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

Actually, I would rely on two performances as a better predictor of VO2max than HR. That's just me though.

Steve

MY ANSWER:

McArdle's patients have a brain and this could protect them from developing rigor.

>>I'm sure they'll be glad to hear that.

My point is that in the absence of any other influence or control, a muscle without ATP cannot relax and hence goes into rigor. That is a biological law. Thus if the muscle cannot produce ATP sufficiently rapidly it has to end in rigor. The idea that the muscle will simply slow down is part of the peripheral model thinking that has gone unchallenged because of the logic that "we know that is how the system works". But how does a reduced rate of ATP production causes the muscle to reduce its force production? I am not sure that anyone has ever really tried to produce an explanation for that mechanism.

>>Of course this is the case. By my point was that McArdles patients, essentially, don't have glycogen because they don't have access to it, and they do fine, even during exercise, if given the second wind.

>>How does a reduced rate of ATP production cause a muscle to reduce its force production? Well, by reducing 1) the number of cross bridges producing force, and as a result, reducing the total convolution of that force, and 2) by reducing appropriate calcium sequestration due to lack of SERCA drive and 3) causing inappropriate depolarization due to inability of the Na/K pump to re-establish the membrane potential.... As availability of resources is reduced, the "machine" slows down. This is the case in any number of systems, whether they be mechanical or economic, or fantasmical (that's a made up word BTW;). My point is, there does not need to be a "catastrophic" failure to see what physiologists term "failure". A reduced force production could result from any number of factors peripheral, and/or central. You keep using the term "catastrophic" referring to the "peripheral model", but I have never stated a catastrophe necessarily has to occur. I am arguing, there could be several levels of control, (including central BTW), but some of those levels may reside in the periphery. One could argue (as you are) there is protection from the potentially damaging effects of exercise, but that protection resides in the periphery.

MY ANSWER:

Muscle cramps occur with increased electrical activity whereas rigor would be electrically silent (as I confirmed by studying a dead body recently - just joking). So I think that cramps are due to a neuromuscular mechanisms whereas rigor is biochemical.

>>Why, yes, that's why I placed rigor and cramps in quotations, I believe, because one can be mistaken for the other. McArdles patients experience non electrical muscle contracture, which by your definition is "rigor". This is reversible though, and they don't die, and their CG doesn't prevent it from happening. Granted, as you are well aware, it can be a serious, dangerous circumstance. The fact remains though, their "brain" doesn't stop them. The failure observed here is in the periphery and the CG doesn't intercede. I don't want to put all my cards on the McArdle model, but it seemed relevant to your point. As you indicated in one statement, you are referring to "healthy people", and this would not fit that criteria.

MY ANSWER:

Good to have some agreement!!

>>Some wonders may never cease;) My point was, you did write this

" so there must be a regulation, either *within the muscle* or via the nervous system"

MY ANSWER:

100m sprinting pace falls off only quite late in the sprint so I am not sure that fatigue happens within the first few "seconds".

>>Well, running speed can be a bit misleading since it is the function of power output and the mechanics involved in movement. So, there is invariably a lag in what is going on within the muscle vs what is evident in speed. If we look at a system like the cycle ergometer, it's clear fatigue occurs within a couple of seconds, and if we look at insitu muscle preparations it's clear force is reduced almost immediately with maximal contractions that don't "break" the muscle. So, I expect that intramuscular fatigue is occuring almost immediately, and certainly by the halfway point.

Your answer continued:

More to the point though, ATP turnover rate is not really regulated peripherally. The rate of ATP use is set by how many motor units are recruited in the exercising limbs (by the brain). Micromanagement may occur peripherally but the overall rate is set centrally.

>>Sure in a paced effort, but in an electrically stimulated contraction, the muscle still fatigues and there is no central input whatsoever. Further, once the MU is activated, ATP turnover most certainly is regulated within the individual muscle fibers by the interaction of the systems that are generating the ATP and the systems that are using it.

In my view sprinting speed is likely regulated to insure that the eccentric load on the hamstring muscles does not exceed their tensile strength. It seems to me that that is the weak point of the sprinter's body.

>>Maybe.

