I don't understand Lactate Threshold

otter wrote:

There are numerous errors in Miss Adventure Pants article.

Also, 4mmols as I stated earlier is not everyone’s LT. It os for some though.

There is plenty of literature specifically defining LT as 4mmol. That's why in my first post I tried to separate out AT and LT. They are the same general idea, but often when you see LT in the literature, it specifically means 4 mmols. I guess you have to be certain what the author's definition is to make sure you are interpreting the article correctly. .

And if the chart from Miss Adventure is an error, it's not specific to this website. Like I said there are hundreds if you do a google search for Anaerobic Threshold graph.

Yes, I was under the impression that acidosis during intense exercise is from non oxidative-phosphorylation-derived ATP splitting. Below VO2max the proton production from ATP splitting can be completely consumed by ATP ox-phos in the mitochondria. When you start using ATP from glycogen/free glucose and phospho-creatine you end up exceeding the H+ consumption capacity of the mitochondria -> acidosis.

I am far from a physiological biochemist but that is my understanding.

Curbside Pickup wrote:

otter wrote:

There are numerous errors in Miss Adventure Pants article.

Also, 4mmols as I stated earlier is not everyone’s LT. It os for some though.

There is plenty of literature specifically defining LT as 4mmol. That's why in my first post I tried to separate out AT and LT. They are the same general idea, but often when you see LT in the literature, it specifically means 4 mmols. I guess you have to be certain what the author's definition is to make sure you are interpreting the article correctly. .

And if the chart from Miss Adventure is an error, it's not specific to this website. Like I said there are hundreds if you do a google search for Anaerobic Threshold graph.

That’s why there is so much confusion. LT does not mean 4mmols. Anyone that has ever done testing knows this.

otter wrote:

Curbside Pickup wrote:

There is plenty of literature specifically defining LT as 4mmol. That's why in my first post I tried to separate out AT and LT. They are the same general idea, but often when you see LT in the literature, it specifically means 4 mmols. I guess you have to be certain what the author's definition is to make sure you are interpreting the article correctly. .

And if the chart from Miss Adventure is an error, it's not specific to this website. Like I said there are hundreds if you do a google search for Anaerobic Threshold graph.

That’s why there is so much confusion. LT does not mean 4mmols. Anyone that has ever done testing knows this.

Yes I agree this is the source of confusion.

This is semantics, but I'd disagree with you when you say "LT does not mean 4mmols" . LT =4mmols, that's very often the definition authors use in papers.

We both agree that 4 mmols does not represent the inflection point of the lactate accumulation curve for every person. Again this is why you have to be careful and it would be nice if the exercise science and coaching community published a set standard.

I reference this page often because the terms are so confusing.

You can all define LT anyway you want, but it will vary from day to day. It’s important to know roughly what pace you should run at, rather than how many mmol you have in your blood. Most LT work should be done just slower than your threshold, for many people this is somewhere around HM pace. You will feel QUICKLY if you are running too fast (faster than threshold)

In Africa where I have trained and done studies, they do not have lactate monitors and calculators for every interval and every run.

You need to learn how to run LT by feel.

Yes. I guess we agree then.

There is so much information out there and some legitimate studies showing LT at exactly that level for everyone.

There is so much information out there. My athletes sometimes come to me to tell me they already know their VO2 max and LT pace because their watch calculated it.

Most of the athletes I train are in high school so even though I have a blood lactate tester, I can’t test them because the parents would not be ok at all with that. So with this group I have to approximate it.

If you can’t test, I guess it is somewhat arbitrary what the lactate number exactly is.

Sorry for posting this much but just saw your post as I submitted mine and yes, we are saying the same thing.

What has been most helpful for me with my post collegiate group is testing runners after a maximum 400 and taking measurements at intervals after. You can without a doubt figure their fiber type by doing this both for maximum levels and the amount of time they take to recover to resting levels.

A good short breakdown of AT, LT, and VT:

http://cprphysicaltherapy.com/index.php/about-us/answer/what-is-the-difference-between-anaerobic-lactate-ventilatory-and-threshold

Alan

Harambe wrote:

I like metabolism more wrote:

Aaaacchhh, you were doing well until you said Lactic acid dissociates into Lactate and a hydrogen ion. Lactic acid isn't produced. The hydrogen ion comes from ATP splitting.

Yes, I was under the impression that acidosis during intense exercise is from non oxidative-phosphorylation-derived ATP splitting. Below VO2max the proton production from ATP splitting can be completely consumed by ATP ox-phos in the mitochondria. When you start using ATP from glycogen/free glucose and phospho-creatine you end up exceeding the H+ consumption capacity of the mitochondria -> acidosis.

I am far from a physiological biochemist but that is my understanding.

Yes that's a good explanation. Although when glycogen is low we will feel acidosis at low intensities, because we have to rely more on blood glucose which produces less ATP than glycogen but more H+.

But that is our body's way of saying stop and eat.

And that is another reason why I love metabolism more :)

I like metabolism more wrote:

Harambe wrote:

Yes, I was under the impression that acidosis during intense exercise is from non oxidative-phosphorylation-derived ATP splitting. Below VO2max the proton production from ATP splitting can be completely consumed by ATP ox-phos in the mitochondria. When you start using ATP from glycogen/free glucose and phospho-creatine you end up exceeding the H+ consumption capacity of the mitochondria -> acidosis.

I am far from a physiological biochemist but that is my understanding.

