Sounds about right from what I've read. Steve Magness (http://www.scienceofrunning.com/), has written on similar themes. He also notes that Vo2Max is a nearly useless measurement (which also seems about right). I think some of these variables have come about simply because they could be measured, and for some reason, physiological studies rarely actually measure the easiest and most meaningful variable (i.e. actual performance).

So now you are gonna be a fan of CP?
Or power duration curve phenotyping?

---

---

Kat Hunter reports on the San Dimas Stage Race from inside the GC winning team
Aeroweenie.com -Compendium of Aero Data and Knowledge
Freelance sports & outdoors writer Kathryn Hunter

I think the argument about lactate threshold is largely just semantics.
The lactate curve itself has no threshold point, but the inflection point of the curve corresponds with a threshold in the power duration curve.

Which is what people mean when they say lactate threshold.

People who talk about lactate threshold also don't imply that the lactate causes it. The lactate is just one signal that fatigue is coming.

But, yes I agree with your point that we focus a lot on what we happen to be able to measure. See - heart rate.

---

---

Kat Hunter reports on the San Dimas Stage Race from inside the GC winning team
Aeroweenie.com -Compendium of Aero Data and Knowledge
Freelance sports & outdoors writer Kathryn Hunter

Maybe this is why a lot of studies just use VT2 or percent of vo2max/HR, even though these measurements also seem a bit arbitrary.

---

Endurance coach | Physiotherapist (primary care) | Bikefitter | Swede

I'd agree.
There may be no threshold, but there is a point that we can reliably tie to performance.

---

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
I also give Training Advice via http://www.ForeverEndurance.com

The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
http://www.AGNCYINNOVATION.com

Having a high heart rate doesn't cause fatigue either, but it's a pretty damn good indicator how close you are to your limit.

I'd agree with Jack in saying it's more of a semantical error than an error in our knowledge of physiology, and our ability to measure lactate is probably the cause of it being such a coined phrase. BUT I'd say that what causes fatigue and lactate production are pretty damn closely related. Using the current definition of LT as fitness indicator isn't going to create any false positives in terms of world class athletes. If your LT is happening around 600w you're still going to be a monster, if it's happening around 200w you're still going to have trouble breaking the hour record. It's not going to produce any false negatives either, because if you're not creating lactate you're going to have a whole mess of other issues hindering your performance.

NOT being able to create lactate is actually a pretty sucky disease called Mcardle's disease- but that's more of a symptom than the etiology of the disease.

Depends on what you mean by a threshold. This graphic shows tests that have been repeated many times:



If you define the Lactate Threshold as the highest steady state effort level where lactate remains at roughly the same level, then one may look at it as a threshold. Something different happens after one passes through it.

For a discussion of the definitions of the lactate threshold see:

http://www.lactate.com/...old_definitions.html

For a long discussion of the various definitions and concepts of thresholds see:

http://www.lactate.com/threshold.html

No serious person in years blames fatigue on lactate.

Actually if you measure lactate at several steady state effort levels, lactate will eventually start to rise above what is called a baseline and the values will lie on a straight line till it hits the maximal lactate steady state. Then the amount of lactate measured each time will depend on how long one takes between measurements. This is what gives the lactate curve its supposedly exponential shape. But this exponential shape is an artifact of how lactate is measured and the lactate curve is really a straight line below "threshold."

A couple references on the Maximal Lactate Steady State

Billat, V., et al. (2003). "The concept of maximal lactate steady state: a bridge between biochemistry, physiology and sport science." Sports Medicine 33(6): 407-426.

Beneke, R. (2003). "Maximal lactate steady state concentration (MLSS): experimental and modelling approaches." European Journal of Applied Physiology 88(4-5): 361-369.

---------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

<yawn>

Did you just pass the yawn threshold?

---

customerjon @gmail.com is where information happens.

Yes, nothing new. I saw George Brooks brief most of this in the 90s.

---

Simplify, Train, Live

Yep, old becomes new again...just give it time.

---

http://www.fuelforendurance.com

True story. Fitness and training theory are very cyclical. At this point, it is rare something is new. Most of the time, people just figure out a clever way to repackage the same old info and market it to people who don't know better.

---

"Just don’t abandon everything you’ve ever learned because of something someone said on the internet." - Eric McGinnis

This was the 1st study that I recall reading that really raised the issue:

http://www.ncbi.nlm.nih.gov/pubmed/3597269

However, if you apply more sophisticated math you can still make a case for inflection points in the lactate-exercise intensity relationship:

http://www.ncbi.nlm.nih.gov/pubmed/8727572

Regardless, anybody in the field worth their salts realizes that the notions of "thresholds" are really just mental conveniences, i.e., that the underlying physiology isn't quite that simple, even though its handy to talk about it that way.

The people at Cologne found that the rise in lactate above baseline is essentially a straight line until the MLSS. Each point in this range represents a steady state. After the maximal lactate steady state there are no more steady states for lactate in either the muscle or the blood. The curve above this point will depend on how fast it is rising in the muscles due to the individual athlete's metabolism and the actual measurement situations, how long it will be between stages and the increase in intensity between stages.

Here is what we have on the CD-ROM we distribute about this.

The effect of short rest - When the effort is long enough and the effort is below the maximum lactate steady state, there is little difference between the lactate readings from steps with short rest and those with long rest. Why? Because once the body reaches an equilibrium (long effort) no further lactate will accumulate if the effort is below the maximum lactate steady state. So whether the body starts from rest or from an elevated lactate level (as long as it's below the maximum lactate steady state) the lactate level will end up at the same equilibrium point if the effort is long enough.

However, once the effort is above the maximum lactate steady state a short rest will tend to accelerate the lactate accumulation. Why? Because the longer rest will return the body to a lower lactate level and complete rest will return the body to resting rates. Hence the step that starts with a higher lactate level (tests with short rest) will accumulate lactate much faster.




When lactate is measured with tests that have long rests and long efforts, the lactate curve is very close to a straight line once it starts to rise. It is not the exponential curve that is seen in most research studies using lactate testing. Thus, an estimate of lactate values from 2 or 3 efforts is valid if the efforts are long (over 5-6 minutes)and are below or close to the maximum lactate steady state. This means that a 2-3 speed test is an equally valid measure of aerobic endurance as a test with several measurements. A test with fewer steps is obviously more desirable if it is equally valid. It saves time and money and both are important for training athletes.

For any athlete, lactate levels above the maximum lactate steady state are affected substantially by two variables, the length of the effort and the rest between efforts. Thus, any test that extends too far above the lactate threshold is problematic. The meaning of a specific lactate value is ambiguous since it is a function of these two variables.

What is of high importance is the maximum lactate that can be produced by an athlete during a short all out effort when fully rested. This is because, if the test is done correctly, it reflects the maximum strength of the glycolytic or anaerobic system. However, it cannot be measured during a step test since the maximum lactate value in such a test is a function of several variables besides the strength of the glycolytic system.

A model of exercise metabolism was developed by Mader and his collegues at Cologne in the 1980's and is described in the published literature. This model is taught at Cologne and is being used for the training of elite athletes in swimming, running, cycling, rowing and triathlon.

---------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Only if you restrict the range of intensities and/or use an exponential X axis. Indeed, even the graph you posted shows a non-linear response below OBLA.

Anyway, the notion of lactate threshold goes back a lot, lot farther than the 1980s...at least to "Owles point" in the 1930s. In part due to misunderstandings regarding exercise biochemistry, though, VO2max becames the primary "measure of a man" (or woman). It really wasn't until Ben Londeree's work in the 1970s and Peter Farrell's paper in 1981 that the pendulum began to swing back the other way (in the English language literature, anyway).

Londeree coined the term, maximal steady state. I never did find the first use of Maximal Lactate Steady State.

Londeree, B. R. and S. A. Ames (1975). "Maximal steady state versus state of conditioning." European Journal of Applied Physiology and Occupational Physiology 34(4): 269-278.

We had a long talk with him one year at ACSM. He was interested in what was happening with lactate research.

Mader after he escaped from East Germany in the early 1970's increased the interest in lactate as a variable when he proposed his 4 mmol/l concept. He had tested his runners in East Germany and they all seemed to exhibit a threshold at 4 mmol/l. He developed the "zweistufigen" test or two speed lactate test. Some call it"zweistrichen."

Mader, A., et al. (1976). "Zur beurteilung der sportartspezifischen ausdauerleistungsfachigkeit im labor." Sportarzt Sportmedizin 4: 80-88; 109-112.

Ten years later he started investigating the effect of the anaerobic system on the threshold and published his ideas in

Mader, A. and H. Heck (1986). "A theory of the metabolic origin of "anaerobic threshold"." International Journal of Sports Medicine 7(Sup): S45-S65.

Thus, began the concept of VLa max or what some call anaerobic capacity and its interaction with aerobic capacity resulting in what is called the Maximal Lactate Steady State.


Well, people who have done over 10,000 tests using lactate passed this linear relationship along to us. It is not something many would do unless they were meticulous and doing it as part of their dissertation. Here are couple more not perfect images from our website and not using an exponential axis.





By, the way thank you for the Cabrera reference. I wasn't aware of it.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Functional Mental Convenience Power!

"Average power during a 1 hour time trial, or functional threshold power (FTP), provides a logical basis for training levels since it correlates very highly with power at lactate threshold, the most important physiological determinant of endurance cycling performance, integrating VO2max, the percentage of it that can be sustained, and cycling efficiency (although, if you define LT as a 1 mmol/L increase in blood lactate over the baseline observed during low-intensity exercise, the corresponding wattage will be some 10-20% lower than FTP). "

You may yawn but you justify Functional Threshold Power by claiming it correlates highly with power at lactate threshold. ( see you quoted above).

There is no lactate threshold, there is no Functional Threshold Power.

Well, logically that doesn't even follow.

---

---

Kat Hunter reports on the San Dimas Stage Race from inside the GC winning team
Aeroweenie.com -Compendium of Aero Data and Knowledge
Freelance sports & outdoors writer Kathryn Hunter

Define Functional Threshold Power. At what duration does it occur? 50 minutes? 70 minutes? 47 minutes? 30 minutes? 92% of 20 minute power? 95% of 20 minute power? 98% of 20 minute power?

Please explain exactly where on the power duration curve this 'threshold' occurs.

I fail to see why you keep tilting at windmills.

Seriously, stop being so pedantic about this "issue" of yours. It's an obsession of yours that matters to exactly 1 person and leaves the rest of us with rolling our eyes. I don't know what "functional" means to you, but it screams "pragmatic" or "working" to me. Given physiology has plenty of day-to-day variability, it may well be a band between 50-70 minutes (given the fall-off in this region is small). Or, even simpler, it's about what you can hold for an hour. Not an exact number, because the confidence interval around that power number is large enough to envelop a decent amount of time.

The more you scream bloody murder about this, the more you're showing that you have no understanding of either math/statistics or the physiology involved.

---

The question of who is right and who is wrong has seemed to me always too small to be worth a moment's thought, while the question of what is right and what is wrong has seemed all-important.

-Albert J. Nock

Interesting that you quote Tim Noakes work here but you replied to me on Jan 28 as if he was a quack.

http://forum.slowtwitch.com/...ring=jaretj;#5418055

I still use 60 minutes.
It is a nice spot within the 'about 60 minutes' window.

