If Tim Noakes "Central Governor" Model is Correct AND there is NO Lactate Threshold, HOW should this effect my train

Actually, if you are talking lactate accumulation in the blood, there is a very close relationship, almost 1:1 due to the lactate/proton cotransport. This is the reason there has been such a misconception regarding "lactic acid" production/accumulation over the years. Of course you are correct though, that lactate production through the LDH reaction consumes an H+, so, intramuscularly, they are not linearly related.

I'm not sure about the pain you speak of though being attributed to H+ accumulation. I'm not aware of any work that has made that connection in a concrete fashion. That is, unless you are speaking of the pain/discomfort associated with the hyperpnea as a result of acidosis compensation through ventilation, but then you get to the linear relationship between proton appearance and lactate accumulation in the blood, and, I'm sorry, but you can't have it both ways;)

Steve

Thanks steve. Great explanation. I had assume a 1:1 relationship. How else was there such an efficient deception. Can you tell me if any processes occur in the bloodstream or is it purely transport. Also i really like the lock-step image you used. Finally what is occurring when someone takes bi-carb soda before entering a lactate state. Cheers

Oh, (if I may call you Oh)

I'm not sure what you are asking regarding processes in the bloodstream. What you may be referring to is the fact that although there is a proton/lactate co-transport out of the muscle, the endogenous bicarbonate buffering system will attenuate the concomitant drop in pH to a certain extent. So, lactate accumulates in the blood, but H+ may not. That's why it is possible to run slightly faster than MLSS (or above the LT) for a while (e.g. 40 min) while lactate accumulates and blood pH remains in check. Or even at faster paces (e.g. 5 km pace) where lactate is clearly accumulating, but again, pH does not decline to critical levels. In the case of bicarbonate loading, it's hard to say what is occurring, maybe nothing (other than gastro-intestinal distress), or maybe something. If one bicarbonate loads, they are in effect enhancing the endogenous buffering system. Unfortunately, there are likely very few effort levels for which this approach is of any benefit. And so, in many cases (e.g. bicarb loading for a 10 km) the only effect is a tummy ache. What is occuring that would be of benefit would be providing additional buffer and possibly attentuating the respiratory compensation that would cause, as Noakes would say, the conscious mind to decide to halt the exercise.

Again, do not misconstrue what I am pointing out above to imply that lactate accumulation per se causes fatigue. Lactate appearance/accumulation is simply associated very closely with processes that do cause/relate to fatigue. Probably more important than the proton accumulation issue is the relationship between lactate production and glycogen utilization. That's the really key factor tied to lactate/proton accumulation. If lactate is accumulating, glycogen is being utilized at a high rate, and if lactate is not accumulating, glycogen is likely being utilized at a lower rate. The hydrogen accumulation is directly associated with glycogenolytic rate, and so impacts performance for say the 3k due to acidosis. OTOH, glycogenolytic rate is the primary determinate in the ability to sustain high workloads in extended efforts such as the marathon. So, that's why I was saying previously that LT will impact efforts as short as the 3k, maybe even the 1500, (acidosis) and certainly the marathon (substrate availability).

dsrunner wrote:

Lopes ran 2:07 for the marathon and 27:20 or so for 10k. He would not be "tempo training" (in any traditional sense) at 3:30/km.

Your problem is you have defined tempo training as too wide a band. Conversely, some have taken the step of saying such archaic terminology is pointless.

If you´re doing, say, 100-150 km/week at 3,30 pace the effect will be similar to doing a few tempo runs each week.

This approach was used by Mike Musyoki as well: 400s on the track and the rest of his training steady distance running.

Steve, the problem I and many others have with MLSS is that it is purely hypothetical. In reality, you can have many different scenarios (scenarii?) for different MLSS

You could have a very high MLSS in a 3000m because 3000m races tend to start fast, and finish fast, in between there is often a gradual slowing of pace. So you could hypothetically have a blood lactate concentration of 12 mmols for 7 minutes

You could have a MLSS of in a 20 mile race with a BLC of 3 mmols for 2 hours.

Thus, the lactate threshold/MLSS concept is very vague and hypothetical.

Isn't it much better just to talk about pace, such as 3.05/km or 4.53/mile or whatever and refer to target paces for each race?

