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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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which is the single most frequently cited non-methods paper ever published in the Journal of Applied Physiology

The conclusion from this study

In conclusion, endurance exercise training induces a number of adaptations in skeletal muscle. Probably the most important of these is an increase in mitochondria with an increase in respiratory capacity. One consequence of the adaptations induced in muscle by endurance exercise is that the same work rate requires a smaller percentage of the muscles’ maximum respiratory capacity and therefore results in less disturbance in homeostasis. A second consequence is increased utilization of fat, with a proportional decrease in carbohydrate utilization, during submaximal exercise. These metabolic consequences of these adaptations of muscle to endurance training could play important roles in 1) the increase in endurance and 2) the ability to exercise at a higher percent of VO 2 max in the trained state, by slowing glycogen depletion and reducing lactate production (i.e., raising “lactate threshold”).


Sounds like changes in aerobic capacity lead to changes in the LT curve. I am going to include this on our lactate threshold page. Thank you. Great cite.

This was also before Mader's work was published which added additional insight into the processes behind the lactate curve.

-------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
Last edited by: Jerryc: Apr 2, 15 7:27
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Andrew Coggan wrote:
Jerryc wrote:
The Dudley study, while done on rats, is one of the original basis for polarized training. It started people thinking about just what affected adaptation to the different muscle fibers.

They then began to apply these concepts to the training of athletes with great success. But not in the US. We were more influenced by the Rocky movies.


Rats, unfortunately, are not humans. Thus, basing one's training decisions on studies of rats is unwise at best, and foolish at worst.

But what if I resemble a rat and love cheese, would this study be more applicable to me?
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Rats, unfortunately, are not humans. Thus, basing one's training decisions on studies of rats is unwise at best, and foolish at worst.

Another absurd statement. I guess you will have to tell all those researchers doing work with rats that they have no relevance to humans.

One of the funny stories I use to tell is that while passing the biology building at a large university, a truck was making a delivery. The truck was full of bags of Purina Rat Chow. there must have been over a 100 bags on the truck.


--------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
Last edited by: Jerryc: Apr 2, 15 7:25
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Re: No lactate threshold [Frost] [ In reply to ]
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Frost wrote:
mauricemaher wrote:

I'll give my opinion, and may be corrected by some of the smarter guys,

If you have an example of say an AG FOP female and VE (lung volume) at peak is for the sake of argument 100 litres then for simple math they are breathing in 20 litres of O2 (I know its 20.8 just keeping the math simple) They may hit VO2 max at 85-90 litres and then say in the last 2-4 minutes of a test, depending on how it's structured the CO2 process will become more dominant and VO2 will plateau.

If that athlete is 50 kilo and hits 3.0 litres then their VO2 is 60, but they are basically spitting out (wasting) 17 or so litres of O2 at the end of the test but maybe only 16 or 16.5 at VO2 max, and maybe only 14.5-15.5 at mid range or event specific levels. So basically 75 to 80% of the O2 delivered is wasted. In some athletes who are long trained they may never hit a V-slope, and may not hit an RER of 1.0

I think this is the debate around anaerobic vs aerobic inputs IE people are incorrectly associating (or overestimating) CO2 and or BL with anaerobic contribution (at least at sub VO2 max levels).

The improvement you stated in your scenario above is usually associated with better patterns of localized absorption IE: you want to be a better cyclist, then you train specifically in that direction and utilization and absorption patterns will (generally) follow.

Maurice


What does ventilation have to do with any of this?

Generally in healthy people nothing, that was my point. I wasn't sure if the poster understood the basics of how much air we breath in and how small a percentage (VE and O2) of it actually gets used for the activity at hand.

Maurice
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
Quote:
Rats, unfortunately, are not humans. Thus, basing one's training decisions on studies of rats is unwise at best, and foolish at worst.

Another absurd statement. I guess you will have to tell all those researchers doing work with rats that they have no relevance to humans.

http://en.wikipedia.org/wiki/Straw_man

(BTW, you'll note that Holloszy himself - you know, the guy who won a $200,000 prize from the IOC for his work studying muscular adaptations to training in rats*? - emphasizes some of the differences between rat and human muscle and cautions against over-interpreting animal studies in that review article.)

