Physiological benefits of "lactate clearance" training?

[padawan]

Pardon me for being a pain but no one addressed this and I'm quite curious about the topic but definitely not a biochemistry whiz.

Training reduces the rate of gluconeogenesis during exercise:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7900783&query_hl=4&itool=pubmed_docsum

So my questions are...

How does reducing the rate of gluconeogenesis during exercise help performance? Is it that, by a reduced rate of gluconeogenesis, we're saving ATP to fuel muscle contraction? Reading about the Cori Cycle seems to suggest that the process of gluconeogenesis results in a net loss of ATP.

I've also read about latate acting as a shuttle, redistributing glycogen from muscles with higher stores to muscles with lower stores. Does "lactate" training help to improve this shuttle system? And is there much benefit to performance from this?

 

[acoggan]

he basically sent me a chart with lactate curve over a long duration, at steady power. Gee, I must have spent 20hr trying to find one just like that.

See Figure 6:

http://ajpendo.physiology.org/cgi/reprint/268/3/E375

 

[SolarEnergy]

SE, why do you think Guy was recording the power and HR measurements at the 2mmol/l and 4mmol/l levels?

I am not sure I understand the question WarrenG. I think you have read something I haven't read yet.

Could you please tell me. When did Guy recorded the power at 2 and 4mmol/L ?

Could it be that he simply wanted to record power & HR at
1) Lactate threshold
2) OBLA

?

 

[SolarEnergy]

See Figure 6:

http://ajpendo.physiology.org/cgi/reprint/268/3/E375

ha ha ha.

Seriously, I have to pay to see figure 6.


Andy, would you mind answering this one, things are starting to make sense now.

How does reducing the rate of gluconeogenesis during exercise help performance? Is it that, by a reduced rate of gluconeogenesis, we're saving ATP to fuel muscle contraction? Reading about the Cori Cycle seems to suggest that the process of gluconeogenesis results in a net loss of ATP.

I've also read about latate acting as a shuttle, redistributing glycogen from muscles with higher stores to muscles with lower stores. Does "lactate" training help to improve this shuttle system? And is there much benefit to performance from this?

Thank you

 

[WarrenG]

I am not sure I understand the question WarrenG. I think you have read something I haven't read yet.

Could you please tell me. When did Guy recorded the power at 2 and 4mmol/L ?

Could it be that he simply wanted to record power & HR at
1) Lactate threshold
2) OBLA

?

It was within the excerpt about the test protocol I mentioned previously. I agree with your 1 and 2. Why would he be interested in HR and power at LT and OBLA?

 

[SolarEnergy]

It was within the excerpt about the test protocol I mentioned previously. I agree with your 1 and 2. Why would he be interested in HR and power at LT and OBLA?

The main benefit he sees into testing LT, is for assessing ones progression. What I mean (or rather, what he means) is that if one can generate lets say 190w at LT, in 2002, and get retested in 2003, and can generate 200w, then there was an improvement. That is the main benefit he sees. That is probably why he focusses on testing at fixed lactate levels.

For what it's worth, because this is my interpretation

 

[SolarEnergy]

I'm not sure what you mean by this.

I re read myself,

I can't tell really.

That is not what I had in mind. I just a bit surprised by your conclusions on gluconeogenesis (that it decreases with training).

I found an article that says the opposite.

Probably the same issue looked at a different angle.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10662708&itool=iconfft&query_hl=3&itool=pubmed_docsum

As usual, I don't mean to confront. You really know that stuff inside out. I am sure you tell the truth. It is just sometimes confusing when trying to learn.

 

[WarrenG]

The main benefit he sees into testing LT, is for assessing ones progression. What I mean (or rather, what he means) is that if one can generate lets say 190w at LT, in 2002, and get retested in 2003, and can generate 200w, then there was an improvement. That is the main benefit he sees. That is probably why he focusses on testing at fixed lactate levels.

For what it's worth, because this is my interpretation

Thanks. Nice that he would share with you.