Maybe you don't get why people even use these kinds of ideas, - it is to extract the idea of ones aerobic power vs the anaerobic power. Knowing how each contribute to your performance has useful meaning. 60 minute power is a quick way to get at your aerobic power. You can use more complex mathematical models of it like coggan does now, you can use 50 minutes, or 70 minutes if you want.

Wouldn't use 1 minute though.


I'm sorry that the fuzzyness bothers you, but that is how physiology is. I suggest a move into the field of number theory or computer science (But not floating point) if you don't like that.

---

---

Kat Hunter reports on the San Dimas Stage Race from inside the GC winning team
Aeroweenie.com -Compendium of Aero Data and Knowledge
Freelance sports & outdoors writer Kathryn Hunter

You're right, it doesn't. OTOH, the notion of a power threshold power is really the same sort of mental convenience as the notion of a lactate threshold.

You jumped to the wrong conclusion there. I've consistently agreed with Noakes ideas about drinking to thirst and I think there is much in his central governor ideas.

I was alluding to the fact Noakes is contraversial and well known.

I most certainly do not think he is a quack. What is you opinion of him?

I like him and his book Waterlogged is a very good book..

Exponential curves have no inflection point...

---

ZONE3 - We Last Longer

Good post...biology is, after all, messy (at best). The trends and ranges over time while factoring for as many variables as possible- the problem is that many want a smoking gun absolute, and we lack the research and tech to identify one.

---

http://www.reathcon.com

This is good to know. No more Z4/Z5 intervals for me since they aren't doing anything different than Z1/Z2.

Isn't this old news?

I read a couple of years ago that (to put it quite simply) lactate was a fueling source and it was excess hyrodgen ions or some other chemical imbalance which caused "the burn".

Going off of memory, here, so excuse any inaccuracies. Point being that this is pretty old, right?

I really like that website. I've read a lot of Steve's stuff. Some very interesting things, there.

I use 50 minutes simply because most of our crits that are supposed to be 60 mins end up being around 50-55 mins and I like using normalized power from those.

Convenience and all.

For those here who are mathematically inclined there is a recent article on cycling and Maximal Lactate Steady State. Here is the cite:

Hauser, T., et al. (2014). "Comparison of calculated and experimental power in maximal lactate-steady state during cycling." Theor Biol Med Model 11: 25.

and can be found here:

http://www.tbiomed.com/content/11/1/25

To indicate the problem of using the MLSS parameter or any other threshold estimate alone for training without any knowledge of what is behind it, here is a quote from the article

Indeed, Bleicher et al. [12] verified, that two different athletes, (soccer and track), had
exactly the same velocity for onset of blood lactate accumulation (OBLA) of 4.4 m/s,
yet the individual parameters of VO2max and VLamax were higher for the soccer player
when compared to the track athlete (VO2max : 70 vs. 63 ml/min/kg ; VLamax 0.93 vs.
0.65 mmol/l/s , respectively). That confirms, therefore that identical MLSS could be
originate by completely different combinations of VO2max - and VLamax values. Using
either VO2max , VLamax or BLC alone, it is not possible to explain differences of Power at MLSS
between two athletes or the effects of training on the MLSS. As such, it would be beneficial
to understand, how MLSS is controlled by glycolysis and oxidative phosphorylation
within the muscle cell.

It includes a bibliography relevant to the issue of thresholds.

Relevant to above quote, several years ago Sebastian Weber sent us information on some cyclists he was working with. Here is a chart that showed the same phenomena as the quote:



Other examples from Weber and his training organization in Germany (STAPS) are on our web page on cycling.

http://www.lactate.com/lactate_cycling.html

The title of one of the abstracts of an article on the STAPS site is (translated by Google)

VLamax, the maximum lactate formation rate - the secret of endurance performance

Food for thought when designing training programs.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Seems like a strange comment since VO2max is one of the two main drivers of the threshold and the more dominant of the two factors and the one to spend most of one's time training for.


---------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Operative word here being "confirms":

https://www.academia.edu/...ol_1988_64_2622-2630

(and before that, http://www.ncbi.nlm.nih.gov/pubmed/6826403)

I disagree. The operative word is "understand." From what was left out of the quote:

and VLamax values. Using either VO2max , VLamax or BLC alone, it is not possible to explain differences of Power at MLSS between two athletes or the effects of training on the MLSS. As such, it would be beneficial to understand, how MLSS is controlled by glycolysis and oxidative phosphorylation within the muscle cell.

Here is an answer which we believe best explains the process



From

http://www.lactate.com/lactate_threshold.html


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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Research and tech are probably much, much, much closer than the day-to-day variability in performance.

We need a new human being. ;)

---

The question of who is right and who is wrong has seemed to me always too small to be worth a moment's thought, while the question of what is right and what is wrong has seemed all-important.

-Albert J. Nock

It's been understood that muscular metabolic fitness (a.k.a. LT) and cardiovascular fitness (i.e., VO2max) are really two different things for a very long time.

Moreover, the regulation of metabolic responses at the muscular level have also long been well understood (which isn't to say that such knowledge isn't growing ever deeper).

As for your schematic, I find it overly simplistic (though probable reasonable when dealing with coaches and athletes, who don't need to know all the gory details).

No, it is not well understood. Also, the LT is the result of VO2max. When one thing is a function of the other, you cannot say they are really two different things. They are not independent. See the above diagram. Change VO2max in some way and the LT will change in the same direction. In other words LT = f(VO2max + other variables)

I am not sure what muscular metabolic fitness is. It is vague. LT as it is used in endurance sports is a measure of effort in the physical environment. It is watts, speed, or some other effort level. It certainly is not a measure of muscular metabolic fitness whatever that is. And VO2max in not just cardiovascular fitness. It varies by muscle group utilized in the different sports. So it is cellular dependent too.

The other main variable which affects LT is VLAmax and when the energy that is a result of these two factors is applied to a physical situation, economy becomes an important issue in the value of the measure for LT. For example stroke mechanics in swimming or cadence in cycling or rigging in rowing or running shoes and surface in running etc. For a triathlete the best way to improve the threshold in swimming is often better stroke mechanics. These are reflected in the above diagram.

The metabolic process is discussed in several of Mader's publications. The summary publication is

Mader, A. (2003). "Glycolysis and oxidative phosphorylation as a function of cytosolic phosphorylation state and power output of the muscle cell." European Journal of Applied Physiology 88(4-5): 317-338.

I doubt that is true. I once asked Bruce Gladden, how does the muscle decide which process to use to make ATP and he said no one had a clue. They know what the processes are but just how much of each one is used in a given situation was still a mystery.

The model above is an attempt to get at that. Which is why the strength of the anaerobic system affects the percentage of VO2 max that can be used at any effort level and affects how ATP is re-synthesized.


It is discussed in detail at

http://www.lactate.com/lactate_threshold.html and on our triathlon site on the anaerobic capacity pages. There are four. Of course Mader's concepts are what is behind it.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

You are mistakenly thinking of FTP as being defined by a value on a mean maximal power duration power curve.

FTP is perhaps better thought of as a property of the curve, than being a specific point along it. It's a functional expression of underlying sustainable aerobic capability expressed in wattage terms. As such it's conceptual but a very useful concept because of the utility of power measurement.

Think of the MMP curve as being a function of a few (useful) conceptual things, with FTP being one of them, i.e.
MMP(t) = f(FTP, A, B), where A and B represent other useful functional expressions of underlying physiological capability that are sufficiently independent of FTP and each other.

Since the mean maximal power curve either side of about an hour is pretty flat, then seeking precision in terms of duration is not required in any case when using this method (i.e. maximal efforts of about an hour) as a means to estimate FTP. IOW don't confuse means to estimate/establish FTP with a definition of FTP.

Naturally, the further you move away from longer durations of about an hour and towards shorter ones, then then MMP expression becomes less dominated by the FTP term (i.e. the A and B terms start to play a greater role in defining the shape of the curve), although FTP is still a dominant factor down to short durations of a few minutes, which should not be surprising given the nature of energy contribution of the various metabolic pathways to maximal exercise over various durations.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

I'd like to take this opportunity to publicly thank Alex and other intelligent individuals like him who have both the understanding and the patience to explain my ideas to people in ways that are often better than I can muster.

Anyone interested in such concepts would do well to pay close attention to what such smart folks have to say, and ignore the trolls who repeatedly try to make things seem "fuzzy" just to forward their own agendas.

"You are mistakenly thinking of FTP as being defined by a value on a mean maximal power duration power curve. "

No I'm saying it can't be defined - I'm pointing out FTP is a vague, blurred, fuzzy concept and there is no threshold. It is variable, all over the place, different whenever you measure it, different indoors outdoors, TT bike road bike, changes with inertia, affected by fatigue, rest, climbing compared to flat etc etc.

"FTP is perhaps better thought of as a property of the curve, than being a specific point along it. It's a functional expression of underlying sustainable aerobic capability expressed in wattage terms. As such it's conceptual but a very useful concept because of the utility of power measurement. "

I agree FTP is not a specific point on the curve. It is no more than an imprecise concept.

"Think of the MMP curve as being a function of a few (useful) conceptual things, with FTP being one of them, i.e.
MMP(t) = f(FTP, A, B), where A and B represent other useful functional expressions of underlying physiological capability that are sufficiently independent of FTP and each other. "

I don't agree FTP is useful. The actual power one can sustain over defined durations is useful.


"Since the mean maximal power curve either side of about an hour is pretty flat, then seeking precision in terms of duration is not required in any case when using this method (i.e. maximal efforts of about an hour) as a means to estimate FTP. IOW don't confuse means to estimate/establish FTP with a definition of FTP. "

The mean maximal power curve is not flat.

"Naturally, the further you move away from longer durations of about an hour and towards shorter ones, then then MMP expression becomes less dominated by the FTP term (i.e. the A and B terms start to play a greater role in defining the shape of the curve), although FTP is still a dominant factor down to short durations of a few minutes, which should not be surprising given the nature of energy contribution of the various metabolic pathways to maximal exercise over various durations. "

The dominant factor is actual power over relevant durations.



(

I read this over on timetriallingforum.

Very entertaining.

http://www.timetriallingforum.co.uk/....php?showtopic=98754




This is a cross-post from Wattage Groups by Nathan Townsend. I thought, in light of some postings on the forum thus far it would make for interesting reading:-


A 30min TT is closer to threshold than a 60min TT


Long winded rant here but with plenty of interesting up to date science. Continue only if you have an open mind and wish to learn and understand about how to train with power....

I'm not going to waste any time whatsoever arguing any of this with Andrew Coggan, but the evidence is clear, 60min for the average trained cyclist is too long and is thus an underestimate of the power at which a true non-steady state metabolism emerges (at a rate which is meaningful for training). Most people cannot maintain threshold power for that long. There is always human variability though so some of you will be able to maintain a true threshold for that long, but the average trained cyclist no.

So by all means do a 20min TT and then estimate your FTP which is itself is an underestimate of threshold and then pretend that when you do medium or long intervals slightly above this power that you are in fact depleting your "FRC". Whilst W' and W'balance are considered to be representative of mechanisms that contribute to peripheral muscle fatigue and there is plenty of evidence to support this, I don't know what FRC is supposed to represent because there is not a shred of science on this made up variable, but what the evidence does tell us is that it probably isn't related to peripheral muscle fatigue (see attached study by Thomas et al).