*Holloszy has also been nominated at least twice for a Nobel Prize, or so I've heard.
Last edited by: Andrew Coggan: Apr 2, 15 8:23
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
Quote:
which is the single most frequently cited non-methods paper ever published in the Journal of Applied Physiology

The conclusion from this study

In conclusion, endurance exercise training induces a number of adaptations in skeletal muscle. Probably the most important of these is an increase in mitochondria with an increase in respiratory capacity. One consequence of the adaptations induced in muscle by endurance exercise is that the same work rate requires a smaller percentage of the muscles’ maximum respiratory capacity and therefore results in less disturbance in homeostasis. A second consequence is increased utilization of fat, with a proportional decrease in carbohydrate utilization, during submaximal exercise. These metabolic consequences of these adaptations of muscle to endurance training could play important roles in 1) the increase in endurance and 2) the ability to exercise at a higher percent of VO 2 max in the trained state, by slowing glycogen depletion and reducing lactate production (i.e., raising “lactate threshold”).


Sounds like changes in aerobic capacity lead to changes in the LT curve. I am going to include this on our lactate threshold page. Thank you. Great cite.

This was also before Mader's work was published which added additional insight into the processes behind the lactate curve.

Speaking of curves, it seems that you (and Mader) were well behind it. As I said, this stuff is the bread-and-butter of the "golden age" of exercise biochemistry, which can be traced to 1) the reintroduction of the muscle biopsy method, and 2) Holloszy and his interests/research/those who coalesced around him.

You can read more here:

https://www.academia.edu/...ics_2014_pp._423-446
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Quote:
http://en.wikipedia.org/wiki/Straw_man

http://en.wikipedia.org/wiki/Red_herring

and

http://en.wikipedia.org/wiki/Ad_hominem

and

http://en.wikipedia.org/wiki/Straw_man

Maybe we should debate what applies to what on this thread.

But I do thank you for the great cites in support of my position that you keep on providing.

-----------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Quote:
it seems that you (and Mader) were well behind it

I haven't disagreed with your cites. I heartily endorse them.

So you finally agree with Mader's work. Thank you. Thank you.

-----------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
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Re: No lactate threshold [mauricemaher] [ In reply to ]
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mauricemaher wrote:
Frost wrote:
mauricemaher wrote:

I'll give my opinion, and may be corrected by some of the smarter guys,

If you have an example of say an AG FOP female and VE (lung volume) at peak is for the sake of argument 100 litres then for simple math they are breathing in 20 litres of O2 (I know its 20.8 just keeping the math simple) They may hit VO2 max at 85-90 litres and then say in the last 2-4 minutes of a test, depending on how it's structured the CO2 process will become more dominant and VO2 will plateau.

If that athlete is 50 kilo and hits 3.0 litres then their VO2 is 60, but they are basically spitting out (wasting) 17 or so litres of O2 at the end of the test but maybe only 16 or 16.5 at VO2 max, and maybe only 14.5-15.5 at mid range or event specific levels. So basically 75 to 80% of the O2 delivered is wasted. In some athletes who are long trained they may never hit a V-slope, and may not hit an RER of 1.0

I think this is the debate around anaerobic vs aerobic inputs IE people are incorrectly associating (or overestimating) CO2 and or BL with anaerobic contribution (at least at sub VO2 max levels).

The improvement you stated in your scenario above is usually associated with better patterns of localized absorption IE: you want to be a better cyclist, then you train specifically in that direction and utilization and absorption patterns will (generally) follow.

Maurice


What does ventilation have to do with any of this?


Generally in healthy people nothing, that was my point. I wasn't sure if the poster understood the basics of how much air we breath in and how small a percentage (VE and O2) of it actually gets used for the activity at hand.

Maurice

Well Andy and Steve are arguing about the role and importance of cardiac output/stroke volume (oxygen pulse) vs metabolic fitness. Nobody mentioned ventilation before your post. I have a feeling you might want to read about the limiting factors of oxygen delivery...
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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I have the book and discussed it with you before. I read your chapter.