This way, no-one is confused, and no-one is talking in a manner which may be construed as overcomplicated or pseudo-scientific, which is what I consider LT and MLSS to be.

Some people like to feel empowered by talking scientific terminology that makes them sound knowledgeable and self important, I don't mean you Steve, it's obvious you know your stuff. And amongst the laymen, ideas such as LT are discussed more because they become fashionable than because they are factual. Just as the old (false) Anaerobic Threshold idea was followed by LT, which is now being followed by MLSS.

Can't we just talk about pace, and what influences pace. I think Richard_ is on the right track on this thread, let's talk about what is going on in the muscles. Training influences muscle contractility in ways which are very noticeably different between trained and untrained runners. This is easy for anyone to understand and much more relevant than currently fashionable physiobabble.

Excuse me while I'm trying to feel empowered by talking scientific terminology, but the definition of MLSS that I'm familiar with is something like "the constant work level over which blood lactate rises no more than 1 mmol between 10 and 30 minutes into the session." I'm not understanding how that is vague, hypothetical, or can be applied to a varying pace 3000 m race in the manner you suggest.

It's fair to question how one most usefully applies such a measurement but it clearly can be made and it clearly is correlated with performance.

??? No you can't. The MLSS is the MLSS. You don't have one for 3000 m or 5000 m or 10 k, you have one MLSS and that's it. I generally corresponds to the speed you can maintain for around an hour. So, in some cases, for a good runner, it would correspond to half marathon pace, for a not so good runner 15 km pace, and for another runner it might correspond to 10 km pace. For the 3000 or the 5000 you will be way above MLSS and hence not at a lactate steady state. It's really not that vague at all. I think what you have a problem with is that you misunderstand the concept. I'm not trying to condescend (sp?), but the MLSS is pretty well defined and very clear. Further, the MSS is even better. If you want to learn a bit more about it, just do a pubmed search for Billat V. and there is some good stuff there. It's not really hypothetical, but quite to the contrary, quite demonstrable.

Why yes it is. I'm not sure why you think I don't want to talk paces. I think talking target paces for the distance is the best way to discuss training. What you can do for a 5 km is all you can do for a 5 k. So, that provides a benchmark for your training. What you can do for the marathon is all you can do for the marathon, and that provides a benchmark for your training. That being said, why would you try to eschew the scientific principles that underlie the training responses? Daniels talks about training responses, but also presents them in the context of the underlying physiological attibute that he is attempting to develop.

Thanks for the compliment above. As for speaking in scientific lingo to feel self important, yes, I agree, that may be the case in some instances. That being said, I don't think we should throw the baby out with the bath water, and totally ignore the underlying physiological principles that support some aspects of training and performance; one of those being LT/MLSS. Because of my background I have a clear bias towards the perceived importance of understanding physiology to clearly understand training and performance. That's not to say a coach can't be great without knowing anything about physiology, but 1) they may need to take a more circuitous route (more trial and error), and/or 2) they are a slave to what they have specifically learned from another coach or through their own empricism. Now, I'm all about empiricism, but the practice of collecting and analyzing data can go alot faster if you have a conceptual framework within which to work. Further, by knowing the physiology, you become a critical consumer of training info. For example, if someone said "I ran a 2:15 marathon by doing 200 repeats everyday", that should ring some alarm bells both from a training specificity and physiology perspective. That's an extreme example. OTOH, if someone told me they did 2 x 30 x 200s on 30sec and 100s on 30 sec, without the physiology, somebody might say, "that doesn't have anything to do with distance running", but the physiologist in me understands that for somebody who has a MLSS of 4:36 m/mi, that's probably a good stimulus for LT (hence relavent to marathon), while incorporating speed that will improve economy. See.... pace, LT, MLSS, economy all in the same sentence without any contradictions. ;) I'm not confused, and because of my understanding of all the concepts involved, I accept that that workout *may* have some value for a given athlete and might contribute to a solid marathon prep.

Of course, another coach who didn't have any understaning of physiology could train specifically at marathon pace to the exclusion of everything else, for the most part, and the athletes could get to the same place.

ANYWAY..... whew,.... again, not sure why you think I wouldn't want to talk pace. The point of my original post was that Noakes' views don't really mean anything new from a practical perspective, and if tempo training worked for you in the past keep doing it. I'm all about doing whatever works. BUT, if you understand the underlying physiology you can determine why or why not something worked so you are not locked into a program that doesn't work for you, or can improve upon a successful program by tweaking it with the understanding of what you are doing.