There are many studies using a wide variety of experimental techniques which lead to these conclusions. In particular, as mentioned in another thread, the fundamental nature of the VO2 slow component means that mammals cannot commence exercising at threshold power and expect to be able to maintain this power for 60min, because the VO2 slow component occurs earlier than this ie: you start to fatigue earlier. Thus, you must either commence at a power output BELOW threshold and then as you fatigue you reach a power which is sustainable for a longer duration, or you commence at threshold, then as you fatigue, you gradually drop the power so that you're always on your threshold. It should come as no surprise that this is exactly how both Brandle and Dennis paced their successful hour record attempts, and is a fairly typical power profile of 40km TTs.

Here are two very recent articles (ie: current April edition of ESSR) which provide commentary on the VO2sc and its relevance to human performance.....

The Critical Power Framework Provides Novel Insights Into Fatigue Mechanisms
http://journals.lww....es_Novel.1.aspx

In particular note the following statement "for many years the VO2 slow component was ignored tacitly because it did not fit with muscle energetics models". It looks pretty obvious that the good Dr Coggan continues to ignore the relevance of the VO2sc and is thus leading all of you down the garden path with this "FRC" non-scientific garbage.

Skeletal Muscle Fatigue and Decreased Efficiency: Two Sides of the Same Coin?
http://journals.lww....ciency__.3.aspx


Also, I've uploaded a very interesting study already known to this forum that contains strong evidence in favor of everything that I've written here on this topic over the past couple of years, yet nothing in favor of the broscience that Coggan continues to carry on with in his perpetual state of scientific denial and/or ignorance....


Central and Peripheral Fatigue in Male Cyclists after 4-, 20-, and 40-km Time Trials.
http://www.ncbi.nlm....pubmed/25051388

Look at the results carefully:

-Average time for 20km TT = 31min, 40km TT = 65min
-Mean (SD) power for 20km TT = 279 (22); 40km TT = 255 (21) W.

So on average about 24W difference there. That isn't quite meaningless is it?

-In the 20km TT the average RER is 0.96. How is this possible if a 30min effort is above threshold? It is not possible. If you are above threshold then the RER must be above 1.0. (I conducted many 30min TTs on elite cyclists, including Cadel Evans when I was a grad student in the AIS physiology lab in Canberra. Using gold standard metcart equipment, usually these elite cyclists could hold right on 1.0, but not once did I see a cyclist hold a higher RER than 1.01-1.02 nor did I ever see that value steadily increasing until the last 5min or so. If FTP is closer to a 60min max effort, then 30min must be above threshold. So why doesn't RER keep increasing even for elite performers? The answer is simple. a 30min TT is not above threshold, therefore approx 60min is lower than threshold and so Coggan is wrong).

-In the 4km TT the subjects achieve a significantly greater level of peripheral fatigue than either the 20km or 40km TT but there is NO DIFFERENCE between the 20km and 40km TT. If a 20km TT is above threshold, then by definition you must be depleting "FRC". If FRC is supposed to be conceptually equivalent to W', which itself is closely related to the mechanisms which underpin peripheral muscle fatigue (see above review by Grassi et al), then what we should see is a difference in the level of peripheral fatigue between the 20km and 40km TT, but there isn't. Why? because the 20km TT is not being performed above threshold and there is little or no difference in depletion of FRC/W' between the two. Ergo FRC/W' is not depleting any faster in the 20km TT than it is for the 40km TT which is impossible in reality (but only possible in Coggan's alternate reality).

-Look at the lactate values (not including the final end spurt values). According to an arbitrary definition of MLSS in the 20km TT the average subject would be above MLSS. Can ANYONE honestly look at that figure and say that lactate has not attained a near steady state but instead is continuously increasing?

-In both the 20km and 40km TT the magnitude of central fatigue is about the same, and in both cases it is greater than for the 4km TT. What this tells us is that over these longer durations such as 30-60min, a contributing factor as to why an average trained cyclist adopts a lower power than their true threshold, is because we experience an additional component of central fatigue that has less effect over shorter durations.


Overall, this study is highly revealing and informative. If we could do a follow up study then a good option would be to repeat the experimental techniques and on separate days do TTs over the following durations 10min, 15min, 20min, 25min and 30min. We know that by the time you arrive at 30min, the level of peripheral fatigue has dropped and central has increased. Even in the 20km and 40km TTs I suspect the level of peripheral fatigue becomes magnified in the last 5min or so as subjects raise the power above threshold and properly start depleting W'. So for example this could be controlled for by simply instructing the subject to maintain the power constant (at whatever it is over the predecing 5min or so) until the end.

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

So there is a lot of criticism here, not of Andrew Coggan himself, but of his biased opinions and lack of scientific rigour. I do not have anything personal against him, but the fact is that the science does not agree with his belief that the original definition of FTP (as stated in his book TARWAPM ie: approx one hour max power) is equivalent to the true maximal intensity at which the physiological mechanisms underlying the threshold phenomenon occur at. The lay cycling world is being led astray due to an incorrect and corrupted presentation of the true science which continue to to be developed throughout the scientific literature. However since blogs and non-peer reviewed books such as TARWAPM are more easily accessible and understandable to the lay public than peer reviewed journals, the incorrect version becomes accepted as de facto evidence and people believe it.

Lastly, whether or not any of this makes a difference to the way people train is irrelevant. It might not make any difference whatsoever to many people, however it does make a difference to factual validity which some people might consider important. Personally I know that if I want to conduct intervals which develop a higher level of peripheral fatigue, then I cannot assume my FTP is the correct boundary. I choose a higher intensity and do my intervals above that. Numerous studies in the literature indicate somewhere in the range of a 20-30MMP is probably a good choice, longer if you are better trained.

Why people conduct a performance measure eg: a 20min TT, and then make some arbitrary correction factor which has an unknown level of error eg: 95% to estimate something which is an estimate of something else, none of which has a scrap of scientific scrutiny to validate the hypothesis, is beyond me. By all means, keep it for your PMC, but when it comes to planning interval training and knowing whether your threshold power has improved, throw that 95% correction factor out the window because you've already got the hard untouched raw data in your hands.


Don't expect me to reply to a continuous stream of ignorant denial because the science is there published in print. If people need further clarification then they should read the science because I'm too busy to spend all my days on this forum. Enjoy and good luck everyone with your training and racing.P

Begone, troll.

One's MMP at any duration is different whenever you measure it, different indoors outdoors, TT bike road bike, changes with inertia, affected by fatigue, rest, climbing compared to flat etc etc. ;)

You are now deliberately confusing measurement methods with an expression of underlying physiological capability. Stop your deliberate obfuscating, it's just trolling.

Noted.

Since FTP and a couple of other key underlying physiological attributes tells you the power one can sustain over defined durations (amongst other things), or can be derived from it, then by your own definition, FTP is useful.

Indeed FTP is more useful than the MMP curve alone because it provides insight into why the MMP curve is shaped the way it is. The MMP curve tells you what you did or possibly can do, and yes that's helpful/useful. Understanding the key underlying physiological attributes such as FTP is even more so, as it explains why the MMP curve is the way it is and arms one with this additional insight to tailor training that is individually appropriate.

I didn't say it was.

I said it was pretty flat at durations of about an hour. And it is.

The dominant factors are the underlying physiological attributes and their relative contribution to power output.

By expressing those underlying physiological attributes in functional terms of energy and rate of energy output (i.e. power), then it provides significant utility for those using a power meter to track their training and performance.

There are of course other means to assess underlying physiological attributes (e.g. various lab tests), but they are only ever going to be occasional snapshots, and lose the significant utility power based measures and such functional expression of attributes provide us, such as constant monitoring, the ability to tailor according to what's happening now/recently, and using the entire data set of work for validation and reliability rather than an individual lab test XX weeks ago.

Without such insight into the underlying physiological attributes, then we are not particularly well informed about why our power over various durations is the way it is. Such insight is very useful for a variety of reasons. If you don't agree that it is, then you really shouldn't be giving out advice about athletic performance.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

So you've cross posted a cross post. How novel.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

You have MMP(t) = f(FTP, A,B). But FTP = f(A,B) so isn't the relationship best expressed as MMP(t) = f(A,B)

I am not sure what you specifically mean by A and B but the main things behind the MMP curve are the same things behind FTP. Actually, I can think of A, B, C, and D and there are probably others.

By the way I am in no way saying that the MMP curve is not useful. Just clarifying what determines it.


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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

You can think of A and B as functional expressions of physiological capabilities other than those provided by sustainable aerobic metabolism, and as such they are not functions of FTP but are sufficiently independent of FTP.

Unless you think, for example, that the physiological factors underpinning one's peak/sprint power over a few seconds and those underpinning FTP are somehow related.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

I look at A and B as internal metabolic processes. And they cause FTP which is an external measure of body movement. So I look at the MMP curve (an external measure of body movement) as a result of metabolic processes and several environmental factors including the actual movement of the body.

I will name the main metabolic processes: aerobic metabolism, glycolytic metabolism and creatine phosphate metabolism. So MMP = f ( aerobic metabolism, glycolytic metabolism and creatine phosphate metabolism plus environmental factors.)

At most points on the curve the creatine phosphate system has little effect but at all the rest of the points the other two metabolic systems are operating and very influential as well as the environmental factors.


FTP and these metabolic processes which are producing the energy are not independent. FTP is very dependent on these processes.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

I said they were functional expressions in terms of energy output and the rate of energy output (power) and there is sufficient independence (but not total) between them. If an individual parameter did not have sufficient independence from the others then it would be redundant and should be removed from the equation/model.

The fact that you've decided to use your own inputs in your own modelling doesn't invalidate what I've said.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

Statistically/mathematically speaking, the best model is MMP(t) = f(Pmax, FRC, FTP). In a sample of ~150 cyclists, Pmax and FRC are positively associated with each other, whereas FTP is inversely related to the other two (based on the covariance matrix).

In such a model, Pmax obviously represents/reflects the combination of muscle mass, muscle fiber type, and neuromuscular control, whereas FRC represents/reflects the factors contributing to resistance to fatigue during high-intensity, non-sustainable exercise (e.g., muscle mass, muscle buffer capacity). FTP, on the other hand, is a surrogate measure of power at maximal lactate steady state.

(Note how VO2max doesn't even enter into the picture.)

One trains to influence adaptations to internal metabolic processes which then drive external output. One also trains to get more efficient in movement. These are the drivers of the MMP curve.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

This means none of these measures are independent of the other.


One of the more absurd statements I have ever seen. Thank you for making it.

VO2 max is having an effect on all these measures and so are other metabolic processes.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Well, FTP only shares ~33% variance with the other two, but, yeah, you're right (and it is exactly what you'd expect from a physiological perspective).


Not absurd in the least (see Alex's comment about excluding parameters for which there is no statistical/mathematical justification for including.


While that seems to make sense physiologically, my point is that you can't show mathematically/statistically that VO2max influences the shape of the power-duration relationship. Presumably, that's because such a curve is really a reflection of fatigue/resistance-to-fatigue, which VO2max influences only indirectly, i.e., by impacting muscle metabolism/energetics. IOW, the role of VO2max is subsumed into FRC and FTP, and doesn't leave an identifiable "fingerprint".

And what has that to do with whether anything I've said is valid or otherwise?