-------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
Last edited by: Jerryc: Apr 2, 15 8:30
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Post deleted by mauricemaher [ In reply to ]
Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Andrew Coggan wrote:
Jerryc wrote:
Quote:
Such examples illustrate that the factors determining each are, to a greater or lesser extent, independent of each other.

I have been reading papers and listening to lectures by top sports scientists for almost 20 years and never heard this before.

Then with all due respect, you must have wax in your ears or something, because such concepts have been discussed for a long time. For example, they are considered in this review article by Holloszy and Coyle:

http://jap.physiology.org/content/56/4/831

which is the single most frequently cited non-methods paper ever published in the Journal of Applied Physiology

Jerryc wrote:
I guess all those mitochondria in the muscles, capillaries, enzymes etc in elite marathoners are a waste of time.

You're confused: the very skeletal muscle characteristics you mention are critical determinants of metabolic fitness.

Jerryc wrote:
what is the definition of metabolic fitness?

I've long used the term "muscular metabolic fitness" as a counterpoint to "cardiovascular fitness", as it helps move the discussion away from precisely how you measure/define lactate threshold. If you prefer, though, you can substitute "lactate threshold" instead...just realize that you are referring to lactate threshold the concept, not lactate threshold the lab measurement.

Is that the same Coyle who tested Armstromg over several years and failed to notice Armstromg's use of EPO, other drugs and blood doping?


Didn't you train under Coyle?
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Re: No lactate threshold [Trev] [ In reply to ]
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Is that the same Coyle who tested Armstromg over several years and failed to notice Armstromg's use of EPO, other drugs and blood doping?

Coyle is a very respected researcher and has done some very good work. His 1988 study on the lactate threshold was good. Just he and his research team missed what was causing the variation between cyclists. The clues were there, differences in glycolytic activity. Identified by Mader a couple years before as the main causes for theses differences.

Now it is quite reasonable to disagree and debate but there is a strong tendency on this site to dismiss out of hand certain explanations.


-------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Perhaps Coyle was so convinced the answer to Armstrong's improvement was from within the muscles he forgot to look at the blood.

http://retractionwatch.com/...re-questions-abound/




This case describes the physiological maturation from ages 21 to 28 yr of the bicyclist who has now become the six-time consecutive Grand Champion of the Tour de France, at ages 27–32 yr. Maximal oxygen uptake (V̇o2 max) in the trained state remained at ∼6 l/min, lean body weight remained at ∼70 kg, and maximal heart rate declined from 207 to 200 beats/min. Blood lactate threshold was typical of competitive cyclists in that it occurred at 76–85% V̇o2 max, yet maximal blood lactate concentration was remarkably low in the trained state. It appears that an 8% improvement in muscular efficiency and thus power production when cycling at a given oxygen uptake (V̇o2) is the characteristic that improved most as this athlete matured from ages 21 to 28 yr. It is noteworthy that at age 25 yr, this champion developed advanced cancer, requiring surgeries and chemotherapy. During the months leading up to each of his Tour de France victories, he reduced body weight and body fat by 4–7 kg (i.e., ∼7%). Therefore, over the 7-yr period, an improvement in muscular efficiency and reduced body fat contributed equally to a remarkable 18% improvement in his steady-state power per kilogram body weight when cycling at a given V̇o2 (e.g., 5 l/min). It is hypothesized that the improved muscular efficiency probably reflects changes in muscle myosin type stimulated from years of training intensely for 3–6 h on most days. ""

Very interesting.

http://sportsscientists.com/...h-errors-evaluation/


Last edited by: Trev: Apr 2, 15 12:22
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
Quote:
it seems that you (and Mader) were well behind it

I haven't disagreed with your cites. I heartily endorse them.

So you finally agree with Mader's work. Thank you. Thank you.

"Sounds like changes in aerobic capacity lead to changes in the LT curve. I am going to include this on our lactate threshold page. Thank you. Great cite.

