T Nation

We don't produce lactic acid.

I recently read an article
(http://www.sportsci.org/jour/0102/rar.htm), which has changed my opinion regarding the lactic acid related "burn" people experience while exercising.

I trust you guys will check out the article, but I'll post a few paraphrased bits, nonetheless.

If you follow how many protons are produced/consumed during lactate fermentation you'll see that the common belief just doesn't hold.

A proton is produced when glucose is phosphorylated with the aid of hexokinase. One more proton is produced when fructose-6-phosphate is phosphorylated with the aid of PFK. Two more protons are produced when 2 G3Ps are oxidized with 2 NAD+s.

So, four protons are produced.

The production of 2 pyruvates consumes two protons. And the production of 2 lactates consumes two protons (the 2 lactates use up another 2 protons but they're from 2 NADHs and therefore would be used in chemiosmosis, so I didn't include them).

So, four protons are consumed, no net gain or loss.

What about the proton from the carboxyl group?

Well, the first carboxyl group containing intermediate produced in the glycolytic pathway is 1,3-biphosphoglycerate. The dephosphorylation of 1,3-bisphosoglycerate results in 3-phosphoglycerate, but the removal of the phosphate from the first carbon makes it the carboxylate form, not the carboxylic acid form, so it's already ionized. And I believe that each "acid" produced en route to lactate is in the ionized form.

Moreover, I read elsewhere (http://www.bio.mtu.edu/campbell/401l16bp1.html) that the carboxylate ion of pyruvate interacts with lactate dehydrogenase (the enzyme which converts pyruvate to lactate and vice versa), so lactate has to be produced, not lactic acid.

The protons, which cause the exercise related acidosis come from incomplete glycolysis (no lactate produced) and ATP hydrolysis.

So, lactate actually delays acidosis by reducing the proton load.

To be honest, I'm surprised I haven?t come across many dissenters on this topic.

I'd be interested to hear what you guys think.

Bumpity bump bump…
come on Goldberg Mr “Student of the year”, and you Berardi-type smart asses…

dude i havent had exercise science classes in a couple of years. I have no clue. i was exercise science student of the year for 99-00. so that means something, right? His post was really hard to follow and i really just glanced over it but in one spot he said something about lactate. If im not mistaken, lactate and lactic acid are one in the same. But again i just glanced so i dont really know. anybody else got the patience to tackle this?

I read the study, and I also agree with Goldberg that I’m not sure what muhr is asking or inquiry about.
But I will attempt to help shed some light on the lactic acid issue. I assume muhr is wondering what role lactic acid plays in fatigue. I’m not sure if this is his intention/question, but I will assume it is, and address it.
Back in the early days of lactic acid research (early 1900’s) it was assumed that glycogen was the precursor of lactic acid. In addition, it was assumed that lactic acid was converted back to glycogen and the energy for this conversion came from the oxidation of remaining lactic acid. This was assumed since oxygen consumption remained elevated for a few minutes after exercise. This was measured by an increase in heat - known as recovery heat.
Then A.V. Hill proposed the theory that the formation of lactic acid was necessary for the contractile process of muscle. In other words, it was thought that lactic acid was necessary for muscle contractions to occur. This theory was debunked when a study was performed by Lundsgaard that consisted of poisoning a muscle with iodoacetate (in order to completely stop lactic acid production) but the muscles could still contract. There goes that idea.
On a similar note, prolonged exercise can be performed without lactate production, and resting muscle can accumulate lactate without contracting.
I could say much more, but I don’t know if this it the type of information you are seeking.

lactic acid is the byproduct of glycolysis, I believe. Glycolysis occurs when the body is in a state of anaerobic activity, i.e. weightlifting bursts. Therefore, the lactic acid “burn” that some feel does exist. Our body doesn’t have lactate sitting around in bundles waiting to be turned into lactic acid, but rather it is produced (causing the burn), then made into something else (removal of the burn).

I wasn't really asking for information on lactate/lactic acid, but rather asking to get your opinions on the assertion that exercised induced metabolic acidosis isn't caused by lactic acid on account that we don't produce lactic acid, we produce it's conjugate base lactate.

Sorry if I didn't make it clear, but I intended for a distinction to be made between lactic acid and lactate. Lactic acid has an ionizable proton and therefore contributes to acidification whereas lactate doesn't have an ionizable proton and therefore doesn't contribute to acidification.

So, if we don't produce lactic acid, but rather lactate, then lactic acid can't be the cause of exercise induced metabolic acidosis.

The "burn" associated with exercise is caused by protons from ATP hydrolysis and incomplete glycolysis ie, no lactate being produced.

in most books i looked at lactate and lactic acid were used interchangeably. In the long run, i dont think it matters too much unless you are on the research side of things.

As Goldberg points out text books use lactate and lactic acid interchangeably. I'm asking that while reading my posts to see those terms as being literal, that is, lactic acid can donate a proton and lactate can't donate a proton.

I'll explain further using an example to clarify.

If we were to make a 1 molar solution using lactic acid (chemical formula: C3H6O3), the pH of the solution would be around 2 (I'm not interested in doing the math so I'm just assuming). Now, if we were to make a 1 molar solution using sodium lactate (chemical formula: NaC3H5O3), the pH of the solution would be 7. Now, lets apply this to a cell within a hypothetical organism. Lets say that the end product of a metabolic pathway in the organism was lactic acid. The pH of the cell would drop if the production of lactic acid exceeded its buffering capacity. Now, lets say that another organism instead of producing lactic acid at the end of the metabolic pathway produced lactate. That organism's cell would not experience a pH change because it didn't have a proton to donate. I'm saying that us humans are the latter organism we don't produce lactic acid and consequently lactic acidosis is a myth. The processes that contribute protons and thus cause acidosis are ATP hydrolysis and incomplete lactate (lactate is a sink for protons) production.

For a biochemical explanation using the glycolytic pathway you can refer to my first post or better yet go to the URL(s) I provided in my first post.

Goldberg, as far as training goes I think your right, it doesn?t matter, but I don?t think we should be perpetuating a myth, I mean damn, this is science.

Its actually a mix or art and science but thats another discussion.