 

[biker-linz]

What's the point of this quote? Doesn't this assume that the removal of lactate from the bloodstream is somehow beneficial?

But maybe the use of the term "lactate clearance training" wasn't the best way to approach this.

Ignore the proxy talk -- I get that. I'm asking specifically about lactate. Is there any physiological benefit at all in improving the body's ability to "clear" lactate?

Stated another way: is there any evidence -- does anyone think, hypothesize, or otherwise wonder -- if lactate itself and its accumulation in the muscles or blood in any way inhibits performance?

And for what it's worth, I started thinking about this because of Warren and Andy's little discussion in the "test results" thread where they both repeatedly used the term "lactate clearance."

I know this is an oldish thread, but my 2 cents!

Everyone seems to be assuming that cellular acidosis is a bad thing, but that might be far from the truth, see:
http://www.ncbi.nlm.nih.gov/entrez/..._uids=15326352&query_hl=2&itool=pubmed_docsum

As far as lactate contributing to fatigue, I don't think so. A great perspective from Hakan Westerblad:

http://physiologyonline.physiology.org/cgi/content/abstract/17/1/17

which should go some way to answering the OP's question. I think that the term lactate clearance might be being employed a little loosely (I haven't read the thread, but perhaps Andy is using it just because it was already there, so to speak).

The horrible truth is... no-one really knows what causes biochemical fatigue (as opposed to substrate scarcity). One nice idea is:

http://ajpcell.physiology.org/cgi/content/abstract/00273.2005v1

Finally, I haven't read it though yet, but this looks interesting:

http://www.physoc.org/publications/pn/issuepdf/53/7.pdf

I'm going to try and spend some time in David Allen's lab in Sydney, he sounds like a very cool guy.

L.

 

[acoggan]

I think that the term lactate clearance might be being employed a little loosely (I haven't read the thread, but perhaps Andy is using it just because it was already there, so to speak).

You know me, a stickler for proper terminology.* So, when I say "clearance" I mean either:

1) the tracer-determined rate of disappearance of substance divided by the arterial concentration, and/or

2) the gross or net rate of uptake across a tissue bed as determined using a-v balance methods divided by the arterial concentration.

In either case, the calculation is an attempt to describe the intrinsic ability of a tissue or tissues to take up a substrate, independent of the mass action effect resulting from the substrates concentration.

(*Ironically, the PET group I'm currently working with calls uptake "utilization" and clearance "uptake"...go figure!!)

 

[biker-linz]

You know me, a stickler for proper terminology.* !!)

Actually I had a sneaky feeling that you might respond to such a scurrilous accusation.

So, when I say "clearance" I mean either:

1) the tracer-determined rate of disappearance of substance divided by the arterial concentration, and/or

2) the gross or net rate of uptake across a tissue bed as determined using a-v balance methods divided by the arterial concentration.

In either case, the calculation is an attempt to describe the intrinsic ability of a tissue or tissues to take up a substrate, independent of the mass action effect resulting from the substrates concentration.

(*Ironically, the PET group I'm currently working with calls uptake "utilization" and clearance "uptake"...go figure!!)

So essentially what you're saying is that when you say 'lactate clearance' you are specifically referring to the rate at which lactate is taken up from the bloodstream and actively used by tissue, as opposed to its rate of clearance *from* (for example) a working muscle.

L.

 

[acoggan]

So essentially what you're saying is that when you say 'lactate clearance' you are specifically referring to the rate at which lactate is taken up from the bloodstream and actively used by tissue, as opposed to its rate of clearance *from* (for example) a working muscle.

It's actually a little more complicated than that, since 1) clearance as determined using a tracer may include removal of a substrate that has never entered the circulation, 2) clearance says nothing about the metabolic fate of a substance (which is why the term "metabolic clearance rate" has fallen into disfavor), and 3) nobody really knows what it is you're measuring when you infuse a lactate tracer and use the resulting data to calculate Ra, etc. But, in the context of the present discussion, when I say lactate clearance I am really referring to mechanisms that result in a reduction in blood or plasma lactate concentration independent of changes in its rate of appearance/production.