This was also before Mader's work"
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
Quote:
Is that the same Coyle who tested Armstromg over several years and failed to notice Armstromg's use of EPO, other drugs and blood doping?

Coyle is a very respected researcher and has done some very good work. His 1988 study on the lactate threshold was good. Just he and his research team missed what was causing the variation between cyclists. The clues were there, differences in glycolytic activity. Identified by Mader a couple years before as the main causes for theses differences.

Sjodin and Jacobs demonstrated that OBLA was more closely correlated to the ratio of glycolytic-to-oxidative enzyme activities than to the latter alone in 1981. IOW, this was already an established idea when we did our study.
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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This was also before Mader's work"

What is your point?????

Of course Holloszy study was before. I never claimed any different. I made the point that Mader's original publication on this area in English was before Coyle's 1988 study. That study did not include the concepts Mader was proffering.

Holloszy and Coyle's study are now on our lactate threshold page as supporting our point of view on what causes the lactate threshold. Done this morning after you referenced them.

Again thank you.

--------------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Quote:
Sjodin and Jacobs

Which one, there are two? I assume

Sjodin, B., et al. (1981). "Onset of blood lactate accumulation and enzyme activities in m. vastus lateralis in man." International Journal of Sports Medicine 2(3): 166-170.

Here is the conclusion:

To summarize, VOBLA is influenced by variables, such as muscle fiber composition, the coupling of the muscle glycogenolytic capacity to the muscle respiratory potential, and training. These variables are in turn interrelated. Thus, it is concluded that the periphery, associated with muscle metabolic characteristics, is of major importance in determining endurance exercise capacity.


Here is the abstract

In an earlier study, we reported close relationships between marathon running performance and the running velocity (V) at which the "onset of blood lactate accumulation" (VOBLA) occurs in a group of marathon runners. Using biopsy material from the m. vastus lateralis of the same subjects (n = 19), we have evaluated the relationship of VOBLA to different muscle enzyme activities together with muscle fiber composition and capillary density in the present study. The activities of lactate dehydrogenase (LDH EC 1.1.1.27), phosphofructokinase (PFK EC 2.7.1.11), and citrate synthase (CS EC 4.1.3.7) were determined. VOBLA was negatively correlated to LDH (r = -0.54) and PFK/CS (r = -0.68). Using multiple regression analysis, the PFK/CS ratio together with the capillary density accounted for 61% of the variation in VOBLA. Absolute training kilometrage was the most significant variable measured and accounted for 77% of the variation in VOBLA. Subjects were divided into elite runners (n = 6) and nonelite runners (n = 13) for an additional analysis of the relationship between VOBLA and the ratios of PFK/CS or LDH/CS. Significant relationships between VOBLA and the ratios were observed only in the nonelite runners (r = -0.77 and -0.66, respectively). The vertical distances between the regression lines for these two subject groups could not be explained only on the basis of the enzyme activity ratios. A greater adaptation to fat combustion in the elite runners might explain the disproportionally high VOBLA in relation to the PFK/CS or LDH/CS activity ratios.


Sounds like the threshold is caused by a the rate of glycolysis. Just what we have been saying all along. Another great reference to add to our lactate threshold page.

Everybody step back a minute. Why is it called the lactate threshold? Because the activity that produces lactate is percolating up to the point where the athlete can not move any faster without an excess of lactate being generated. In other words, the glycolytic activity is different from athlete to athlete and this is one of the determinants of the threshold. Shall I mention the term, anaerobic capacity.

Again, thank you.

--------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
Quote:
This was also before Mader's work"

What is your point?????

Of course Holloszy study was before. I never claimed any different. I made the point that Mader's original publication on this area in English was before Coyle's 1988 study. That study did not include the concepts Mader was proffering.

Holloszy and Coyle's study are now on our lactate threshold page as supporting our point of view on what causes the lactate threshold. Done this morning after you referenced them.

Again thank you.

--------------------

You claimed is that we overlooked the possible role of differences in glycolytic enzyme activity as contributing to our findings. In point-of-fact, however, we were well aware of this hypothesis, as it had been previously presented in the literature (seemingly well before before Mader).
Last edited by: Andrew Coggan: Apr 2, 15 12:02
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
the glycolytic activity is different from athlete to athlete and this is one of the determinants of the threshold.