I've never come across that definition. The name Maximal Lactate Steady State implies the highest lactate value that can be maintained at a more or less constant level for most of the distance of a race.

If you put a lot of limitations on the definition, such as the one you have given, then doesn't that imply that the definition is rather shaky, and that the person making that strict definition is trying desperately to imply that MLSS applies only to 20 minutes of effort?

The point I am making is that lactate steady states can be observed over a very wide range of distances. Also, the word maximal should, if it is to be applied strictly, should be applicable to the higest lactate steady state, which is really rather impossible to do, becasue blood lactate concentrations can rise quickly, remain more or less constant for short time and then rise again or fall.

Steve, Jan Olbrecht and Alois Mader write about a 20 minute MLSS, Renato Canova says you can have an observable MLSS in a 13 minute 5000m race, others say it is strictly 1 hour race pace.

VAGUE VAGUE VAGUE. HYPOTHETICAL HYPOTHETICAL HYPOTHETICAL.

let's talk facts instead.

It is possible for a runner to have around 12 mmmols for 7 minutes in a 3000m race, but the pace would be falling.

or he could have 11-12 mmol for the same time, with only a gradual decrease in pace. If he maintained a constant pace from the end of lap one to the beginning of the last lap, then his blood lactate would be rising.

Also, in a one hour race. you might have 3-5 mmols or 5 down to 3 or a constant 3 for most of the race or a constant 4 or 5 or a slight increase or decrease, a huge amount of possible variations.

That's why we shouldn't really talk about LT or MLSS.

I don't wish to imply that you wouldn't rather talk in real pace terms, I just want to point out the confusion surrounding the LT MLSS terminology.

wellnow wrote:

I just want to point out the confusion surrounding the LT MLSS terminology.

I have to agree, you do seem confused.

A quick pubmed search for MLSS comes up with 278 refs. Of those, I will bet you dollars to donuts that you won't come up with more than a couple (so, less than 1%) that will suggest you can see a *maximal* lactate steady state for any duration less than 15 min, and if they do, it's to validate a cool protocol that can be done in a short time frame. The effort they identify will likely correspond to around 60 min. Further, in an all out effort such as a 13 min 5 km, I doubt that you will see it. If you are determining it based on the proper definition, I'm not sure how you would know. Generally, you take the first sample 3-5 min into the test, then again at the end, typically 20 min. So, in a race (e.g. 13 min 5 km), I really don't know how you could possibly see a steady state. If so, *I* want to see the data. (I presume that's all out, unless you're riding a bike);) I would be very impressed to see someone stop 3 min into this remarkable 5 km, have a blood sample drawn (actually 2 or 3 so we have duplicate samples we can have some confidence in), then start running again, then as soon as they cross the line (presumably in first) they stop and give another blood sample (or 3). Now that I think of it, I'd really like to see that data. Impressive implementation and must be a very fast 5 km runner, likely 11:30 without the stop, eh?

From your reply to the previous post where you admit you've never seen the actual scientific definition of the concept, it's clear you misinterpret what it is. THE GREAT PREPONDERENCE of the evidence (not one or two anecdoctal reports that we have no evidence for) clearly show that the MLSS corresponds to an effort that can be maintained for about an hour. Here is a sampling:

1. Baron B, Noakes TD, Dekerle J, Moullan F, Robin S, Matran R, and Pelayo P. Why Does Exercise Terminate At The Maximal Lactate Steady State Intensity? Br J Sports Med 2007.

2. Billat LV. Interval training for performance: a scientific and empirical practice. Special recommendations for middle- and long-distance running. Part I: aerobic interval training. Sports Med 31: 13-31, 2001.

3. Billat LV. Use of blood lactate measurements for prediction of exercise performance and for control of training. Recommendations for long-distance running. Sports Med 22: 157-175, 1996.

4. Billat V, Bernard O, Pinoteau J, Petit B, and Koralsztein JP. Time to exhaustion at VO2max and lactate steady state velocity in sub elite long-distance runners. Arch Int Physiol Biochim Biophys 102: 215-219, 1994.