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

You are using in your equation, factors that you are not training. The factors reflect training not what is actually being trained. FTP is not was is being trained. FTP will change because of metabolic adaptations within the body or for economy reasons. These are the things that should be in your equation. It is what one wants to train in the right direction so that the FTP gets better.

So the equation should reflect the things that are actually driving all the points of the curve. Each point represents a time to exhaustion at a different power. What affects this time at all these power levels? If you knew, then that is what would guide training. I happen to believe that the main driver is VO2 max. And the second one is VLa max.

There is an impasse here. I disagree strongly with Dr. Coggan on what are the main causes for the MMP curve. Readers will have to decide on their own what makes more sense. It will affect how one trains.

-----------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

I take that to mean that you're a strong believer in lots and lots of VO2max intervals for all athletes, endurane or not? After all, your claim seems to be that VO2max is the primary determinant of performance at all durations ("the main driver is VO2max").

Thank you for asking the question. Blogs are certainly not the place for complete exactitude. However, my guess is that the vast numbers will never see these exchanges.

The MMP curve is essentially a series of races from a few seconds up to I guess several hours. Nobody probably does any more than a few points on this curve though I would be interested in any here who read this just how often they actually do the various times/distances.

We discuss on our triathlon website in a brief way this concept in a page titled

"What does it mean to be faster in a race?"

http://www.lactate.com/...riathlon_faster.html

We take the point of view that each point on the MMP curve (though it is a term I have never used) is determined primarily by three metabolic factors: aerobic capacity, anaerobic capacity (using VLA max as the definition) and creatine phosphate.

If one wants to delve into the energy contribution of various races, the obvious answer is that the results are due to the strength of these three energy systems plus some other factors such as muscle strength. There is a lot of literature on this and it varies by researchers as to the contribution of each of the systems at the various time frames. I sat through a presentation on this by Uli Hartmann last December and he showed differences between what US and European researchers have found on this.

I once asked Jan Olbrecht about this and he replied for a 50 m freestyle or about 21-24 seconds aerobic capacity had almost no factor in the race. Whatever oxygen was used was already in the blood or muscles and while the swimmer obviously breathes during the race, the oxygen did not get to the muscles.

But he said that these swimmers spend most of their time training aerobically. Why? His answer was that they needed to be strong aerobically in order to do the other workouts efficiently that would lead to success in these races.

For the first 10 seconds, it is mostly creatine phosphate with some glycolysis and for the next 20 seconds, it is mostly glycolysis. After 40 seconds the races are strongly affected by VO2 max. World champions at these distances will almost certainly have high VO2 maxes. But what determines one VO2 max from another in how well they will do in these races is anaerobic capacity.

From a few minutes up to extreme distances the VO2 max will be the primary driver of performance but not the only one. Anaerobic capacity is always there, providing a lot of the energy at the shorter end and then determining how much of VO2 max can be accessed at the higher end.

Hope this clarifies things. And by the way, I am just the messenger here, providing what I have found to be the most consistent system to explain performance at both ends of the MMP curve.

When we first got involved in this business we searched for anyone who could explain it to us. It wasn't till we found Olbrecht 2 1/2 years after we started that we found someone who made sense out of it all. And by that time I had read about a thousand documents on it including many with Coyle's and your name on it.

As far as VO2max intervals, certain types of intervals are obviously beneficial for all athletes but by far, most of the training will be at lower intensities and this has the effect of building VO2 max too. Probably few track sprinters do low intensity stuff, possibly fearing it will erode anaerobic capacity. Swimmers don't have that problem. There are lots of philosophies on training.

I suggest you read Olbrecht's book if you want to understand his approach to training. His ideas are 1) a different perspective on energy metabolism from most, one that explains a lot of things; 2) a system on how to test these energy systems which is definitely different from everyone else; and 3) a system of training the various energy systems reflecting differences in fiber type.

It is this third part that most here are interested in. Many coaches and athletes just want to know how hard, how long and how often and whether intervals should be short or long or the rest short or long. There is obviously mechanical things that have to be trained.


----------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

VO2max sets the upper limit to aerobic ATP production, yes. In terms of the power-duration relationship, though, that means it influences the vertical position of the curve, not its actual shape (in fact, as I already pointed out, it isn't possible to mathematically/statistically identify any "signature" of VO2max from power-duration data).

Furthermore - and probably more importantly - individuals with the same VO2max can have markedly different power-duration curves, both in terms of their vertical positioning and in terms of their shape (cf. our 1988 paper on "Determinants of endurance in well-trained cyclists", in which time-to-fatigue @ 88% of VO2max varied over a 6-fold range in 14 individuals all with essentially the same VO2max).

IOW, VO2max is not the "primary driver" as you claim.

Something that alters the vertical position of the MMP curve, is most definitely a determinant of performance, isn't it ??

And therefore a determinant of FTP (since ftp IS the Y coordinate of MMP at around 1 hour)

And therefore a determinant of MMP

AND... by a hell of a lot. Its not uncommon for riders following the old school training model as recommended by Joe Friel for example to add 20-30w from a few weeks of vo2 intervals.

I find it interesting how you immediately go to discredit. You will notice that I have continuously said that anaerobic capacity is right in there with aerobic capacity affecting performance. I couldn't agree more with your comment:

in which time-to-fatigue @ 88% of VO2max varied over a 6-fold range in 14 individuals all with essentially the same VO2max

I would look to differences in anaerobic capacity as the factor in this. Your comment just makes my point. Thank you.

Here is the conclusion of the paper you cite

In conclusion, the present results indicate that individuals with a similar VO 2 max can vary greatly in glycogen utilization and time to fatigue *when cycling at the same work rate and percentage of V02max. These differences in performance ability during high-intensity submaximal cycling are highly related (r = 0.96; P c 0.001) to a combination of lactate production (i.e., %VO~ max at LT) and muscle capillary density (e.g., lactic acid removal). Muscle mitochondrial activity, which can be a primary determinant of lactate production (12, 21), was not different in groups L and H, nor was their blood lactate responses when running uphill. The factors associated with a high %VO2 rnax at LT when cycling and performance ability were years of cycling experience and percent type I muscle fibers. It appears that intense cycle training performed for -5 yr compared with 2-3 yr promotes continued neurological and/or muscular adaptations that reduce muscle glycogenolysis specifically when cycling.

You came across VLA max, but just didn't recognize it. You should have been reading Mader as he was coming to grips with the concept at that same time. Olbrecht was also in the midst of his doctoral research on the topic at the time.



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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Yes, clearly - however, when performance can vary 6-fold in subjects all w/ the same VO2max, it's hard to support the claim that it is the primary determinant.

EDIT: To help illustrate my points, here are the fitted power-duration curves for two cyclists with essentially the same VO2max (and economy). Note the differences in performance, not only at shorter durations but also at longer durations (where the average difference in power is 10%). For comparison to our 1988 study, also shown is the power that would elicit ~88% of VO2max in both subjects, as well as the predicted time-to-fatigue at that intensity, which differed by ~2.5 fold (i.e., these subjects are not as radically different as the extremes of our published study).

The difference isn't due to varying anaerobic capacity, at least in any normal sense of the term. Now if you and/or Olbrecht wish to attempt to redefine the term, be my guest...but I think you'd find communication a lot easier if you didn't use terms to mean something that they don't.


Lots and lots of people were aware of the fact that VO2max was not the be-all and end-all as an indicator of endurance performance ability. As the saying goes, though, credit goes to those who do the work (publish the data).

I don't think the fact that it isn't readily comparable between riders stops it being a determinant.

Although absolute vo2max can't be readily compared between riders to determine how much power they create, you could be pretty sure that if a rider increases their vo2max, they will probably go faster.

Whether vo2max work is actually working by forcing muscle adaptations, well I'm not sure. But if that was the case, why would athletes go faster on EPO or blood doping ? - all you've done is increased the oxygen in their blood, and lo and behold they go faster with the same metabolic fitness (same aerobic machinery and plumbing) still in place.

Why would that be the case if O2, and hence VO2, wasn't a primary determinant of performance ?

Here are some graphics we just put up on our lactate threshold page in the last couple days:

http://www.lactate.com/lactate_threshold.html



From later on in the page:



The data was provided by someone who also was educated at Cologne and like Olbrecht was primarily interested in training athletes, not academia. I am not sure how he measures anaerobic capacity. He is now a coach of a high level cycling team and has been involved with TDF cyclists since 2005.

If you want to maintain that VO2 max is not the main driver of top performance in endurance races, then fine. Many will disagree.

Our point of view explains why some do better than others and how to train anaerobic capacity so they can do better in endurance races. I would think many would be interested.

Have a good day, I do not have time to go on at the moment. This discussion will make some great future web pages.

But your power curve just above makes my point better than anything I have said already. The cyclist with the red curve obviously has a higher anaerobic capacity and will be better at shorter races and not as good at longer races.

Thank you, I will use it in the future to support my position.


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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

You might ask yourself this: what happens to the shape of the power-duration relationship when VO2max is altered by blood-letting or transfusions? What about severe iron deficiency combined with transfusion? Aging?

(These are all examples of cases where changes in VO2max exceed changes in performance or vice-versa, i.e., performance in a relative sense moves in the opposite direction...thus demonstrating that the primary determinant of performance lies elsewhere, i.e., within the exercising muscles themselves.)

To state things in a Boolean way: having a sufficiently high VO2max (whatever that is) is a necessary but not a sufficient condition for elite (or any particular adjective you choose to use) endurance performance.

That would seem to be a problem...

Thanks, I'll need to chew on this and dig out those articles. Might even need a glass of red to get through it !!

I'm still stopped on the EPO question though, just.... why does it work ? Perhaps its because the body has less work to do in actually pumping the blood around ? e.g. lower HR for the effort, slower breathing, so athlete autonomically less stressed at that power ? less to do ? I dunno ! :)

Fatigue is caused by many things. The unconscious mind / reptilian brain/ brain stem / central governor is constantly monitoring heart, blood, muscles, temperature, fuel, hydration, internal organs, chemical balances etc etc; often the conscious brain is engaged in an argument with the unconscious brain and is trying to override the discomfort and pain messages it is receiving. The power we can sustain is to an extent down to motivation and how much discomfort and pain we are prepared to endure. Some are prepared to endure more than others in training or competition than others.

These interactions between body and mind are incredibly complex and there is much to be discovered and much argument about the little we already claim to know. The scientists don't agree with each other.

What we do know is that the pace or power we can sustain or average drops the longer the duration. We can't hold the same power or pace over 20 minutes as we can for 10 minutes, or for 20 minutes or 50 minutes. We can't hold what we can hold for 50 minutes over 60 or 90 minutes.

We can't even necessarily hold the same pace or power over a given duration on different days, in the cool or extreme heat, different inertia different riding position, uphill or on the flat etc etc. You are never sure exactly what power you can hold for a given duration on any particular day.

Get someone on a trainer and tell them to ride a 30 minute test then after 25 minutes ask them to just carry on and complete 60 minutes and they will slow down.

Do a 60 minute test. Start at the power you expect to be able to average over the entire 60 minutes - the first 10 minutes will feel really easy. After 20 minutes you will start to feel that an hour is a long time. The last 20 minutes becomes hard. Very hard and at about 50 minutes you might start thinking 'well I've done 50 minutes I'm sure I could hold this for 60 minutes but it's only a test I really don't need to hurt myself anymore.'
The same pace the same wattage, the same 'threshold' power was easy then incredibly hard and you couldn't do it for 70 minutes or 90 minutes, if you could, it wasn't your best effort over 60 minutes.