And this is news how? One of the more well-known adaptations to endurance exercise training that contributes to the reduction in lactate production is a generalized down-regulation of glycolytic enzyme activity:

http://www.ncbi.nlm.nih.gov/pubmed/4270315

Note, however, that the magnitude of such changes (i.e., typically 10-20%) are much smaller than changes in mitochondrial respiratory capacity (which can increase by up to 100%).
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Quote:
And this is news how?

You do realize that everyone of your comments supports my point of view and Mader's ideas. It seems like you do not understand his ideas and just spout things you think will be detrimental to me and to his ideas. Else you would not be making the comments you do.

As far as the magnitude of the changes in glycolytic activity over time, it may be much higher than you believe for some athletes due to the right kind of training. I would trust the people training the athletes rather than some academic research study.

The 1988 study certainly missed the implications of the findings of the study or else there would be a concerted effort to change glycolytic activity as a means of training the cyclists to raise the threshold. Have you recommended training to reduce the activity of the glycolytic system for your cyclists?

That is an implication of Mader's ideas and should be standard training practice. Somehow i don't think it is.

------------

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom
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Re: No lactate threshold [Jerryc] [ In reply to ]
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Jerryc wrote:
You do realize that everyone of your comments supports my point of view and Mader's ideas.

I don't know why you persist in giving him credit for ideas that have been around for as long as I have been studying exercise physiology (starting in 1976).

Jerryc wrote:
As far as the magnitude of the changes in glycolytic activity over time, it may be much higher than you believe for some athletes due to the right kind of training. I would trust the people training the athletes rather than some academic research study.

I would tend to trust those who have actually stuck biopsy needles into peoples' legs before and after training to directly measure changes in glycolytic enzyme actitivies (like I have done).

Jerryc wrote:
The 1988 study certainly missed the implications of the findings of the study or else there would be a concerted effort to change glycolytic activity as a means of training the cyclists to raise the threshold.

Our study wasn't in any way intended to influence how people actually train.

Jerryc wrote:
Have you recommended training to reduce the activity of the glycolytic system for your cyclists?

Why yes, as a matter of fact I have (it's called endurance training).
Last edited by: Andrew Coggan: Apr 2, 15 16:03
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Re: No lactate threshold [Andrew Coggan] [ In reply to ]
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Andrew Coggan wrote:
Jerryc wrote:

You do realize that everyone of your comments supports my point of view and Mader's ideas.


I don't know why you persist in giving him credit for ideas that have been around for as long as I have been studying exercise physiology (starting in 1976).

This.

TBH, I'm surprised this is news to you Jerry, lactate.com is your website ?
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Re: No lactate threshold [Derf] [ In reply to ]
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Derf wrote:

It's really best to think of these systems in parallel. A marked improvement in any one portion of the system will have a modest improvement in the overall system.

O2 supplementation (and EPO eventually, once RBC count comes up) will both have immediate salutatory effects, as O2_sat will remain higher at exercise. This allows you to train at a higher level, thus (ostensibly) eliciting a stronger adaptation response from the body's various subsystems (read: fitness!). Your body will assuredly not linearly benefit from that extra oxygen, but still benefit (and plenty).


Derf wrote:

Hence AC's comments about high VO2Max being a necessary, but insufficient selection guideline for an elite endurance athlete.



This bit in bold is the point I was trying to establish, and I've spent a couple of days googling and pubmedding around looking for evidence in studies, WIP.

It seems that O2 availability is necessary for mitochondiral biogenesis/gene expression (its an aerobic process?). So does the presence/availability of additional O2 in the blood bring about more adaptation in the muscle? leading to more blood flow=more oxygen availability and more mitochondria??

Taking a step back, I started by proposing that doing vo2max work enables you to put out more power. And backed that up with the logic that EPO works, vo2 training works, etc. And then, AC comes along and says no, its a necessary condition but not a determinant. I happen to think he is probably right, since its the muscles creating the power, and all the o2 in the world won't make any difference if the muscles can't absorb it. So if additional O2 doesn't makes you faster, then additional O2 must somehow bring about metabolic adaptation that makes you faster.