5. Billat V, Dalmay F, Antonini MT, and Chassain AP. A method for determining the maximal steady state of blood lactate concentration from two levels of submaximal exercise. Eur J Appl Physiol Occup Physiol 69: 196-202, 1994.

6. Billat V, Gratas-Delamarche A, Monnier M, and Delamarche P. A test to approach maximal lactate steady-state in 12-year old boys and girls. Arch Physiol Biochem 103: 65-72, 1995.

7. Billat V, Sirvent P, Lepretre PM, and Koralsztein JP. Training effect on performance, substrate balance and blood lactate concentration at maximal lactate steady state in master endurance-runners. Pflugers Arch 447: 875-883, 2004.

8. Billat VL, Sirvent P, Py G, Koralsztein JP, and Mercier J. The concept of maximal lactate steady state: a bridge between biochemistry, physiology and sport science. Sports Med 33: 407-426, 2003.

9. Hawley JA, Myburgh KH, Noakes TD, and Dennis SC. Training techniques to improve fatigue resistance and enhance endurance performance. J Sports Sci 15: 325-333, 1997.

10. Laffite LP, Mille-Hamard L, Koralsztein JP, and Billat VL. The effects of interval training on oxygen pulse and performance in supra-threshold runs. Arch Physiol Biochem 111: 202-210, 2003.

11. Lepretre PM, Lopes P, Koralsztein JP, and Billat V. Fatigue responses in exercise under control of V.O2. Int J Sports Med 29: 199-205, 2008.

12. Schabort EJ, Killian SC, St Clair Gibson A, Hawley JA, and Noakes TD. Prediction of triathlon race time from laboratory testing in national triathletes. Med Sci Sports Exerc 32: 844-849, 2000.

You'll note the first is a recent study by none other than the Noakes group, and although the original poster indicated that he (Noakes) claimed there was no LT, lo and behold, by his determination of the MLSS, the subjects fatigue at.... wait for it.... 55 min. Of course you will reply that it was on a cycle ergometer, so, if you look at these reviews, you will see the concept validated using running as the exercise mode.

1. Billat LV. Interval training for performance: a scientific and empirical practice. Special recommendations for middle- and long-distance running. Part I: aerobic interval training. Sports Med 31: 13-31, 2001.

2. Billat LV. Use of blood lactate measurements for prediction of exercise performance and for control of training. Recommendations for long-distance running. Sports Med 22: 157-175, 1996.

3. Billat VL, Sirvent P, Py G, Koralsztein JP, and Mercier J. The concept of maximal lactate steady state: a bridge between biochemistry, physiology and sport science. Sports Med 33: 407-426, 2003.

**Them's the facts Jack.**

Again, if you go by the proper definitions, there really isn't any confusion. There may be some confusion in the coaching world, or the lay literature, and there may even be the rare outlier. What can we do about that though. Just because someone doesn't understand multidimensional universes, Physicists should stop talking about String Theory? Or the practicioners, astronauts who may plan to go to Mars, shouldn't be aware that there may be wormhole out there that could drop them into another universe, or bring them back home quicker?

As you point out, I've already stated I would rather talk in terms of paces, but see value in these concepts. You've clearly empirically shown there is confusion on the topic. On that we must agree.

Among 15 articles/studies in your bibliography, 13 are from the same person V. Billat or she is co-author, and the 2 others are both from Noakes. If you quote the same source you will get the same MLSS or MSS definition. Veronique Billat denies the interest AT as training pace zone and she says that MLSS is a dubious concept.

And you say that we the physilogists they all have the same definition of MLSS. No they don´t. You need to read some more physilogists and you will see that they tend disagree one each other. They do. It doesn´t matter what´s the subject. rather be the Central Governator or MLSS. As Renato Canova once point out in physilogy whe you don´t get the expected result the physiologist thinks that´s not the physilogist that´s wrong but the person he tests. Them's the facts Jack.

ANAEROBIC THRESHOLD - A RELATIVELY USELESS CONCEPT FOR COACHING – by V. BIllat

(...)Practical Implications

When scientists cannot agree upon a concept's definition, let alone the appropriate label to use, as well as the appropriate method/protocol of assessment, then the practical use of the "general implications" of the concept is foundationally prohibited. Until this situation is clarified and discrepancies removed, field testing for "lactate-threshold" should be avoided. There are more profitable and useful activities for athletes and coaches to be engaged in. (...)

