I don't understand Lactate Threshold

otter wrote:

Ganbatte wrote:

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

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.

Ganbatte wrote:

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?

Ganbatte wrote:

Dairyland wrote:

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?

Ganbatte wrote:

It is the most confusing topic ever. It seems like there is no clear consensus on what lactate threshold is.

The most common definition I see is that it is the point at which lactate is accumulating in the blood faster than the body is able to clear it. But then it seems like anaerobic threshold is the same thing as lactate threshold but I've seen other things that say anaerobic threshold is different. And then the science behind it is confusing as well some people make the distinction between lactic acid and lactate, but others don't.

What is bothering me is that I will go and read an article that explains lactate threshold or anaerobic threshold and I will understand it just find but then I will go read another article and they will seem to contradict each other! I can't keep it straight. Anyone else have this problem?

Harambe wrote:

Ganbatte wrote:

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?

A lot of what you said is fine but the common error is that lactate production is acidifying. It is not, it actually takes one proton from solution and one from NADH to make lactate from pyruvate.

https://en.wikipedia.org/wiki/Lactate_dehydrogenase

The current model is that ATP hydrolysis is the truly acidifying reaction. Every time ATP is hydrolyzed to ADP a proton is released. If these ATP molecules came from the mitochondria (generally aerobic respiration) then the proton released can be consumed by mitochondrial ATP synthesis.

Under intense exercise, you need generate ATP from free glucose and glycogen, these ATP molecules are then used releasing more protons that the mitochondria doesn't have the capacity to consume. This leads to acidosis.

Regardless, accumulation of lactate correlates strongly with acidosis so it's a good biomarker of anaerobic energy production even if it isn't the mechanistic culprit of fatigue.

Ganbatte wrote:

Harambe wrote:

A lot of what you said is fine but the common error is that lactate production is acidifying. It is not, it actually takes one proton from solution and one from NADH to make lactate from pyruvate.

https://en.wikipedia.org/wiki/Lactate_dehydrogenase

The current model is that ATP hydrolysis is the truly acidifying reaction. Every time ATP is hydrolyzed to ADP a proton is released. If these ATP molecules came from the mitochondria (generally aerobic respiration) then the proton released can be consumed by mitochondrial ATP synthesis.

Under intense exercise, you need generate ATP from free glucose and glycogen, these ATP molecules are then used releasing more protons that the mitochondria doesn't have the capacity to consume. This leads to acidosis.

Regardless, accumulation of lactate correlates strongly with acidosis so it's a good biomarker of anaerobic energy production even if it isn't the mechanistic culprit of fatigue.

ahh darn, I thought I got it.

Ok so I looked up ATP hydrolysis and I'm not seeing anything about acidosis... Do you have a source?

Ganbatte wrote:

I like metabolism more wrote:

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