blame along with "lactic acid" as being the cause of fatigue, because these accumulations coincide, even though this has never been proven.

Isn't it fair to say that the amount of energy derived from anaerobic pathways is greater at 3K pace than at marathon pace -- to use the system you suggest?

This is a really interesting question. It depends on what you refer to when you say greater. If you mean that there is more anaerobically derived energy at 3k pace vs marathon pace, then you are correct. If you mean that there is more anaerobically derived energy than aerobically derived energy at these different intensities than I am not sure. In other words, lets say that marathon pace is 90% aerobic and 10% anaerobic and that changing to 3k pace becomes 60% aerobic and 40% anaerobic. I am just making these numbers up to make my point so please don't hold me to them. This may seem like a simple comparison, but it is not. Since it takes more total energy to run at 3k pace than marathon pace, you can't just look at the percentages and say it is more anaerobic. The aerobic pathways are greater as well. I am trying not to make this more confusing. I hope that this helps.

[quote]The Light wrote:

I also see the point wellnow is trying to make. I still want to know if anaerobic production of ATP produces lactate, why is it a mistake to use the word anaerobic? I don't speak about what happens at the end of a 5K race, or in a VO2max test, but I'm thinking more in the context of interval training. What shall I call the interval sessions which trigger so much anaerobic production of ATP, that subsequently accumulates lactate faster than our body can process it? I say it is still appropriate to call them anaerobic intervals, because it is precisely the anaerobic production of ATP that is the key attribute. For someone else to say, wait a minute, don't you know that lactate is being used as an aerobic fuel? True or not true, it's just beside the main point that the whole goal of the training session is triggering lactate accumulation with the anaerobic production of ATP. I say it is appropriate to call this anaerobic, because it is more anaerobic than tempo runs, or easy runs, or recovery runs.

Is my use of the term anaerobic wrong, incorrect, or confusing, in this training context of interval sessions?

[quote]

When lactate is produced, two ATP molecules are also produced from each blood glucose molecule, and 3 ATP from muscle glycogen.

This ATP, known as Glycolytic ATP is broken down to release energy anaerobically.

The lactate is broken down through a series of reactions which take place inside the mitochodria to produce ATP from aerobic respiration.

The formation of lactate was wrongly named Anaerobic Glycolysis, because many decades ago, it was thought that the products of this reaction were glycolytic ATP and Lactic acid, which was thought to be only useful after the excercise was finished.

We now know that lactate formation produces BOTH ANAEROBIC AND AEROBIC fuel.

When you sprint 100m, the glycolytic ATP helps you to maintain your pace for several several seconds after creatine phosphate levels have become severely depleted.

During this time and for several seconds after the race, lactate accumulates.

So 100m races are mostly anaerobic because aerobic respiration cannot provide energy fast enough, but it does supply most of the energy after the race is over.

If you run 10x400m @ 1500M pace, the first few seconds of each 400 are mostly anaerobic and the rest of the 400m is mostly aerobic. In all session is about 80+% aerobic.

Nobby, there is a small oxygen debt during track races, because the creatine phosphate system can only be fully replenished when you either stop running or slow down, and this re-synthesis requires oxygen.

The increase in breathing rate comes from a combination of steadily increasing oxygen consumption, (because the pace becomes harder and harder to maintain) and constantly increasing carbon dioxide production, which is a consequence of the constant increase in carbohydrate breakdown for respiration.

Remember this one from biology class?

C6 H12 O6 (glucose)+ 6O2(oxygen)---> 6CO2(carbon dioxide) + 6H2O(water) + ATP( energy)

For the most part there is a lot of good discussion here.

A few things... Indeed hydrogen ions seem to be a major source of fatigue and that is the model that I use. I have seen some data which conflict that (may have been in vitro stuff), but I have also seen a lot to support that. Indeed lactate is "guilty by association," and in fact it has been demonstrated that lactate is not related to fatigue, breathing heavy, etc.

Tests have been performed to dissociate the two. Two that come to mind are infusing muscles with lactate so that lactate levels are high before any exercise even begins, and fatigue is basically unaffected. So, the lactate itself clearly is not the cause of fatigue. Additionally, some interesting studies have examined this using hypoxia (altitude simulation) and McArdle's disease patients. Research has also dissociated the ventilatory threshold from lactate levels. So it is not theoretical that lactate is not associated with fatigue but has been demonstrated many times with many creative methodologies. Yes unfortunately, the idea that lactate is a bad thing causing fatigue exists.

Just a clarification from another post - recovery from sprinting is also very much aerobic. Even though sprinting is not aerobic, the CP pathways are restored through aerobic metabolism - hence people breathe hard after finishing a sprint.