ANAEROBIC THRESHOLD - A RELATIVELY USELESS CONCEPT FOR COACHING – by V. BIllat

Of significance to coaching is the concept itself. The common misunderstanding that the anaerobic threshold is the state where aerobic activity is dominant and maximal and anaerobic activity constant but "insignificant" is very prevalent. There are few competitive activities or events where such a circumstance is desirable.

Most activities do not require all body parts to be involved in an activity at the same intensity level. A cyclist will work the legs extremely hard but, by comparison, the rest of the body will function comfortably in an aerobic zone of metabolic activity. A swimmer pounding out stroke after stroke in a 1500 m race works the arms at an intensity that employs a high level of anaerobic energy supply but the rest of the body is "relaxed" and functioning at quite a basic aerobic level. Even in running, in a marathon the legs work hard while the arms and upper body "save energy." In these activities, lactate is produced by the primary working muscles and resynthesized by the muscles engaged in mild supportive activity. Those muscles cleanse or "sponge" out lactate so that the blood supply to the hard working muscles is quite low in acidity when returned to those muscles. Thus, any lactate measure is a measure of the "general functioning" of the body, not the actual work performed by the primary sporting muscles. Differences in technique most probably would account for a significant portion of many inter-individual differences in lactate assessments than work levels or movement economy.

In many "aerobic" sports the actual prime mover muscle groups work at an anaerobic level rather than aerobically as is inferred from anaerobic threshold testing. The common perception of anaerobic threshold does not give any information or understanding of what actually is happening in important aspects of a performance. Even the slightest improvement in movement economy (technique) in the "anaerobic prime movers" could make a significant difference to performance.

Of all the concepts of anaerobic-type thresholds or measures that are proposed perhaps the maximum lactate steady-state (MLSS) is the one that is most applicable to the field of sports. In cycling events of one hour, athletes have been measured to "tolerate" and demonstrate sustained lactate levels in the region of 7 mM/l. In most events where "effort" is required as part of the competitive strategy, lactate levels will be sustained in a competitive performance in excess of the anaerobic threshold (if one can be demonstrated). There is a much greater proportion of many competitive performances that is more anaerobic than is generally acknowledged. If appropriate and sane anaerobic training is ignored then an athlete will not be trained optimally and a theoretically "best" performance will not be possible.

How can one test for maximum lactate steady state? Simply ask trained, experienced athletes to perform a task equal to the duration of their competitive event and they are likely to produce a performance that is close to demonstrating the MLSS. To be sure of this, if performance intensities, usually velocities, are performed at an increment above and below the first trial, verification should be forthcoming. Repeating many trials usually is not necessary. Is this too simple of a concept for complicated science? In practical circumstances it works. But since this could be a procedure that is implemented by coaches would it be endorsed by scientists which would seemingly remove a coach's dependence on them?

But a central perplexing question still remains: what does one get from measures of lactate and performance? What do they tell more than is already known? If lactate values are specific to the task/testing-protocol/event there can be no inference beyond the observations themselves.

When two athletes with the same physiological capacities perform the same activity, one using arms only the other using arms and legs, the performance results are often different, particularly when energy supply is an important aspect of the task demands. In this case, it is not the "anaerobic threshold" that differentiates the two but the movement economies, one using more muscle mass to produce a performance outcome. An attempt to shift the anaerobic threshold by further training of a particular type in an hypothesized metabolic zone with appropriate heart rates is clearly the wrong approach to solving the less-efficient athlete's problem. A skill element change to reduce unnecessary movements would result in greater movement economy and would shift the velocity that supports the MLSS to the right.

It is dubious to attribute shifts in anaerobic threshold values to physical training. Given that so many variables render field tests of this phenomenon practically unreliable, what is attributed to score differences obtained between two tests is more of a guess than an informed judgment.

Sport scientists can produce graphs of swimmers, runners, rowers, etc. showing an "inflection point" that occurs in a region of performance velocity. Equally, other athletes tested with the same protocol do not show any inflection or exhibit measures that cannot be interpreted in terms of a traditional anaerobic threshold. A few selected demonstrations do not prove the existence of a phenomenon that can be applied universally. The trend in field testing is rather one of more people not demonstrating a clear "anaerobic threshold" than doing so. Complicate that further with deciding upon which threshold protocol fits the sport from the existing array of definitions and confusion results rather than a clearly usable training tool.