The point about the Cheetah is simply to take the extreme case of turning on ATP production so rapidly and to show how exquisitely the rate of ATP production and use must be matched. Again I argue that the only way this can really be done is if the extent of muscle recruitment is matched to the muscle's capacity to produce ATP.

>>But the muscle's capacity to produce ATP is intrinsic to each muscle fiber. It's not like it's a collective ATP pool that all the fibers have access to, so, by not recruiting some fibers, you are sparing ATP for something else.

You made reference in a previous post to the EMG data out of Dempsey's lab, and I was really waiting for you to comment on that. I really think that is the strongest argument in favor of your model. If you look at the "Arterial oxygenation paper."" (I think, I don't have it with me), you'll note that in the hypoxic condition, there is no "endspurt", doesn't that deflate your argument?

Thanks again for remaining engaged. I can't help but take advantage of it.

Steve

Hi Steve,Actually, what I meant was that, for my purposes, I don't really need a better predictor of VO2max -- these were examples of bad estimaters, compared to lab testing.BTW, are you familiar with Polar's Fitness Test? It's a passive test in which you lay down for 5 minutes, without actually doing any intensive exercise. It estimates your VO2max and HRmax based on measurements of your HR variability. This could be useful if the athlete is 100+ pounds overweight, and traditional tests might be problematic, or fatal.I'm not a slave to my HR, but was just checking out some of the advanced features of my expensive watch. Anyway, it seemed to independently correlate my VO2max (and HRmax!) estimates from my race performances. It happened to work for me, but I've read it fails for a lot of people too (so I don't place too much stock in that either!).Thanks for your replies,

Steve McGregor wrote:

Actually, I would rely on two performances as a better predictor of VO2max than HR. That's just me though.

Steve

Let me get into a point that is often misunderstood. It has been remarked that Lopes could not change pace during races. That is not true.

On 26 June 1982 Carlos Lopes ran a European Record of 27:24.39 in Oslo, beating Fernando Mamede. During that race, Lopes took the lead at 7 km. He broke away by increasing the pace to 57-58secs for both of the next two laps. He then ran the last 1500m in about 3:52 and the last 1,000m in 2:32. Is that not change of pace?

What Lopes did not have was a good final sprint, but that is because he was essentially a slow-twitch runner (ST) and Mamede was a fast-twitch runner (FT). And this is a topic myself and Hadd hope to develop more fully within our thread, because it is fundamental to knowing how best to train, and what events will best suit each individual.

This difference in the physical properties of both Lopes and Mamede basically pre-determined their different training and race strategies.

Lopes knew by trial and error (like all ST’s – see Radcliffe) that he needed to take the lead at some point in the race and run away from the lead pack if he wanted to win. He knew that if he was with anyone at the bell who had a better kick than he did, he was almost certain to lose. We saw this in global finals with Radcliffe who would lead for something like 24 laps and then get passed by three runners in the final sprint (e.g.: Ribeiro, Tulu, Wami).

Mamede, on the other hand, who knew he was fast over 200-400m, simply needed to bide his time within the pack and then try to out-kick the opposition on the final lap. Both of these race tactics had their roots in the physiological differences between both runners. The title of the Cabral & Hadd thread is “Two types of runners…”, and both these world-record holding Portuguese runners offer ideal examples of both types: Lopes (ST) and Mamede (FT). Hadd and I will get into this more deeply in future posts on that thread.

What happens in a race is that Lopes does not have a huge reserve of anaerobic capacity to call upon at the bell. He does not have a sizeable percentage of FT fibres (unlike Mamede) to recruit and use to fire up a faster final minute in a 5,000m or 10,000m race.

In saying that both runners were physiologically different in muscle fibre type, and that this necessitated different race tactics to best suit their individual strengths, it should now be understood that both of these runners (types) also needed different training approaches to maximize their individual abilities. And these training approaches were different despite the fact they both trained under the same coach.

Moniz Pereira’s coaching methodology was strongly based in the intermittent and interval-training style. Later, I will continue the discussion on what his coaching methodology was based upon.