There is a sustainable pace or power for each specific duration. There is nothing special about any duration. There is no magic threshold pace that you can sustain for 20 minutes or an hour or longer.

Obviously if you row for 2,000m 6 to 7 minutes that duration is relevant. If you cycle for 25 miles then 50 or 60 minutes is special to you. But there is no 'threshold' you can hold for 20 minutes 40 minutes 60 minutes 70 minutes, which if you go over you tire easily. It isn't as simple as that, we fatigue and fatigue is complex.

Then you have motivation. When you do a 20 minute or 60 minute test and improve are you fitter or did you just try harder than ever before?

The brain plays a big part, and you can trick it. Just wash the mouth out with carbs and the brain thinks it is going to get carbs and allows you to speed up or continue longer at the same pace, yet no carbs have reached the muscles.

It's all very complex.

So for training purposes do we really need to know anything other than power / pace and distance / duration?

Do we really need to know blood lactate numbers?
Do we need to know Functional Threshold Power?

All we need to know is our power over durations which are relevant to our events and our training.

Training should be based on percentages of known performances rather than an estimated vague FTP number which might correlate well with blood lactate threshold or not depending on how you measured the blood lactate and how you estimated the FTP
and there is strong evidence there never was a lactate threshold anyway.

Doing a 20 minute test then taking a percentage and calling that FTP, then doing training at intensities based on percentages of the estimate is daft when you have real performance data over the durations you do in training.

If you really want to know your 60 minute power do a 60 minute test. If you decide doing 2x 20 minutes is the sort of training you want to do base the intervals on your 20 minute power. If you do 5 min intervals base them on previous 5 min intervals.

There is no need to use mental constructs, or imaginary thresholds.


So back to the original post and Noakes view that there is no lactate threshold. There does not need to be a threshold for lactate numbers to be of use.

I'm not disputing that those who know how to measure blood lactate and use those numbers to train athletes don't know what they are doing. They do know what they are doing, but most of us don't have access to blood lactate testing or have the know how to use the results in our training.

I am saying we don't necessarily need it to train effectively.

As far as FTP goes I think the name is just plain misleading. Functional OK fine, Power yes obviously, but Threshold? There isn't a threshold, not a lactate threshold or a power threshold. As for 60 minutes, well there is nothing special about 60 minutes. As for somewhere around 60 minutes between 50 minutes and 70 minutes or FTP based on a percentage of 20 minute power, here we visit Alice in a mathematical wonder land. The power curve may not be steep but it is still a curve, it isn't flat, there is no threshold.

Why on earth base your training and the quantification of your training on a vague wooly estimate, a mental construct, when you have real numbers from actual performance?

Not true, I think: you've tricked the brain into thinking that refueling is imminent, therefore it is safe to release more of the reserves that are already present. You can't increase or maintain output without increasing or maintaining fuel usage, can you? No matter how tricky your brain is.

---

----------------------------------
"Go yell at an M&M"

Correct and therefore the pacing strategy is limited ( at least in part) by the brain and not peripheral fatigue.
The fuel was there all along, but the brain is regulating your work load based on the information it has. "Anticipatory Regulation"

They've done numerous deception trials where the body can out perform if fed incorrect information.

---

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
I also give Training Advice via http://www.ForeverEndurance.com

The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
http://www.AGNCYINNOVATION.com

Limiting factors in trained individuals are in some regard central and not peripheral.
We know this because if you look at the oxygen uptake of a leg when both legs are working simultaneously it is lower than when that leg alone is exercising.

Therefore, tissues are competing for oxygen.
If you are able to utilize EPO (synthetic or altitude or ????), you are able to deliver more oxygen through increased red blood cells. This increased oxygen delivery is taken up by the local tissue and results in increased performance.

---

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
I also give Training Advice via http://www.ForeverEndurance.com

The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
http://www.AGNCYINNOVATION.com

Comparing absolute threshold power values with relative VO2Max values is ... well bit funny. Subject A could be 100kg and subject C 50kg.

Thank you. The brain is tricked into releasing carbohydrate it would otherwise withold?

You alluded to other instances where the brain is tricked into improved performance. Amphetamines, pain killers? Given false times or power readings? Placebo?

So the same muscles at the same level of fitness, same capilliaries etc can output more power just because there are more red blood cells?

No improvememt in the fitness of the muscles, just an improvememt in blood?

No improvememt in heart stroke volume or increased sustainable heart rate just blood which delivers more oxygen per heart beat per pint of blood?

From deceiving about how warm it is to blocking information from muscles to the brain, can all have an affect on exercise performance.

To your other post:
Yup:same body, more red blood cells = more power.
(Technically if you re-infuse a pint your volume is increased transiently and therefore stroke volume and cardiac output, but that goes away relatively quickly).

Increasing blood volume itself (say be using glycerol) hasn't really decreased HR, but may show an improvement for exercise in the heat due to increased sweat rate (banned by WADA as a masking agent). What Osmo Proload and Skratch Hyperhydration are attempting using high electrolyte load.

Study on autologous blood reinfusion: http://www.ncbi.nlm.nih.gov/pubmed/3623787
Limiting factors for oxygen uptake: http://www.ncbi.nlm.nih.gov/pubmed/10647532

---

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
I also give Training Advice via http://www.ForeverEndurance.com

The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
http://www.AGNCYINNOVATION.com

Sort of- cognitive tasks given while performing vigorous exercise has been shown to increase performance compared to the same workload and no cognitive task.

Google Ministry of Defense, Dr. Marcora, etc, for more info...Runner's World did fluff article on it a couple months ago I think. This is why assessment and selection programs use a high amount of cognitive testing during exhaustive exercise...weeds out the physically and mentally weak.

---

http://www.reathcon.com

So you are not actually measuring the underpinning physiological changes occurring at cellular level, but other proxy integral measures for the result of such changes, such as VO2max and BL response.

How is that any different to using another integral measure like power output (other than they lack utility and are not measures of performance in the way power output is)?

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

How do you track real improvememt in fitness using power alone without blood lactate testing or heart rate other than by doing maximal tests?

How do you know there is a real fitness improvement as opposed to improved motivation or just simply trying harder than in the previous test?

Improvements in fitness are not just improvements in maximal performance - often you want to be able to sustain a given power easier so you have more in reserve for the finish or a major climb or for the run after the bike.

How do you measure improvememt or lack of it without maximal tests without some other reference like blood lactate levels or heart rate?

In rowing it is common to test at sub max power levels and look at blood lactate and or heart rate. This gives real evidence of improvememt in fitness. Maximal tests can still be used so I don't see why additional evidence and information should be ignored or discarded.

Unable to deal with the refutation of your earlier comments, you instead try to bleed over into unrelated matters.

i. who cares? We're discussing testing athletes for their racing performance, not the frail.

ii. there are (some pretty straightforward) ways, but what makes you think BL or HR response is any better at revealing motivational factors?

This is contradictory.

If you can ride at a given absolute power more easily than before / have more in reserve, then by definition you are now capable of sustaining a higher power output than you were before, or of sustaining the same power output for longer. Hence your maximal performance has improved.

Choosing not to ride maximally for the duration is simply a tactical / strategic choice. You could have done that before as well. You'd just go slower.

Who cares? This is racing after all and racing tends to require maximal efforts at some stage to sort out the wheat from the chaff.

The real evidence of rowing fitness is improvement in race power output and race performance.

HR adds nothing of particular value to the assessment of performance, and BL is inconvenient, expensive, infrequent and often quite unreliable unless performed with great care.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

Flawed logic on your part.

Just because it can't be agreed what is happening at the (arbitrary) different Zones, it doesn't follow that the different zones aren't eliciting different responses.

The type of argument in this thread can be applied to any of the tools used to simplify exercise physiology.

Why are the zones defined as so?
Why do we use 4 minute intervals and not 4 minute 23 seconds? Is there no chance that the 4:23 is better?
How about Tabatha intervals? Why aren't they 23 seconds on 11 seconds off - was that even studied?

Simplicity is the thread that ties exercise physiology together.
People pretending to know the answer is what keeps us apart.


"Uncertainty Is an Uncomfortable Position. But Certainty Is an Absurd One.” – Voltaire

---

#######
My Blog

OK so I've gone through all this and yes it would appear that vo2max is not itself a primary input (after all, its the muscles that create the power, not the oxygen) but that additional O2 availability is a key cause of muscle adaptation (the muscles adapt to use that o2) and therefore, from a point of view of all the poor buggers on TTF and here trying to make sense of all this, we should really be considering that VO2 work (or any other way of getting MORE oxygen to the muscle) can have a substantial effect on fitness (call it metabolic or cardiovascular, its really at the point where the two meet, i.e. the O2 uptake of a muscle).

If thats correct, then (for example) wearing an oxygen mask, or injecting EPO, etc, wouldn't have much same-day effect on an athlete, but in a relatively short time frame, if you kept it up and kept training, the muscle would adapt, it would start utilising that o2, and then it would generate more power.

I'm just a trying to get my head around something thats very complex in a simplistic way ! feedback welcome and appreciated :) thanks

 
Yes, and no.

At the most basic level, one is interested in the gene expression of various proteins as a result of various exercise processes. These proteins will lead to various changes in cellular structure and chemistry.

No one yet understands this but they are studying it and learning more all the time. These changes result in changes to the energy producing capabilities of the muscle which will reflect in the ability of the person to contract the muscles in terms of speed and sustainability.

There is more than one energy producing system in the body but for most races there are only two that matter, aerobic metabolism and glycolysis. These two systems affect performance from races of 20 seconds up to ultra marathons. Thus, it would be prudent to understand just how these systems work to produce the energy necessary for contraction.

One system dominates energy production after 40 seconds and that is aerobic metabolism. There are contributions of energy from glycolysis after this time up till ultra long races. One can still contract the muscles without glycogen or a source of glucose so obviously there are examples where almost 100 % of the energy is from aerobic metabolism, nearly all of it the metabolism of fats.

Because of the small amount of energy from glycolysis in long races, exercise scientists essentially discounted it as a factor in endurance races. But there was a problem as several have pointed out, people with the same ability to produce energy by aerobic metabolism often exhibited very different abilities in long races. And one of the consistent findings was that the out put of glycolysis was causing this differential ability to utilize the aerobic metabolism. Hence the origin of the terms such as anaerobic threshold, lactate threshold, maximal lactate steady state (MLSS) and OBLA (onset of blood lactate accumulation.)

Most who study this just referred to some unknown factor or pointed to a result in the environment, not in the muscle as the cause of this difference. However, some looked for a metabolic explanation and they believe they found it. This metabolic explanation, not at the level of gene expression, but at a subsequent point in the process involved the interaction of the aerobic and glycolytic systems and the strength of each.

They named a process in the body for glycolysis similar to what exercise scientists had named for aerobic metabolism. They called it anaerobic capacity or VLA max to represent the rate of pyruvate production in the body. They also found that this capacity varied widely in people and obviously athletes. Now aerobic metabolism and glycolysis are the result of several things but rather than look specifically at each of the sub components, it became important to look at the two systems as a whole. This does not mean that there is no interest in the causes of each but for explaining muscle contraction it was easier to consider them as wholes within the cell.