Anaerobic threshold results must be reliable, that is, capable of replication. When a particular protocol is used for a series of periodic assessments, as is commonly followed in "sport science testing" programs, if that protocol is altered, the previous results cannot be used for comparison purposes. A protocol change will produce unrelated results, often different response phenomena, and above all different implications and interpretations. The definitions and discrepancies listed above all originate from different testing protocols. Thus, results from one protocol to the next, no matter how small the change is explained to be, should not be compared. Essentially, a new data base is developed.

An unavoidable dilemma. Sport scientists are ethically bound to represent the worth of lactate testing and the inferences that are commonly proposed. This is what is known.

1. Lactate concepts and measures are limited/specific to each testing protocol.

1. Results from one protocol cannot be used to generalize or infer values to other testing protocols.

2. If one cannot infer from one lactate testing protocol to another then it is illogical to generalize lactate testing results to a competitive performance.

3. It is a greater stretch of the imagination to leap conceptually from an inferentially-limited measure under controlled conditions to the dynamic circumstances of a competitive or practice setting.

4. At most, lactate and lactate threshold measurements reveal changes but have limited to possibly non-existent inferential capacities about future performances (even training performances let alone competitive performances).

5. Lactate and lactate threshold measurements can reveal that they have changed as a result of training, but, if those changes are unrelated to competitive performances what is their value?

6. There are no national or international competitive events that reward medals for lactate threshold changes, levels, or testing protocols.

A story. During the spring of 1996, this writer attended the ARCO Training Center in Chula Vista, California. One day a USOC testing group had completed lactate threshold and aerobic parameter testing sessions on the US men's heavyweight rowing eight that was to compete later that year at the Atlanta Olympic Games.

The eight had just completed a European tour and performed worse than at any time in the previous three years. Based on comparative racing performances, it was a boat in trouble.

The head USOC scientist related that the members of the eight were still improving in fitness as the measures that were taken were better than previous test results.

Despite improved "fitness measures" the eight recorded a performance that was worse than any in the previous four Olympic Games, and compared to the boats that it had raced during the recent European tour, it had also degraded in racing capability. The fitness measures indicated that training was progressing satisfactorily. Unfortunately, racing performances were declining. Training improvements in physiological indices were negatively correlated with racing achievements. In 1994, the eight were world champions, in 1995 world bronze medalists, and in 1996, when they had the best testing results, were fifth out of six at the Olympic Games.

Just what is the value of lactate and lactate threshold/MLSS testing for making coaching decisions that relate to competitive performances?

Indeed, there are numerous studies in which MLSS is defined as the highest lactate steady state measured in 20-30 minute tests of constant velocity (speed).

Here is brief bibliography I recently posted on therunzone.com which may be of help/interest.

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From my post on therunzone.com:

"Maximum Lactate Steady State Studies

To further inform runners and readers of therunzone.com on the correlation between maximum lactate steady state and distance running success, please reveiw, at your leisure, the brief bibliography shown below, from my files:

Maximum Lactate Steady State Bibliography by Tinman:

J Sports Med Phys Fitness. 1999 Dec;39(4):300-8

J Sports Med Phys Fitness. 2004 Jun;44(2):132-40

Eur J Appl Physiol. 2002 Dec;88(3):214-26. Epub 2002 Sep 19

Int J Sports Med. 2004 Aug;25(6):403-8

Int J Sports Med. 2003 Feb;24(2):138-43

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

Below are articles to read which don't specifically discuss MLSS in detail, but the information about lactate measurement and performance parameters may be of interest to you:

Br J Sports Med. 2007 Dec 18 [Epub ahead of print

Eur J Appl Physiol Occup Physiol. 1997;76(4):295-301

Eur J Appl Physiol. 2001 Aug;85(3-4):351-7

Int J Sports Med. 2003 Oct;24(7):486-91

J Sports Sci. 2007 Jan 1;25(1):87-96

Scand J Med Sci Sports. 2000 Oct;10(5):286-91

Eur J Appl Physiol. 2006 May;97(1):1-8. Epub 2006 Feb 3

J Sports Sci. 1997 Aug;15(4):403-10 (3km time = velocity at LT (87% of variation shown in this factor, alone).