But what I can note right now are some fundamental differences between the training of Lopes and Mamede:

Lopes ran long outdoor tempo runs several times per week: MaxLaSS runs almost daily. He used interval training like cruise “soft” training.

Mamede was the opposite: very easy runs on a daily basis, but then he regularly performed very strong track workouts and most of them as intervals with short recovery.

Lopes would take a longer recovery for the same interval workouts that Mamede did, and he would not be able to run the intervals as fast as Mamede did. This difference is fundamental to the training of both types. ST’s do not need to (and indeed, cannot) run the reps as fast as FT types, plus they need more recovery.

Allow me to clarify one aspect of the training of Carlos Lopes that I have read recently on this board, as well as often heard mentioned in several threads and in Noakes’ book as well as in studies by Billat and other articles.

Those who say that Carlos Lopes did not run tempo runs are wrong. Very wrong.

First we need to decide which Carlos Lopes we are talking about: The young Carlos Lopes junior runner, or the Carlos Lopes from the European Championships of 1971 or from the 1972 Olympics who was lapped in the heats of both events by Lasse Viren?

Or are we talking about the Carlos Lopes after 1975, when he won his first World Cross Country Championship (76 Chepstow WCCC) and was second in the 1976 Olympics, at the finish line just some feet behind the self-same Lasse Viren who had lapped him four years before?

Because if we are to talk about Lopes after 1975, let me assure you he was running very fast on a daily basis and no-one could live with him on those tempo runs.

One of the main aspects that characterized Lopes’ training during his best seasons up to the 2:07:12 World Marathon Best or his 27:17 10,000m run, or the 1984 LA Olympic Marathon win or leading up to his 3 WCCC wins (and 2 seconds) was that fact that he would run 20-40 mins of tempo runs at a paces ranging from 2:55 to 3:05-3:07 per km, several times each week. We might consider these efforts as MaxLaSS and LT pace.

(Note here that Hadd makes a distinction between both paces, Lactate Turnpoint (LTP) pace and Lactate Threshold (LT). “LT corresponds extremely well (and is useful) with training for marathon performance, while the Lactate Turnpoint correlates better with MaxLaSS (Maximum Lactate Steady State) and thus HM and 10k performances.”)

Also on the runs that Lopes considered “easy days” he would often cover 16-17 km or even 18.5 km for a one hour run.

You can believe me on this, because I am Portuguese and the above information has been related in a number of books, interviews and studies, as well as from the mouth of Lopes’ coach and Lopes himself. I trained and followed Lopes by direct observation on a near daily basis for a period of almost 20 years. I was personally present when he (and Mamede) would do their track workouts. I spoke to many runners who would try and go with him on his tempo runs. No Portuguese runner of that period, including Fernando Mamede (13:09 and 27:17 WR) could live with him when he decided to run his 20-30-40 mins tempo runs. Okay, Mamede could, but he chose not to, because he knew he would not be able to handle his planned training for the day after !

I read that Mr Noakes insists on evidence, that only from evidence shall we have a reliable source. Is scientific evidence somehow different from empirical? But then I also realise that he draws some wrong conclusions from wrong information.

I do not know from where Mr Noakes got his information about the training of Carlos Lopes. I am left doubting the conclusion he draws from what he claims are facts and evidence. I believe he had some source of information, but it must have been the wrong source, and I would urge him to go back and check the information once more. No scientist can draw correct conclusions if the initial data/evidence is flawed.

If required, I can provide copies of several publications stating that Lopes performed what we call hard tempos on a several times a week basis. I still have regular access to Lopes and see him frequently – indeed I saw him last Saturday. So, if you are interested, you can come to Portugal, and I can arrange for you to hear what I say confirmed from the mouth of Carlos Lopes himself or his coach !

Soon I will write something I consider very curious and interesting about how Lopes and Mamede trained differently in the 3-day period between the Oslo 5,000m run on 28 June 1984, and the Stockholm 10,000m WR set on 2 July 1984 (in which Mamede ran 27:13 new WR and Lopes ran 27:17 PB).

Post on Cabral & Hadd thread

2 kinds of runners. Which are you?

http://www.letsrun.com/forum/flat_read.php?thread=2375989&page=2