They also found that two capacities interacted and affected how much of each capacity could be utilized in a race. The stronger the anaerobic capacity the more the contracting muscles used glycolysis and the more metabolites were produced which eventually limited contraction or the amount of aerobic energy that could be utilized.

So it makes sense to consider both in any athletic event. Aerobic capacity is best measured by a VO2max test but there are other ways of approximating it. One is blood lactate because the fuel for the aerobic system at VO2max is almost 100% pyruvate or lactate. Lactate is also the product of glycolysis so it can be used to assess the strength of the other system too. But any lactate test that does this is subject to the same problem that any other non VO2 max test has, it does not reflect the contribution of each system to the effort level. But lactate also reflects the output of glycolysis so can be used to try an assess anaerobic capacity.

It is not VO2 max and lactate. It is lactate as a window into both systems. Some find it easy to estimate VO2 max this way since the window into the aerobic system only requires a 4-6 minute sub-maximal test and not a one hour all out test. It is just as precise or maybe more so than a FTP test. The lactate test gets even more precise with multiple readings. Any maximal test to estimate anaerobic capacity is less than a minute so not onerous on any athlete.

Now you have offered up the MMP curve as an example of what can be done without lactate. Each point on the MMP reflects the input of the three energy systems but after 10 second it reflects just glycolysis and aerobic metabolism. The curve that Dr. Coggan provided above is a perfect example of two athletes with the same aerobic capacities but differing anaerobic capacities. The one with the greater anaerobic capacity will excel at shorter distances as the curve indicates but at some point will start to get slower at longer distances. It is an almost perfect illustration of Mader's theory which is the basis for my comments.

Go to http://www.lactate.com/...riathlon_faster.html for examples of athletes that differ in time to exhaustion at various distances which is the basis for this curve.

I have been patiently pointing this out for a couple years but it seems to get lost in the rhetoric and the mocking. Now one can disagree with this assessment but it is something that one should carefully consider and not just reflexively dismiss it.



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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Alex, you have not said anything I felt worth refuting. But I will go over your recent posts and reply to them in detail seeing as you challenge me to do so.

You should be aware I have no objection to maximal tests. I only object to doing too many or doing them at the wromg time.

You should be aware some older people, people with long term health problems or injury or anyone recovering from illness may need to avoid maximal tests. Even entirely healthy athletes in danger of overtraining or recovering from overtraining may want to avoid maximal testing.

Your statement "who cares" is frankly an insult to any athlete who has ever been ill or injured, thousands of older athletes, and any athlete who may have health problems from time to time.

I note you are unable to track performace improvememt without doing maximal tests.

You should remember, those who do sub maximal tests can still do maximal tests when necessary.

Many Olympic class athletes do sub maximal tests. It isn't only the weak who do sub maximal tests.

And to stay on thread. - do you beleive there is a heart rate threshold?

Would you agree that threshold heart rate is reasonably stable despite changes in fitness?

The standard test for performance in rowing is a 2000 m test simulated on an erg. In the US, this is nearly always a Concept II machine.

Shannon Grady who works with various athletes, mostly runners, also works with some high level rowers. She worked with a male light weight four and this boat eventually had the best time in the US about a year ago and was one of the best in the world.

Each athlete in this boat's 2000 m test were all time bests during this process but for the previous 3 years each athlete had stagnated at lower power levels. So yes, the 2000 m test is relevant but how to improve the 2000 m score is the real issue.

So it is best to ask what causes the result in a 2000 m test rather than just constantly repeating the test over and over which may not be optimal training.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Alex, in a triathlon, where one must complete a run after the bike section, I very much doubt the best strategy is to do the bike section maximally. It is a race yes but a race in which the art of pacing is very important. A rider who paces him or herself better is likely to beat an athlete who is fitter but does not leave enough in the tank to stay in contention in the run.

Also, regarding your weaklings comment, triathlons and road races and timetrials, all sports in fact are full of people who don't win. Races of all sorts are full of weaklings with no chance of winning. But they take their sport just as seriously as elite athletes.

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).

---

The question of who is right and who is wrong has seemed to me always too small to be worth a moment's thought, while the question of what is right and what is wrong has seemed all-important.

-Albert J. Nock

Yes indeed. I just know that there are riders and coaches who don't put the cardiac side high enough on their list.

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.

A while back I found this comment on another forum from a very well respected physiologist. I hope he won't mind me posting it here !

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

There's a lot of other things that will determine how high a %age of that VO2Max one may sustain for longer and shorter intervals. Ergo, it's utility as a marker is fairly limited.

---

The question of who is right and who is wrong has seemed to me always too small to be worth a moment's thought, while the question of what is right and what is wrong has seemed all-important.

-Albert J. Nock

I think both you and the physiologist you quote are living in the pre-1960s. The simple fact of the matter is that endurance performance ability is more closely correlated to muscular metabolic fitness (expressed or power or pace at threshold) than it is to cardiovascular fitness (measured as VO2max). Moreover, the scope or magnitude of possible improvement is greater for the former than for the latter (since threshold can, and does, move closer to VO2max). Thus, while having an adequately-high (whatever that means*) VO2max is important for elite performance, and all endurance athletes should consider how their training may (or may not) increase their VO2max, such considerations should be secondary, not primary.

*When I was younger, mine was ~80 mL/min/kg, yet I never made it beyond cat. 1, so the bar must be higher than that. ;)

EDIT: So now having look up the context in which Jamie Pringle made his remarks, I've edited my post, as clearly he was speaking specifically about how to improve VO2max, not how to improve performance in general.

I assumed (perhaps wrongly?) that mcmetal was simply being sarcastic.

Thanks Jerry.

In the UK it is the same, a Concept2.

I know from bitter personal experience that 2000m on a Concept2 requires training other than maximal efforts over 2000m.

Training incorporates maximal efforts yes, but over shorter durations and sparingly. Maximal efforts over longer durations like 15 minutes 20 minutes or 60 minutes are done for specific reasons.

Where did I say a 2000m test was the best way to train? The question was about performance tests, not training.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

And I said that the premier performance tests in rowing was inadequate. It doesn't tell the coach or athlete what has to be trained. You focused on the last phrase of the last paragraph when the heart of remark was elsewhere, on the relevancy of this test.

-----------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Where did I say one should do the bike section maximally?

For those who are competing (either against others or themselves) then it's a maximal effort for the duration of the event.

The vast majority. So, are you saying that only winners should ever do a maximal effort?

I never said weaklings. I said the frail.

Assuming they are healthy then there is nothing wrong with maximal tests to determine your fitness. Your fitness might suck, but doing a maximal power-duration effort isn't a particularly big deal or something to be avoided like the plague.

But there are a number of people for whom a maximal test efforts are as inappropriate as racing, or even just participating. For some that might be because they have a temporary condition (e.g. doing a maximal effort while you have a bad viral infection is dumb), while others have chronic issues (e.g. heart disease, obese, or other serious medical conditions) and of course maximal performance tests are not appropriate. But then they aren't racing either, which is what discussion about athletic performance tests are about.

If all they are doing is a walked fun run, then they don't need a test of athletic ability, they need a check by their doctor to make sure they wont die. That's hardly relevant for the discussion of testing for athletic performance.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

Where did I say that such a test was the only one that should inform a coach about an athlete's training?

Having a mean maximal power duration curve would be as instructive for coaches of competitive rowers as it is for cyclists.

But if 2000m is the race, then you surely need to test for it?

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

Then why don't you say that rather than attack maximal tests in the first place.

Has anyone on this thread ever suggested high frequency maximal testing? It's a strawman.

Another strawman. Suggesting an argument that doesn't exist to knock down. It's rather tiresome Trev.

When you've finished stating the bleeding obvious, then do let me know.

Come off it Trev. If a maximal test is obviously inappropriate, then then nobody cares about such tests because they are obviously inappropriate.

Another strawman.

That's an unfounded claim about my capabilities.

So?

Since our heart beats when performing a threshold level effort (however that happens to be defined), then one can define such a thing, but it's likely to be in a typical range than a specific number.

HR response varies with fitness.

---

http://www.cyclecoach.com
http://www.aerocoach.com.au

I think I'm one of the largest proponents of lab based testing but anyone who says that Lab based testing is a better measure of performance than actual performance is just plain wrong.
I think lab based is a great resource to understand changes, but the fact of the matter is you can either be improved, the same or worse on your lab testing and still faster or slower in the real world.

When someone has increased threshold wattage, I tell them their threshold wattage has improved... I don't tell them they're a faster cyclist.

Do you know wattage at threshold is a better predictor of performance than say VO2max? Because it integrates more components such as economy, effectiveness etc.
Field testing integrates the physiology with the motivation etc. You can't focus on one while losing sight of the other.

For those who are not "performance" athletes but recreational, ask them if they can ride up that hill easier or finish that century. If they say yes, that's all that matters.
Ultimately it's not about fitness, its about performance.

---

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
I also give Training Advice via http://www.ForeverEndurance.com

The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
http://www.AGNCYINNOVATION.com

I'm not saying that.

I'm saying we have performance testing, we can all do maximal tests unless ill or injured. I'm not against maximal performance tests.

I'm against discarding sub maximal tests. I'm against ignoring heart rate and I'm against ignoring blood lactate testing and I'm against ignoring lab testing if you have access to it.

I'm against ignoring or disparaging any form of testing.

I'm all for maximal testing and I'm all for specific testing over relevant durations / distances when appropriate.

But I'm also saying that sometimes you want more than maximal tests alone in isolation.

I'm also saying that it is a mistake to ignore data that is available.

Why ignore heart rate or blood lactate data if you have access to it?

I don't ignore power data, I use it. I do maximal tests. I do sub maximal tests.

It's daft to ignore available data.

I note you mention motivation - I'm aware some coaches on this forum don't see it as their concern, but motivation is a part of performance a big part. One of my earlier questions is how do you know if improved performance is due to improved fitness or improved motivation?

I ask these questions again, if you use power in isolation without heart rate and without blood lactate testing, how do you measure improvement without doing maximal tests?

When you do maximal tests without heart rate or blood lactate testing how do you know if the improvement is due to increased fitness or because you just tried harder and were better motivated?

I'm not convinced it's useful to characterise cardiovascular fitness as exclusively measured by VO2max.

Suppose we have a cyclist with a max HR of 190bpm and a threshold HR of 170bpm. Then, many years later, their max HR has dropped to 180bpm, but their threshold HR is still 170bpm. If nothing else has changed, e.g. their cardiac output at the HRs they can still achieve is still the same, their power at threshold would be unchanged. But their VO2max would have decreased, purely because their HR doesn't go as high as it used to. It's like fitting a rev limiter to a car, we wouldn't expect it to have any impact at all on the car's performance at rpm below the limiter. Sure, yes, one aspect of the cyclist's cardiovascular fitness is worse, in that their heart can't pump at the maximal rate it used to, but it's outputting just as much per beat below that HR as it did previously, and that seems to me to be a measure of cardiovascular rather than metabolic fitness.

So I don't see the above situation as demonstrating that the limiter is in the exercising muscles. Threshold may have moved closer to VO2max due to the "rev limiter" effect, but the limiter at threshold HR can still be oxygen delivery rather than the ability of the muscles to utilise it. Improve the amount of O2 pumped per beat with EPO or a blood transfusion and their power per heartbeat will increase, increasing power both at threshold and their max HR.