Sports Med. 1985 Mar-Apr;2(2):83-99 (use of fat as fuel source is a key factor in marathon running performance, as is specific economy and VO2 max)

Int J Sports Med. 2002 Jul;23(5):336-41 (Bilat) (Fractional use of VO2 peak is key factor in Marathon performance of elite runners. Raising VO2 peak did not effect submax VO2 economy, so the fractional percent at MP decreased significantly)."

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by Tinman

runfastcoach@gmail.com

Umm... so you take the bulk of a statement made by Billat en bloc and paste it? Why not simply refer to it instead of pasting a bunch of words that confuse the issue.

The issue at hand,... if I recall, was LT, which morphed into MLSS. I never even brought up the that AT, let alone supported it. Further, I NEVER ADVOCATED using the LT or the MLSS as a means of determining training paces, let alone actually testing it. That is why I also made reference back to the MSS to remove the issue of lactate testing all together. The conversation then got pulled away from discussion of the conceptual nature of the LT/MLSS to more semantics of the MLSS. If the bibliography I posted is a bit skewed, that was inadvertent, but probably reflects the fact that Billat is deserving of great weight when it comes to citations in this area. The fact that you yourself replied with a post by her further strengthens that. If one were to wade through the hundreds of studies that have used or looked at the MLSS concept, I am quite certain there will be exceptions to the rule. But the fact that one such as Noakes who does not necessarily subsctibe to the underlying tenents of the LT/MLSS still finds that the approach results in an effort that can be sustained for ~60 min lends further credence to the principle in my view. As I said in my previous post, I rely on the preponderance of the evidence which points toward the MLSS corresponding to an effort of ~60 min.

All that being said, *the point* keeps getting obscured, is that the underlying concept of the LT/MLSS is relevant to training principles. Are you going to say the concept of the VO2max is irrelevant, and/or inconsistent? It's true, if you perform a VO2max using one protocol, the actual number that you measure may be different than using another protocol. Or, let's say you pick VO2max velocity determined using Billat's protocol vs some other, the time to exhaustion will likely be different between the two. Further, if you perform intermittent work, the time limit at VO2max can be doubled. Does that mean VO2max doesn't exist? Does that mean VO2max has no relevance to understanding training principles?

Still, if you go back and look at all of my previous posts in this regard, I NEVER ONCE advocated using the MLSS or LT lab tests to set training zones or intensities. I don't personally believe a VO2max test should be used to determine training paces, and I wouldn't perform a LT or MLSS test to determine training paces, but that doesn't mean the attributes aren't relevant to target, or aren't of value to get a firm handle on understanding training adaptation and approaches. Also, as I pointed out in one of my previous posts, due to the multitude of definitions of the LT I prefer to simply refer to MLSS because it has a consistent definition (despite what you argue), and will move with the LT and/or the CV. The concepts are all related, and contribute strongly to the physiological aspect of endurance performance.

Depending on the group I am speaking to, if I refer to adaptations that depend on LT, I invariably get caught up in defining the LT. Therefore, it is simpler to refer to the MLSS which has a standard definition, again, despite what you argue.

Steve

Another:

Braz J Med Biol Res. 2004 Oct;37(10):1551-6. Epub 2004 Sep 22. Links

Effect of the aerobic capacity on the validity of the anaerobic threshold for determination of the maximal lactate steady state in cycling.Denadai BS, Figuera TR, Favaro OR, Gonçalves M.

Laboratório da Avaliação da Performance Humana, Instituto de Biociências, Universidade Estadual Paulista, 13506-900 Rio Claro, São Paulo, Brazil.

