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Fatigue is biochemical, not biomechanical.
- Andrew Coggan, PhD

That was a good summary, but I think people are missing the point with the values from these tests.

LT and VO2max should be two separate tests. Especially when you do an LT test, relating the HR data to the LT (depending on how it is defined) is often 85-90% of the VO2max. Likewise, AT/VT are also two different values of the VO2max, and could be 75%-85% of VO2max. I don't know about others, but when you're trying to get BP (if you don't have them set up to lead lines), HR, blood values, monitor all of the equipment, and encourage the individual, it's better to pick one "goal" for the test and leave it at that.

This goes back to being specific to the goal- if you want to assess LT, do an LT test. A person shouldn't do a VO2max and LT at the same time and expect the values to be optimal for training. Especially if a person is going to base their training intensity off of LT values, and the test is done from a VO2max protocol, chances are the values will be overestimating the ranges from which to base training.

Both tests are worthwhile, but the OP needs to perform the tests for the purpose of training and racing goals and improving the data assessed.

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http://www.reathcon.com

Matt,
As an observer, you are the one who has anger issues. Go back and look at your post. You asked a question, he answered it. You asked a second question, he answered it. You then asked a third question, he answered it ( "Aerobic threshold and lactate threshold are referred to interchangably - do they not mean the same thing?") answer: Paulo: "The answer to that is no, they don't, even though AT and LT are correlated. Using them interchangably is not correct.")

Then you proceeded to launch into an attack, calling him an "unhelpful asshole" even though he answered your question, insult his clients, and question his upbringing. Maybe you should stick to decaf.

Kyle

really? his answers were all partial non-answers. it's as if he was just messing with me rather than recognizing what I was looking for.

compare his answer to mckenzie's first post. one really helpful, one really not.

he also started with the hostilities.

I wouldn't have said that but he is Always like that in other people's post's, too.

I really hope he was going to keep his word not to post to me again but he seems to have not been able to resist for what, more than an hour?

he's a unhelpful assclown. I though when he first responded if I was nice he might not be, but I was wrong.

When anaerobic metabolism occurs, lactic acid is produced because there is not enough oxygen to use the aerbic pathways (which are after the anaerobic in the chain of events). Lactic acid is almost immediately dissociated into lactate and a hydrogen ion (H+).

The lactate can be safely transported in the blood, but the H+ cannot. The H+ then reacts with bicarbonate HCO3, which produces water and CO2 (which can be safely carried in the blood).

Increased levels of CO2 will stimulate ventilation to 'blow off' the excess, and maintain the balance of the bicarbonate pathway (if CO2 is retained, it will reverse the reaction and leave H+ in the body). This is the point where hyperpnea (increased ventilation) becomes hyperventilation (over-ventilation). This is the ventilatory threshold.

Hyperpnea is where ventilation is above normal, hyperventilation is when ventilation exceeds the bodies metabolic needs (used to 'blow off' CO2 instead of provide more oxygen).

To bring it all together, non-metabolic CO2 rises as a result of lactate accumulation and H+ buffering, so VT and AT should occur almost simultaneously. They don't always, but in theory they should.


mckenzie



"In Reply To
"however, in many cases these values will be very close to each other (either in HR or VO2) because the two are linked (yeah! bicarbonate buffering pathway)"

Real question, not sarcastic (I have to warn :-p): Like Trey said, I thought the exact mechanism was not known, has this been clarified in the last years? "

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mckenzie

So what about the people that have VT that is not associated with increased lactate levels? What's the connection there? I thought that was the link that wasn't explained by the mechanism that you explained.

"Simply because lactate can go through that process and "convert itself" into glucose doesn't eliminate all the other, performance limitation characteristics of that compound."

Lactate can actually go either direction. It will convert into glucose in the liver, but it can also be converted back to pyruvate in other tissues (especially muscle, most importantly the heart, and the brain). At this point it goes directly into the aerobic pathway (bypassing the anaerobic). This is especially important in the brain and heart, which do not have the capacity for anaerobic metabolism. They require the excess lactate from other tissues to provide a fuel source. In this case, lactate provides an easier fuel source than glucose.

Lactate is not the bad guy. The literature from the early 20th century supports this, we just forgot about this until the last 10 years (oops!), so now we are relearning all of it.