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:
Untrained state: threshold power 150W, VO2max power 190W, 78.9%
Trained state: threshold power 300W, VO2max power 360W, 83.3%
Power at VO2max has increased by 89%, and we know that improvements in power at VO2max are dominated by improvements in cardiac output. So we would expect the same increase in cardiac output to be increasing power at threshold from 150W to 284W, leaving only 16W of the increased power at threshold being due to increased metabolic fitness.

Or some data from my own training:
20 minute max effort 233W 176bpm CTL=29
20 minute max effort 322W 174bpm CTL=89
How would you determine the relative contributions of metabolic and cardiovascular fitness to that change in performance? HR is essentially identical for the two efforts, so clearly I am somehow delivering more power per heartbeat. If it isn't possible to determine the relative contributions of metabolic and cardiovascular fitness from the above data, what data would be required to make that assessment?

Trev, it's not daft to ignore data if it doesn't contribute to your understanding and you or your coach don't need it to modify training programs. You could do a hundred tests a week with every variable tracked. Is that better than doing one or two simple tests with only power data? What about just tracking training data? That is hours of sub maximal testing every week.

You've created so many straw man arguments, it's nearly impossible to respond to your posts.

FTP is a way to structure your training around a simple concept that condenses a lot of physiological and performance research. The fact that FTP might be different indoors vs outdoors is about as relevant as saying your HR swimming is different than it is running.

I'm not sure what you're trying to say, but VO2max is considered the best overall measure of cardiovascular fitness. That's why, e.g., it is used to help make important clinical decisions, such as whether or not someone goes on the list for a heart transplant.


If maximal cardiac output is reduced, then obviously cardiovascular function isn't the same as it used to be. IOW, cardiovascular fitness has declined.


Where your lactate threshold lies in relation to your VO2max is an indicator of your muscular metabolic fitness.


I don't, as it is an irrefutable fact.


You're looking at things the wrong way. Power at VO2max has increased by 89% (yeah, right!), but threshold power has increased by 100%.


For starters, measurement of VO2max.

That's what happens to trolls: they become so focussed on winding people up that they lose track of their own positions.

The only person I've ever encountered who is 100% consistent in their arguments is 'perfection' (which leads me to think that he's either a bot, or that he actually believes the nonsense he posts).

But if max HR reduces, with everything else constant, threshold has improved relative to VO2max yet there has been no change in muscular metabolic fitness, just the addition of a "rev limiter".



But the majority of that 100% has been achieved by an increase in cardiovascular fitness not metabolic fitness. So in that scenario I would argue cardiovascular fitness has led to ~8x the improvement in threshold power that metabolic fitness has (134W attributable to cardiovascular fitness and 16W to metabolic fitness).

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?

It would probably help if you talked about stroke volume instead of cardiac output/cardiovascular fitness.

I take it you don't agree with Noakes about there being no lactate threshold?

Incidentally I thought you might find it entertaining that I've been training on a Concept2 for 2 months without heart rate. I've even done a few all out performance tests, one of them was a 60 minute test.

It is an interesting experiment.

+1

Andy is the one who wants to split everything into cardiovascular and metabolic fitness, in which case stroke volume is one component of cardiovascular fitness.

If we take every underlying element and decide whether we want to lump it in with cardiovascular fitness or metabolic fitness, then consider the case of someone's max HR decreasing with everything else remaining constant - this would constitute a decrease in cardiovascular fitness (but only one of the elements of it, one which has no impact on performance at threshold provided max HR is still above what was their threshold HR, while other elements of cardiovascular fitness do impact performance at threshold) and there would be no change in any of the underlying elements that we are classifying as metabolic fitness. Threshold would move closer to VO2max, but there would be no change in any of the underlying elements of metabolic fitness.

I've pointed out numerous situations in which changes in lactate threshold (an indicator of muscular metabolic fitness) and changes in VO2max (an indicator of cardiovascular fitness) can diverge from each other, not only in magnitude but even in direction. Such examples illustrate that the factors determining each are, to a greater or lesser extent, independent of each other. Moreover, endurance performance ability has been repeatedly shown to better track (correlate) with lactate threshold than VO2max. If you wish to overturn this scientific literature, I think you're going to have to marshall a more cogent/convincing argument than changes in your own personal power:heart rate ratio.

Yeah, me...and 10s of thousands of people like me (although "split" is too strong - it's more that one needs to recognize that they are different, albeit interrelated, things).

I have no problem with anything I have ever read in the scientific literature on this subject, only your characterisation of it. I have described a scenario where threshold can move closer to VO2max without improvement in any of the underlying elements of metabolic fitness. I do not agree that the fact that lactate threshold and VO2max can move in different directions shows that the factors determining each are independent of each other. It shows that there are some factors independent of each other, but the size of the common vs independent factors is important. An increase in stroke volume will increase both VO2max and lactate threshold, thus a change in lactate threshold cannot be said to be purely a measure of metabolic fitness, as it also reflects elements of cardiovascular fitness. So I still do not see anything in what you are saying that backs up your statement that metabolic fitness is more important than cardiovascular fitness for endurance performance, in that nothing that you have said shows that the influence of metabolic fitness on lactate threshold is greater than the influence of cardiovascular fitness. Perhaps you could point me to a paper that took untrained people, trained them, and analysed the underlying adaptations they experienced to quantify the relative contributions of cardiovascular and metabolic fitness to their increase in lactate threshold?

Maybe I'm just not understanding what you mean by the terms metabolic and cardiovascular fitness. When I first saw you make the statement, many years ago now, that metabolic fitness is more important than cardiovascular fitness for endurance performance, I looked up what you might mean, and the definition I found was that metabolic fitness is simply everything that isn't cardiovascular fitness. 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:

You inhale 20 litres and exhale ~15 litres. So what do you breathe?
Apart from that - what it got to do with anything?

---

#######
My Blog

Apparently not. The "take home" message is that the key determinants of endurance performance reside within the exercising muscles themselves, in particular the ability to balance aerobic ATP production to ATP demand. This is something not entirely reflected in the measurement of VO2max, and in fact is to a greater or lesser extent independent of VO2max (cf., for example, our 1988 study).

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

I guess all those mitochondria in the muscles, capillaries, enzymes etc in elite marathoners are a waste of time. They should have been focusing on metabolic fitness whatever that is. Oh, wait, what is the definition of metabolic fitness? Is it strictly those with a high LT. I guess all those sprinters of the world are headed for metabolic oblivion.

Here is a study published a couple years ago about the effects of low intensity training on the metabolic fitness of a world class runner. His VO2 max and LT went up at the same time after changing his training approach.

Ingham, S. A., et al. (2012). "Training distribution, physiological profile, and performance for a male international 1500-m runner." International Journal of Sports Physiology and Performance 7(2): 193-195.

A summary of this is on our website on our lactate threshold page. Anyone who wants to know what causes the LT curve should read it. It includes training advice on how to change it.

http://www.lactate.com/...hreshold.html#vo2max

The VO2 max referred to in the above model is the VO2 max of the day of the race. In practice over a season, measured VO2 max varies quite dramatically, and as just pointed out varies from sport to sport with the same athlete. It changes from time to time, due to training, racing, illness or inactivity. But a performance during a race will depend on what it is the day of the race.

A recent research presentation at ACSM 2011 showed the variability of VO2 max during a season and from season to season with an elite 1500 m runner over a 2 year period.

VO2 max varied from a low of 4.8 l/min to a high of 5.6 l/min in a 18 month period which is a 16.7% improvement, hardly a trivial change. Within the first year, the change went from 4.8 l/min to 5.16 l/min. Using ml/kg/min the low was 70.5 ml/kg/min and the high was 79.6 ml/kg/min. Performance changed substantially as the runner's best time in the 1500 m race went from 3:38.9 to 3:32.4 min:s from the beginning of year 1 to the end of year 2 (3:32.94 was the winning time at the Beijing Olympics in 2008.)

Ingham, S. A., B. W. Fudge, et al. (2011). Training monitoring; training delivery; middle distance running. American College of Sports Medicine, Denver, CO.

So training to raise VO2 max is very rewarding. This study has several interesting aspects and will be referred to at other parts of this page and in other sections on this web site.

As the athlete's VO2 max goes up or down the lactate threshold will do the same. In the above study, the velocity at the lactate threshold went from 16 km/hr to 18 km/hr over the two year period, a 12.5% improvement. These corresponded to increases in VO2 max. So improvements in VO2 max will also affect the threshold positively.

This was later published in a journal. Here is the cite.

Ingham, S. A., et al. (2012). "Training distribution, physiological profile, and performance for a male international 1500-m runner." International Journal of Sports Physiology and Performance 7(2): 193-195.

Shows the value of polarized training.



Yes, a well recognized result but there is a reason for this. Some types of training will affect VO2 max in a negative way while raising the threshold. Here is a visual from our website which reflects this. See the lower right hand box. I can point you to the type of training that does this. It is highly recommend on Slowtwitch.



Here is another visual which we are now trying to get animated which also shows this issue



From Olbrecht's book

Shift of the Lactate Curve: Interaction of the Aerobic and Anaerobic System on the Lactate Curve

there are not 3 but 13 ways to explain the shifts of the lactate curve, making the interpretation much more intricate, complex, and delicate but actually more accurate and reliable

I know he is such a crank, advising all those world championship and Olympic medal winners (over a hundred). But maybe he needs to know what metabolic fitness is. I know, I know it is not published in the literature except it is. See Mader.

I suggest you read Olbrecht's book.

-----------

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

You just contradicted yourself.


I would agree...and since lactate threshold (a surrogate measure of muscular metabolic fitness) can move closer to (or away from) VO2max, it follows that there is more room for improvement (or reduction) in it than in cardiovascular fitness (i.e., VO2max).


You need to learn to think in both absolute and relative terms.


There are literally dozens of studies out there showing performance is more highly correlated with lactate threshold (expressed as power or pace) than with VO2max. Indeed, in fairly homogeneous groups of subjects there is often little-to-no correlation between VO2max and performance. (Our study just takes that a bit further by matching subjects on the basis of VO2max and finding that performance still varied 6-fold...and was highly correlated with lactate threshold.)


While (again) there are dozens of such studies that speak to this issue, here are a few that leap to mind:

http://www.ncbi.nlm.nih.gov/pubmed/6725086

(Longitudinal study showing lactate threshold moves closer to VO2max with training)

http://www.ncbi.nlm.nih.gov/pubmed/1385806

(Longitudinal study showing relative magnitude of changes in parameters of the cardiovascular Fick equation)

http://www.ncbi.nlm.nih.gov/pubmed/1474063

(Cross-sectional study showing that metabolic responses are more closely related to lactate threshold than to VO2max)

http://www.ncbi.nlm.nih.gov/pubmed/6373687

(A bit dated, but still excellent, review of the role of skeletal muscle adaptations in training-induced improvements in endurance performance)

http://www.ncbi.nlm.nih.gov/pubmed/17901124

(A more recent review that approaches the question from a slightly more whole-body/applied perspective)

Your study missed an underlying cause for your findings. If you had read the literature, there were publications indicating why your findings were perfectly reasonable if you considered the right variables.

Mader's ideas explain the findings in the 1988 study and your MMP curves etc. You may reject them but at least admit there are concepts that explain all these findings.