I would like to think that H+ is innocent until proven guilty. Scientists have been trying to pin the blame on those "nasty protons" for 100 years or more and there is still not enough evidence for a reliable verdict.

I would like to introduce another concept; that those "nasty protons" are actually nothing of the sort. The pain generated from the H+ is an extremely reliable guide to pace judgement for us and all mammals and has been for millions of years.

Without the pain from H+ to guide us in our energy output, how would the human race have survived?

The same survival instinct helps us to pace our training and racing.

Message:

Nobby wrote:

I know what wellnow is trying to say because we've been exchanging e-mails privately as well! But here is my question on this topic (and wellnow is more than welcome to jump in here); I also thought it's misleading to describe "anaerobic" as "without oxygen". In fact, I personally described "anaerobic" as "without ENOUGH oxygen". So, Mr. "Yes and No", when you were gasping air and when you were in fact using MORE oxygen, was your body REQUIRING even MORE oxygen than your body was actually using? In other words, were you getting into OXYGEN DEBT?

I'm glad I caught this.

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So in a 5K race, when a runner slows down about 100 meters from the finish, staggers and falls to his hands and knees for a couple of seconds; then slowly gets up, staggers about 10 to 15 meters further; falls to his hands and knees again for a couple of seconds; slowly gets up and continues to do this until he crosses the finish. Would you say he has gone into oxygen debt?

I hope that he would receive prompt medical attention. I certainly wouldn't give a medical diagnosis since I'm not a doctor and obviously, neither are you.

I saw the above situation happen. We have heard that he was examined and no physical problems were detected. Some have said that it was similar to a 400 runner who pushes himself to the limit or maybe beyond. If this was the case, my question still is - could this then, be an example of oxygen debt if there is such a thing?

Thank you.

No, it's not oxygen debt that would cause such a collapse, I am sure that there is no such true medical diagnosis. If he has a healthy heart, then it is more likely that the runner may have been depleted of glycogen and/or dehyrated.

I have seen this in a road 10k where a man was staggering in the last half mile and after the race hes was weak, dizzy and unable to talk. I told his wife and the medics who attended him that I had seen him staggering in the last half mile and that I was sure that he was glygogen depleted and so I got him some energy drink and food, after making sure he was not diabetic.

The term oxygen debt as most people use it is not an accurate description of what is really happening physiologically when we are gasping for breath.

The term oxygen debt is attributable to A.V. Hill, the most famous and infleuntial physiologist of all time.

In 1923 Hill coined the term oxygen debt to describe his hyopothesis that lactate could only be removed by oxidation after an excercise, and that the cost of this removal used 20% of the energy contained in the accumulated lactate to send the other 80% back to the liver for recoversion to glycogen.

He also suggested that there was an oxygen deficit in the early part of excercise was also incurred an oxygen debt. In this idea he was correct, there is a small oxygen debt to be repaid for the resynthesis of creatine phosphate.

Hill's description was so plausible and his inflence so great that the term oxygen debt became ingrained in public consciousness and there it will remain.

Ongoing research has shown that there are several reasons why we are gasping for breath at the end of a race such as a 5000m.

Towards the end of the race, the runner has reached maximum oxygen consumption. Also, the rate of carbohydrate breakdown for fuel is very high, causing a large production of carbon dioxide to be exhaled.

Carbon dioxide also helps to buffer the acidosis which is the accumulation of hydrogen ions which always occurs to a very high degree in a 5000m race.

Extra CO2 is produced above the level of carbohydrate oxidation bringing the ratio of CO2 exhaled to O2 inhaled the respiratory exchange ratio; RER to 1.2 Although the true ratio is more accurately measured by RQ the respiratory quotient. Perhaps JD can help us out here with more info?

Here is a review of "oxygen debt" along with the proposal of another, more accurate term from Gaesser and Brooks; excess post-exercise oxygen consumption EPOC which has since been adopted by the scientific community:

Med Sci Sports Exerc. 1984;16(1):29-43.

http://www.ncbi.nlm.nih.gov/pubmed/6369064

Metabolic bases of excess post-exercise oxygen consumption: a review.

Gaesser GA, Brooks GA.

The classical "oxygen debt" hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2 consumption in excess of resting that occurs after exercise. The O2 debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between initial, fast ("alactacid"), and second, slow ("lactacid"), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2 consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2 debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2. The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a "reservoir of carbon," which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2 may be understood in terms of those factors which directly or indirectly influence mitochondrial O2 consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise. The terms "alactacid debt" and "lactacid debt," which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., "excess post-exercise oxygen consumption" (EPOC) and "recovery O2," will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.

Some interesting info here from JD on a recent thread:

http://www.letsrun.com/forum/flat_read.php?board=1&id=2318932&thread=2318650