Yes that's a good explanation. Although when glycogen is low we will feel acidosis at low intensities, because we have to rely more on blood glucose which produces less ATP than glycogen but more H+.

But that is our body's way of saying stop and eat.

And that is another reason why I love metabolism more :)

Ok so let me see if I understand this. I've been reading about it and watched a few khan academy videos on cellular respiration. I think I'm going to mess this up so please correct what I get wrong.

When the muscle needs energy Glucose enters the cell to undergo glycolysis. Glycolysis will breakdown the glucose and release 2 ATP and pyruvic acid. If there is oxygen present the pyruvic acid will undergo oxidative phosphorylation and produce around 30 something ATP. If there is not enough oxygen present pyruvic acid will oxidize NADH into NAD+ and then NAD+ goes back to glycolysis? Can someone explain that? What happens to NAD+? When Pyruvic acid oxidizes NADH it picks up the the H+ ion and becomes lactic acid but it immediately dissociates into lactate and an H+ ion. Lactate isn't a problem since it can be converted back into pyruvate but the hydrogen ion causes pain. Someone said that when the H+ consumption capacity of the mitochondria is reached it results in acidosis which I assume is when there are a bunch of H+ ions in the cell? The reason we measure lactate is because the more lactate there is in the blood the more hydrogen ions there are in the cell?

I've heard that Lactate Threshold is roughly the pace that you could sustain for an hour. So lets say some random guy can run 6:00min/mile for and hour. At a pace faster than 6:00min/mile the mitochondria is not able to consume as much H+ than is being produced resulting in the cell becoming more and more acidic? But at a pace of 6:00min/mile the amount of lactate in the blood is relatively constant and thus the level of H+ ions in the cell is relatively constant? So the goal of LT training is to increase the pace at which the mitochondria is able to use up the H+ ions as quickly as they are being produced so that the levels of acidity of the cell does not increase too quickly?

If what I explained is correct could we begin to call this type of training Hydrogen ion training? haha

How did people ever train without lactate threshold training???......

.....the world may never know.....

Alan

If I don’t mind asking Ganbette, have you taken a biology course in school? If you are older, then maybe the opportunity to ask a teacher is less available.

Biology is such a complex topic. You could spend months, if not years, finding the intricacies of cellular respiration. Each component could likewise be analyzed for years.

The science is not the important part when we talk about running though.

The important part is making practical use out of the science.

I would highly recommend picking up a book at your local library on cellular respiration, or maybe a biology textbook. The people are trying hard on this thread. But very few people will be able to give a thorough explanation of anaerobic respiration.

And the goal of LT training is to run faster while maintaining a largely aerobic component. Or “bumping” your threshold up a notch.

Not in school anymore and hated biology when I was there.

I understand that this science isn't very important for me to know but I find it interesting when it relates to running. Lactate threshold always bothered me because it seemed like there were so many different definitions and seemed very confusing. I think I have a better grasp of it now, but are there any books that you would recommend on cellular respiration? I felt like this was a good question for LetsRun because a lot of biology videos will be able to explain the science but they won't translate it to running.

If the goal of LT training is to run faster while maintaining a largely aerobic component could that also be defined as limiting the amount H+ ions in the cell? The more aerobic the less H+ ions?

Runningart2004 wrote:

How did people ever train without lactate threshold training???......

.....the world may never know.....

Alan

? I guess we/they, just did intervals @ desired race pace. ?

So yeah, to start glycolysis produces 4 ATP, but only nets 2 because 2 were used up just by the process.

Then, yes it goes through oxidative phosphorylation in which it starts with the Kreb cycle and on to the electron transport chain.

I don't know if was intentional or not but I like how you said 30 something ATP is produced because if you understand the electron transport chain you know that there is a maximum yield that probably never happens. The most fascinating thing about it for me is the idea that the ATP synthase actually mechanically binds the phosphate back on to the ADP to create ATP again. It's kind of crazy and unbelievable to think that this is how the process happens.

To your point, you train to increase the size and amount of mitochondria to basically do more of this kind of work. So what you have said is kind of true in that at a greater size and surface area the mitochondria can do more.

Runningart2004 wrote:

How did people ever train without lactate threshold training???......

.....the world may never know.....

Alan

This sort of stuff wasn't widely understood in Lydiard's time and his athletes didn't do specific threshold training.

There is common reference to "raising" the threshold, but afaik, the threshold is largely genetic and can't be raised as such. It is more about training so that this intensity is more comfortable.

Best thread on letsrun in a very long time. Thank you!

Disciple wrote:

Runningart2004 wrote:

How did people ever train without lactate threshold training???......

.....the world may never know.....

Alan

This sort of stuff wasn't widely understood in Lydiard's time and his athletes didn't do specific threshold training.

There is common reference to "raising" the threshold, but afaik, the threshold is largely genetic and can't be raised as such. It is more about training so that this intensity is more comfortable.

Yet, Lydiard stated in his books that his athletes were running at paces around 3:00 per kilometer during their Marathon Conditioning Phase. If you looked at Snell and Halberg at the starting line back then you probably would not have thought they could win anything. Snell was built like a tank and Halberg had a lame arm.

Same thing in a different package. It doesn't matter how you get there as long as you do.

Thanks, Otter!

It was intentional that I said 30 something ATP. I don't understand the electron transport chain but in a khan academy video, they said that the amount of ATP produced varies.

I know it's a spectrum but I thought that higher intensity training increased the efficiency of the mitochondria more than increasing the size and amount.