Logically (just rewording your bold bit really) if you hold your vo2max slightly higher through the winter then you can do your winter miles at X watts higher, and thats likely to lead to more adaptation as long as you can absorb that work (in my experience, when I look at times where I've done a block of vo2 work after a block of volume work, RPE connects more to heart rate than power despite an increase of 20w, so I don't think those extra X watts are necessarily more fatiguing provided you fuel correctly). This would also help explain why polarized seems to work for some. You step up your power with a bit of vo2 work, you do some long steady miles at a higher power than you would have otherwise, adaptation occurs (more adaptation occurs), and then you do a bit more vo2 work, and more long miles at higher power, its like a cycle of stimuli working together. Its a way of training at higher power for the same stress.

Personally I'd get blatted in no time if I did vo2 work week in week out, but I find sweetspot or greater can provide enough stimulus to step onto this ladder, it doesn't have to be vo2 work for me, but it does for some people, moreso but not exclusively it seems those who are well trained. And I also find that training at a relatively higher power is much more enjoyable, so mentally this model works better too.

Simplistically if more oxygen availability in the blood did not enable rapid adaptation of oxygen uptake in the muscle, EPO wouldn't work much, and vo2max intervals wouldn't work much. But we know they do work - a lot.

Looking at a study of hypoxia in mountaineers at altitude for ~5 weeks, their muscle mass decreased by 10% and mitochondria volume decreased by 25% despite capillary density staying the same. The only stimulus that caused this change would appear to be less O2. They were still "training" by doing mountaineering. What will happen when they get back to sea level ? More oxygen, carry on climbing, will mitochondrial levels return to their original ? I think it would. But what would be the stimulus for that? More oxygen alone? (More oxygen with training is fine, since we're not interested here in people who don't train). O2 is the only thing we're changing here. I'd like to find more studies that connect hyper-oxia to mitochondrial density increases and explain mechanisms, WIP

The other possibility here is that the additional o2 availability has nothing to do with muscle adaptation, and its simply that hard training associated with vo2work is bringing about adaptation within the cells which then enables more oxygen uptake. I'd also accept that as an explanation, but if thats the case, why does EPO work ?


paull wrote:

The take home message about vo2max not being a determinant, while it may be technically true, is hugely misleading. That could easily fool your average Joe Athlete into thinking that oxygen availability and hence vo2max is not relevant !! Seems to me its incredibly relevant, and to almost all training.


Steve Irwin wrote:

I also think it's misleading to talk about the scope for metabolic fitness improvements being greater than the scope for VO2max improvements based on the observation that threshold can move closer to VO2max. This would be true if the only source of improvement in threshold power were metabolic fitness improvements, but of course improvements in cardiac output will improve power at all HRs, including threshold. To illustrate, suppose we have:

Steve Irwin wrote:

I tried for some time putting your advice into action by focusing on training that would be expected to primarily improve metabolic fitness rather than cardiovascular fitness, and the results were as poor as they were for the animals in the studies this refers to:


These quotes are clear demonstrations that the statement about Metabolic fitness being a determinant CAN BE misleading. Here we have an intelligent rider with a good education in science, including some physiology, and many years in sport as a swimmer and cyclist. He took on board AC's advice and (I'm assuming) wasted one or more seasons trying to get fast by doing the wrong training. Lifes too short to have that going on.

So while I maintain that AC might be technically correct, the take home message needs to change, but first I don't yet see the science that explains why Polarized works? why vo2 work raises power? why EPO works? why do Steve Irwin and other riders go better on a polarized model? Why does Ric Stern recommend some threshold work even through the winter? Why is 60's music so good? Why do other riders thrive on long miles and some need polarized? HOW SHOULD RIDERS DECIDE ON THE INTENSITIES TO TRAIN AT ALL YEAR AROUND FOR OPTIMAL PROGRESSION?
Last edited by: paull: Apr 3, 15 1:50
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