Lactate has been long regarded as a 'poison', which is outrageous. The caveat however, is that the hydrogen ions associated with lactic acid will cause problems (metabolic acidosis), but the lactate itself is very beneficial.

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mckenzie

I know patients with Mcardle's syndrome will not produce lactic acid, but will still show a VT and hyperventilation.

I don't have an answer for why (sorry, I'm not really a clinical ex. phys. guy). It's an interesting scenario, and I'm not sure that we have the answer for it.

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mckenzie

My understanding of this subject is that if those patients still exihibit VT, then the mechanism that you described is not what is responsible for VT. Looks like it's still an open question.

 
it appears as though I was correct last night except it was "assclown" vs. "fucktard".

Gotta love OP's who ask an honest question and get an honest answer only to decide that honest answer isn't "good enough" and is only a "half answer".


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[reply]
this is correct. Although I'm sure somebody will have to refer to you as a "fucktard" and then explain how you add nothing to the forum and bad mouth it to your clients before this thread is done :-)

Oh yeah, and piss and moan about how you shouldn't "sell" your advice.


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[.reply]
Only "finger prick" will allow you to test for LT.[./reply][/reply]

Are you talking about someone who has reached VT breakpoint, but hasn't met any criteria for LT?

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http://www.reathcon.com

Probably I am. It's not like I understand the subject in depth, I just questioned mckensie because I thought that there might be new research that cleared this. He's the PhD student in Exercise Physiology, not me ;-)

"his answers were all partial non-answers"

No, he gave a pretty specific answer to your pretty specific question, then you went on your wikipedia tangent.

If you want to complain that he limited his response only to answering your specific question and didn't elaborate on the topic as others did, that is your choice. It just didn't seem like his answers warranted a personal attack from you.

You mean like this explanation for reduced La- while working at the AT?

"This study examined the relationship between minute ventilation (VE), CO2 production (VCO2), and blood lactate concentration ([La-]) during incremental exercise performed with reduced muscle glycogen stores. Nine untrained female subjects (25.3+/-4.2 year) performed incremental cycling in a normal glycogen (NG) state and under conditions of reduced muscle glycogen (RG) content. To reduce muscle glycogen stores, subjects cycled to exhaustion (124+/-33 min) at a power output corresponding to their gas-exchange anaerobic threshold. Peak oxygen uptake (VO2peak) was unchanged with glycogen reduction, even though subjects achieved a significantly lower maximal power output in the RG state (p<0.05). Peak blood [La-] decreased significantly by 37% in the RG state (p<0.001). "

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compare his responses to some of the other pretty brilliant responses.

not only is he unhelpful, but he's wrong. question was which was superior, he said one didn't exist and was intentionally as dense as possible.

it's as if he you ask him 'where can I go to the bathroom' and he points at your crotch and smirks. but wait, that would be a correct answer.

doesn't matter. I got some great answers to take to pubmed and make a better decision (thanks all), there was some serious discussion and sharing of ideas among other forum members, and I got a signature file. win-win-win.

so they must have been delivering much more oxygen to their muscles in the glycogen depleted state since lactate levels were lower, right?

;-)

tongue out of cheek now - those who suggested oxygen delivery as being responsible for lactate levels, please carefully read this last post.

No. Mckensie described a mechanism for VT that is linked to the increase of lactate concentration in the bloodstream. But if even people that don't have an increase in La exhibit VT, then maybe an increase in La is not what causes VT.

I did a little bit of homework (yeah, about 10 min., but it's sunday) on Mcardle's syndrome.

these patients lack phosphorylase, which means they can't break down glycogen (and therefore, don't create lactate), but will still exhibit a VT (without an AT).

another study showed that after glycogen depletion athletes (non-mcardle's) showed a larger difference between AT (higher intensity after) and VT (lower intensity after) than before depletion (sorry, no citation - sunday).

while this is completely my own idea, with no backing by experimentation (at least for now), there may be an effect of fuel substrate. In both of these cases the suybjects must be relying on lipolysis (fat metabolism) as an energy source, which should change the relationship between AT and VT.

I can't back this up, but it seems a plausible explanation. That said, I'm not sure that there has been enough study to confirm of refute this idea.