bdenadai@rc.unesp.br

The maximal lactate steady state (MLSS) is the highest blood lactate concentration that can be identified as maintaining a steady state during a prolonged submaximal constant workload. The objective of the present study was to analyze the influence of the aerobic capacity on the validity of anaerobic threshold (AT) to estimate the exercise intensity at MLSS (MLSS intensity) during cycling. Ten untrained males (UC) and 9 male endurance cyclists (EC) matched for age, weight and height performed one incremental maximal load test to determine AT and two to four 30-min constant submaximal load tests on a mechanically braked cycle ergometer to determine MLSS and MLSS intensity. AT was determined as the intensity corresponding to 3.5 mM blood lactate. MLSS intensity was defined as the highest workload at which blood lactate concentration did not increase by more than 1 mM between minutes 10 and 30 of the constant workload. MLSS intensity (EC = 282.1 +/- 23.8 W; UC = 180.2 +/- 24.5 W) and AT (EC = 274.8 +/- 24.9 W; UC = 187.2 +/- 28.0 W) were significantly higher in trained group. However, there was no significant difference in MLSS between EC (5.0 +/- 1.2 mM) and UC (4.9 +/- 1.7 mM). The MLSS intensity and AT were not different and significantly correlated in both groups (EC: r = 0.77; UC: r = 0.81). We conclude that MLSS and the validity of AT to estimate MLSS intensity during cycling, analyzed in a cross-sectional design (trained x sedentary), do not depend on the aerobic

What the hell are you doing tinman? If you cannot present information in your own language then please don't at all. Steve is presenting the situation very clearly and bridging the gap between theory and practise nicely if verbosely. Please cease tinman you aren't helping.

Are you providing these for me? Of the references you provided, I have already read a substantial proportion. Thanks anyway, but I'm quite comfortable with my knowledge/understanding of the topic.

Steve

Steve. Can one think about the MLSS as task specific? So if you have to run 3000m there an observable level of lactate you need to stabilise at in order to only overload after the finishing point. The earlier you stabilise the better as well. Even the 800m would have some level to stay under until the end. Is this more of a maximal lactate increasing rate.

Typically, I avoid making reference to less prominent journals such as this. That is one issue with many of the published studies that may *appear* to contradict or provide evidence of outliers. That being said, since it's published it's still better than anecdoctal evidence (actually, that's not always the case as published bad data can serve as a red herring,.. but I digress). Further, I also try to avoid talking specifics with only an abstract to look at, but this provides a nice demonstration of why I like to use the MLSS as a term of reference. As I pointed out in one of my earlier posts, the MLSS pace will correspond to 10 km pace for one individual, 15 km pace for another and for an elite 1/2 marathon. So, if I am speaking to a group of runners and use an elite as an example, if we talk about the adaptations (or training intensities) stictly in terms of distance/pace for the elite (e.g. 1/2 marathon pace), those paces are totally irrelevant to the recreational runner (some might say jogger) in the group who takes 48 min to run a 10 km and likely almost 2 hr to run a 1/2. But when speak about adaptations/paces in terms of MLSS pace, then the adaptations are relevant to anyone in the group, regardless of ability level. I know some on this board might poo poo the idea, but there are runners who take their training very seriously, and will take more than 40 min to run a 10 km. We shouldn't entirely neglect them by talking about adaptations, or even training approaches only in terms of elite, or even highly trained paces. This is really the same tack Daniel's takes with his tables. By presenting a range of Vdots, he is addressing the disparity in ability levels and appropriate training paces and talking about paces and adaptations in terms that are relevant to all.

So, instead of having to use 10 km pace as a reference for one runner, and 1/2 marathon pace for another, it's simpler just to refer to MLSS pace. This abstract supports that case, that the MLSS was not different between untrained and trained, so, broadly applicable. In this case, the powers (not paces but power is proportional to pace) were substantially different, as one would expect. If we perform a little exercise to demonstrate the value in this approach, we could use the power values presented and simply convert them to paces in m/min then convert those to paces in min/mi, the trained would perform at MLSS pace = 5:42 min/mi, while the untrained would perform = 8:55 min/mi. Holy cow, that's a huge difference in pace, and again using the paces for the trained based soley on performance for a given distance would be totally useless for training the untrained. Some will say, "who cares about the untrained", but like I said before, there are those who may not be much faster than untrained and still take training seriously.

Again, don't get caught up in the actual *values* of the lactate for MLSS, they are irrelevant. The investigators in the abstract reported them, and showed they were not significantly different, but that may have simply been due to high variability which there certainly is. Regardless, the actual lactate value holds no...well, value to me. That's why I don't use OBLA as a recerence other than for specific purposes, and certainly not in the context of this discussion.

Sorry for being so verbose "similarities", but I think this is a fairly important issue worth resolving to some extent.

Steve