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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

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.


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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

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


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

Our study wasn't designed to identify causes of fatigue, and the results were not at all unexpected. IOW, the purpose of the study was to drive home the point that endurance performance is primarily determined by muscular metabolic fitness (a.k.a., lactate threshold the concept), not cardiovascular fitness (a.k.a., VO2max).

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

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

But what if I resemble a rat and love cheese, would this study be more applicable to me?

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

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

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.

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

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

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

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...

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

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?

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

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 (V&#775;o2 max) in the trained state remained at &#8764;6 l/min, lean body weight remained at &#8764;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% V&#775;o2 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 (V&#775;o2) 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., &#8764;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 V&#775;o2 (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/

"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"

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.

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

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

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).

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%).

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

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).


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).


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


Why yes, as a matter of fact I have (it's called endurance training).

This.

TBH, I'm surprised this is news to you Jerry, lactate.com is your website ?

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 ?







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?

You seem to be confusing the determinants of performance with the stimulus for adaptation...and I never advised Steve (or anyone else) to train a particular way.

Another thought (stimulated by various prior posts):

While I have done ~100 VO2max tests in my life, only a handful were when I was training hard for competition and at peak fitness (most were in the off-season, for research studies and/or as a biological control of the equipment). The three best results (at different institutions using different metabolic carts, but all constructed/validated by yours truly) all put my VO2max at 5.35-5.45 L/min, or w/in a ~2% range. Prior to each, I had been training for ~8 h/wk, but with different approaches. Specifically, in one case I had been doing nothing but what is now known as "sweetspot", in another I had been following a highly polarized program with 3 d/wk of VO2max intervals on an ergometer, and in the third I had been training using more of a mixed approach. I interpret such data to mean that the above value likely reflects my genetic limit for VO2max, such that I was bumping up against it no matter how I trained. What is relevant here, however, is how my actual performance varied depending on how I trained...as you would expect based on the specificity principle, the first approach led to more success in longer road races and TTs, whereas with the second I got really good at going hard for a few minutes at a time, and the third seemed to leave me better prepared for, e.g., criterium racing. This gets back to my point that one should structure train to meet the demands of an event and let the physiology take care of itself, rather than chase particular physiological adaptations per se.

Apologies for using the word "advice", that was of course incorrect. I'm sure you can still understand what I was getting at though. People are reading this stuff and making training errors as a result.

As far as stimulii vs determinants. They are one and the same for the purposes of what I'm trying to find out here. And I don't think Steve, or Derf, or me, or others, would have bothered posting at all in here if they didn't think the discussion might help establish where, how and when to apply training stimulii in order to influence those determinants.

Anyway, I'm just interested in finding answers to this question. Given the Seiler/non-Seiler type stuff flying around recently, it seems quite a pertinent question for many riders, coaches and physiologists.

I think I have the EPO answer now, that it does not bring about muscle adaptation, but I'd like to verify that first. more to come later. But if thats correct I do think Derf's point about being able to train at a higher level is logical.

They are not one and the same. Unfortunately its just how it is.
Additionally, many times people post because they want their voice to be heard, not because they think their thoughts are helping.

Back to your original points:
1. The muscles can absorb additional oxygen that is sent to them. This is why EPO and Altitude and increased cardiac output helps.
2. VO2max oxygen consumption being held higher does not necessarily allow you to hold submax watts higher.
3. VO2 intervals are not about training your muscles to uptake more oxygen.
4. Climbers lose muscle mass for a multitude of reasons. One includes the increased metabolic rate of trying to complete strenuous tasks in a cold, low oxygen situation. To conserve energy, you can kill off some hungry muscle tissue to lower metabolic demand
5. I already pointed out how EPO works in a previous post.

6. Polarization works (maybe, depends who you ask) by maximizing volume and thus stimulus of low intensity work on aerobic ability and maximizing your ability to complete high-intensity work to work anaerobic systems. The main tenant is that too much "in the middle" training leaves you tired to complete high intensity work at the highest workloads and that decreasing you low intensity a bit gets you most of the adaptation without as much fatigue.

---

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
I also give Training Advice via http://www.ForeverEndurance.com

The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
http://www.AGNCYINNOVATION.com

Thanks for this.

Point 1 is something I learned today from papers so thanks for confirming.
Point 2 its certainly my experience, and others I have regular contact with, although I've never tried it all winter. Perhaps it varies between athletes also. But certainly when I've done a vo2 block, or even a much smaller amount of vo2 work, my easy rides have moved up in power/hr and power/rpe at all intensities.
Point 3 I think all training trains just about all possible adaptations, but to varying degrees, so what vo2 is "about" is what effect it has on everything we're interested in training. I strongly suspect that a lot of muscle adaptation occurs when you do vo2 work, as well as cardiac and vascular adaptation
Point 4 my interest was more around what happens when they get back to sea level, just a thought experiment
Point 5 thanks and I just wanted to find some decent papers, currently on this one (pity they werent well trained!) http://www.ncbi.nlm.nih.gov/pubmed/25128327
Point 6 I'm working on it :--)

Here's the thread on hyperoxic effects (primarily focused on folks living up high, where they're already behind on o2 delivery): Hyperoxic Set up?


I was more trying to give mechanism of things (to my, humbly admitted, limited understanding). I said parallel systems before, but I should have said serial. Any improvements in any systems/pathway will ultimately be beneficial, BUT the greatest effect will be realized when the lowest-performing (rate-limiting) pathway/system is improved. That, by and large, is your metabolic "fitness".

So, simply put (to first order), supplementing with oxygen does allow you to work harder (even though that gain is pretty modest unto itself). That working harder elicits a much stronger adaptation signal. It's not from the oxygen itself, it's the ergogenic effect of oxygen under maximal efforts. You're stressing your metabolic fitness even more than usual .

EPO does help with that, but the extra RBC's are probably helping buffer/shuttle byproducts out of the primary working muscles, too, which could have a material effect on metabolic fitness. (I'm guessing)

As far as any of this being practical? Not really. Determine what events you're trying to optimize for, find your rate limiters within that event/competition, and target efforts that are in kind, especially as you close in on the event/competition. Otherwise a lot of consistent (more important than the composition!) work at a moderately-high level, polarized or sweet spot or whatever, is going to yield you some awfully good results.

Pretty much what everyone's been saying, though.

---

The question of who is right and who is wrong has seemed to me always too small to be worth a moment's thought, while the question of what is right and what is wrong has seemed all-important.

-Albert J. Nock

" This gets back to my point that one should structure training to meet the demands of an event and let the physiology take care of itself, rather than chase particular physiological adaptations per se. "

Oh bugger - I agree.

I would add though that I don't think that means everyone should train the same for the same event. One should identify strengths and weaknesses and slew training accordingly.

I've heard this one before....

"It's an aerobic sport dammit!"

What was your low-point during that time and what was the training load/intensity prior that? ie. what kind of a VO2Max responder are you?

I'll have to go back and look. In general, though, I've never considered myself to be particularly responsive to training. (OTOH, up until recently I've had few significant interruptions in my 40+ y of endurance sport, so perhaps I've never detrained enough to really understand how well I do/do not respond.)

In my 50 odd years, I have had several occasions where I have de trained and at times have given up a sport in which I was fit and switched to a different sport.

Particularly interesting is how when one switches from one endurance sport to another how unfit one is for the new sport.

This must be an indication as to how muscles adapt to specific sports.

The cardiovascular system may be fit but the muscles are not adapted to the new sport. It's amazing how much more power the muscles can sustain after training.

Same heart, same lungs, same blood, so the improvememt must be within the muscles.

Good point ! Despite my penchant for thought experiments and sanity tests its amazing how easy it is to get lost in pubmed and forget about the blatantly xxxxing obvious at times :)

Thanks for the study links. So, taking the one above, a 26% increase in VO2max was observed, and a 39% increase in O2 consumption at 2.5mM.

This still suggests to me that cardiovascular changes were more important than metabolic changes, in that 26% of the 39% is accounted for by cardiovascular changes, so the metabolic changes only provided half as much improvement as the cardiovascular changes.

The other thing I struggle to reconcile with what you are saying is the slide from Maglischo's presentation that I posted previously:


The time to exhaustion test ranged from approx 2 to 9 hours. The best performance, even over such long durations, was achieved by the rats that only did training that is usually regarded as improving cardiovascular fitness. Is this because cardiovascular fitness is more important, or because VO2max training also improves metabolic fitness more than the lower intensity training done by the other groups?

As you mentioned relative vs absolute, could you define more clearly what you are saying? Are you saying that metabolic fitness is more important than cardiovascular fitness for the entirety of the absolute change in power at lactate threshold from untrained to trained, or only for the component of that change relative to power at VO2max? I would have no problem with the latter.

Re one of the other studies:
http://www.ncbi.nlm.nih.gov/pubmed/1474063
perhaps it illustrates a source of where we are at slightly crossed purposes, as I don't see it as relevant to the matter being discussed, whereas clearly you do. The reason I see it as irrelevant is that it was cross-sectional in nature, and tells us nothing about the trainability of the difference identified between the two groups, so it could simply be due to an innate difference between them. If talking about "fitness" in a general sense, including innate characteristics, then it would be relevant, but what I mean by fitness in this context is adaptations brought about by training. So if you would regard the high lactate threshold group as having better metabolic fitness, even if it's an innate characteristic rather than acquired through training, then I wouldn't disagree with that, it's just a slight difference in the concept of fitness from what I'm interested in.

I don't think it is so cut and dried. Changing, for example, from cycling to running the biomechanics of running are significantly different.
I have experienced many problems myself due to imbalances and weaknesses in my lower limbs when running that have limited my performance and caused difficulty (strain/injury).

Mark

No, because if you acutely increased VO2max by 26% via transfusion, lactate threshold would have increased by less than that.


The latter (although again, extrapolating from studies of rats to humans is risky at best, so I wouldn't read much into this particular study).

Agreed.

My post was more about power output. e.g. Cycling compared to a Concept 2, but then there are questions about how the power is measured. There is more technique in rowing compared to cycling on a turbo or Wattbike etc etc. Power on Concept2 only measured at flywheel. Power going up and down slide not measured.

I can't measure power running, and even if I could runnimg is about pace. One man's 250 watts running might be considerably slower than another man's 250 watts even if they are the same weight.


But all that said, anyone who has taken up a new sport, or returned to a sport after a lay off of several years will confirm that their cardiovascular fitness will only carry over to the new activity to a limited extent.

If this were not the case we would see athletes switching sports and being as competitive in the new sport instantly.

There is lots of information that suggests that VO2 max is muscle specific and will vary sometimes widely between the muscle used in the test. There is also lots of information showing the importance of the delivery system in determining VO2 max. There is no way one will be a top athlete involved in endurance races without a high VO2 max and a good cardio vascular system.

You need both a good delivery system and well trained muscles at the periphery using the oxygen. This is simple common sense.


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

---

Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Agreed. If you take up a new endurance sport or return to one after a long break having a trained cardiovascular system means you are already a long way down the line, it will just take time to train the specific muscles.

Even a muscle well trained in one sport seems to still need training to be specifically fit for the new sport.

Sorry, but this statement is simply incorrect. If you can't achieve the same upper limit to VO2 using a particular exercise modality, then that's not VO2max, just a VO2peak.