I will agree that this phenomena is not solved by any stretch, but there are some very solid ideas on what is going on. besides, controversy makes for good science, right?

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mckenzie

There's that too. I found it strange, but what do I know, I'm just a hack.

do you have a citation for that (seriously, I would like to read it. It can wait - I realize it's sunday, especially since i haven't cited anything in this thread).

Thanks for the contribution.

I can't get it all quite straight in my head yet, but it does make sense.

glycogen depleted subjects show lower Lactate levels. This could be due to higher lactate consumption due to comprimised muscle glycogen levels.

In this case, you still should see a VT, at a intensity lower than AT, because H+ is still being dissociated. even though circulating Lactate levels are low, it is still being produced, but it's being consumed more than at a normal glycogen level.

just a thought,

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mckenzie

Quote:

Ventilatory and gas-exchange responses to incremental exercise performed with reduced muscle glycogen content
Journal of Science and Medicine in Sport, Volume 9, Issue 3, June 2006, Pages 267-273
S. Sabapathy, N.R. Morris and D.A. Schneider


Interesting thought- I never looked at it that way.

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http://www.reathcon.com

thanks, just requested it through the library (full text online is nice, but having the library deliver it when it's not is such a great luxury - there are advantages to staying in college for 10 years)

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mckenzie

You have this one?

http://jap.physiology.org/...nt/abstract/54/2/470

I do now.

thanks paulo - it seems you might be only half as bad as everyone says (j/k - maybe)

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mckenzie

Here's another- let me know if you want it and I'll email you the complete .pdf -
doi: 10.1519/1533-4287(2004)18<260:SLDDLA>2.0.CO;2
The Journal of Strength and Conditioning Research: Vol. 18, No. 2, pp. 260–265.
Short-Term Low-Carbohydrate Diet Dissociates Lactate and Ammonia Thresholds in Men Józef Langfort, Dariusz Czarnowski, Magorzta endzian-Piotrowska, and Jan Górski

Department of Physiology, Medical University of Biaystok, Biaystok, PolandJózef Langfort

Laboratory of Experimental Pharmacology, Medical Research Centre, Polish Academy of Sciences, Warsaw, PolandRyszard Zarzeczny

Department of Physiology, Academy of Physical Education, Katowice, Poland

ABSTRACT
Langfort, J., D. Czarnowski, M. endzian-Piotrowska, R. Zarzeczny, and J. Górski. Short-term low-carbohydrate diet dissociates lactate and ammonia thresholds in men. J. Strength Cond. Res. 18(2):260–265. 2004.—A low-carbohydrate (L-CHO) diet has been shown to shift the lactate threshold toward higher workloads. The aim of the present study was to examine the effect of an L-CHO diet on the ammonia threshold and to compare it with the lactate threshold in men. The plasma catecholamine threshold was also measured. Eight young, untrained men participated in the study. Two exercise tests with graded workload were performed. The workload was increased every 3 minutes by 40 W until volitional exhaustion. The first test was performed after 3 days of a controlled mixed diet. After the first test, the mixed diet was switched to a L-CHO diet. Three days later the same test was repeated. The blood concentration of lactate, ammonia, noradrenaline, and adrenaline was measured before and after each workload in both groups. It was found that the concentration of the examined compounds in the blood increases exponentially with graded workload after each kind of diet. This led us to calculate the blood ammonia, lactate, epinephrine, and norepinephrine thresholds. The thresholds were defined as points at which the concentration of a given compound starts to increase in a nonlinear fashion, which is calculated using 2 segmental linear regressions. After the mixed diet, the threshold for each compound occurs at the same workload. The L-CHO diet resulted in dissociation of the lactate threshold from the ammonia threshold: the lactate threshold was shifted toward a higher workload, whereas the ammonia threshold was shifted toward a lower workload. The norepinephrine threshold was also shifted toward a lower workload, and the epinephrine threshold remained unchanged. The results obtained indicate that an L-CHO diet accelerates production of ammonia and delays production of lactate during graded exercise, as well as that diet must be strictly controlled when ammonia and lactate thresholds are measured.

Key Words: ammonia, lactate, catecholamines, blood, diet, exercise, man

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http://www.reathcon.com