 

[SolarEnergy]

I know this is an oldish thread, but my 2 cents!

Everyone seems to be assuming that cellular acidosis is a bad thing, but that might be far from the truth, see:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15326352&query_hl=2&itool=pubmed_docsum

L.

With all due respect, Linz, here up North, some people are dying as a result of metabolic acidosis. Go tell the parents of these kids that cellular acidosis isn't a bad thing.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&dopt=Detailed&tmpl=dispomimTemplate&list_uids=220111

Morin et al. (1993) described the clinical findings of 15 of the 34 patients referred to by Merante et al. (1993) who had biochemical evidence of COX deficiency. Fifteen patients in whom clinical findings were reported in detail were aged 6 months to 11 years; 11 children died in episodes of fulminant metabolic acidosis

 

[SolarEnergy]

I may have sounded a bit rude in my post above, and now that "edit" button isn't available no more.

Sorry Linz

I think those kids are dying from something other than acidosis.

But the pattern always seem to be the same. They don't have enough Cytochrome Oxidase, they suffer from that during their short little life. Then they get a flu. Their body needs to fight against the virus. Sever acidosis is a consequence of this fight against the virus, and they die.

A friend of mine, P. Lavoie, world record holder in age group 40-44 for the Ironman distance (9h02), created a foundation to help these kids, his dauther has the desease.

Sorry again if I sounded rough.

 

[biker-linz]

I may have sounded a bit rude in my post above, and now that "edit" button isn't available no more.

Sorry Linz

I think those kids are dying from something other than acidosis.

But the pattern always seem to be the same. They don't have enough Cytochrome Oxidase, they suffer from that during their short little life. Then they get a flu. Their body needs to fight against the virus. Sever acidosis is a consequence of this fight against the virus, and they die.

A friend of mine, P. Lavoie, world record holder in age group 40-44 for the Ironman distance (9h02), created a foundation to help these kids, his dauther has the desease.

Sorry again if I sounded rough.

Please don't worry at all, it's easy to get upset when the subject matter is 'close to home', intentional or not.

I wouldn't doubt that systemic acidosis is very bad indeed (whether it was responsible for the tragic deaths of the children you mentioned or not); this is the reason the body has so many complex mechanisms for maintaining pH homeostasis.
The point of the 'Science' article I think is just that in terms of *localized* acidosis in working muscle it probably isn't the primary cause of fatigue.

L.

 

[WarrenG]

The point of the 'Science' article I think is just that in terms of *localized* acidosis in working muscle it probably isn't the primary cause of fatigue.

L.

In that article it mentions that the acid may help with the excitability of the muscle. When a rider finishes a very hard effort, like in a kilo event, what is causing the condition at the end where the rider simply can not move their leg muscles?

 

[acoggan]

When a rider finishes a very hard effort, like in a kilo event, what is causing the condition at the end where the rider simply can not move their leg muscles?

It's probably mostly due to inhibition of actomyosin ATPase activiity as a result of a change in the cell's "energy charge" (i.e., concentrations of ATP, PCr, etc., and their hydrolysis products). Failure of excitation-contraction coupling may also play a role, but that's probably more important in explaining the fatigue that occurs during even shorter duration, higher intensity exercise.

 

[WarrenG]

It's probably mostly due to inhibition of actomyosin ATPase activiity as a result of a change in the cell's "energy charge" (i.e., concentrations of ATP, PCr, etc., and their hydrolysis products). Failure of excitation-contraction coupling may also play a role, but that's probably more important in explaining the fatigue that occurs during even shorter duration, higher intensity exercise.

I understood some parts of that. Babelfish was of no further help with the translation.

 

[acoggan]

I understood some parts of that. Babelfish was of no further help with the translation.

So you're saying that I should dumb it down for you even more?

 

[WarrenG]

So you're saying that I should dumb it down for you even more?

Don't bother. It was just a curiosity for me. I'm sure many other people here understood all of what you wrote so maybe one of them can explain it in a way that is more appropriate.