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

Perhaps you could enlighten me?

Spaniel chooses to ignore or dismiss George Brooks 40 years of research all too readily.

Your knowledge of physiology is laughable. You must be joking right?

Richard_ wrote:

Every muscle in your body is composed of individual muscle fibers of various types (slow twitch, fast twitch A, fast twitch B are the usual classifications). Each muscle fiber has individual contractile properties - how much force it produces when it contracts, how fast it contracts, and how long it can contract before it fatigues.

Because of the way muscle fibers are recruited during exercise and because of the individual contractile properties each fiber possesses, any normal training run such as a tempo run only trains a subset of the muscle fibers. In the case of the tempo run, it generally trains the Fast Twitch A fibers. The Slow Twitch and Fast Twitch B are undertrained or untrained during a tempo run.

Richard_ that makes sense, but it also suggests that either several different types of tempo run are necessary, from long runs just below marathon pace, to short tempo runs such as 5-7k @ 10k pace, or alternatively, progression runs starting at a medium pace and gradually building?

I believe that the logical application of the muscle factor model is multi-paced training.

I think 6 distinct training paces/workouts are minimally required to train as many of the fibers as is reasonably possible.

1. Marathon and slow pace, long duration (15 or more miles)

2. 1/2 marathon pace, 10 - 13 miles

3. 10k pace workout, 5 - 7 miles

4. 5k pace workout, 2 - 4 miles

5. 2-3k pace workout, intervals of 2-3k

6. Sprint workout, 1200m and less sprints/intervals

Structuring the training program so that all the workouts are include on a regular basis and in such as way so that the athlete is optimally trained is where a good coach is so important.

It is ridiculous to say that spaniel is out of date or off target about phyiology when his primary opponent is basing so counter-evidence based on a THEORY. Yeah, a THEORY!

Granted, George Brooks is a brilliant man, but his intra-cellular lactate shuttle model is still theoretical; currently nowhere near being solid. Other researchers such as Sahlin & Fernstrom (et al) in one camp and Yoshida & Holloway in another have replicated Brooks (et al) studies and found little to no evidence that intra-cellular lactate shuttling exists. At the most, they say it is less than 1% of total ATP turnover.

The point is, just because spaniel is not in agreement with the terms another person uses doesn't mean spaniel is an idiot.

Have a good day!

citations:

http://jp.physoc.org/cgi/content/abstract/2002.016683v1

(evidence against lactate shuttle within mitochondria) (Yoshida & Holloway)

http://jp.physoc.org/cgi/content/abstract/582/3/1317

(yr 2007) (no evidence of lactate shuttle to mitochondria)( by Yoshida, Y and Holloway, G.P.)

Richard_ wrote:

3. 10k pace workout, 5 - 7 miles

4. 5k pace workout, 2 - 4 miles

wellnow wrote:

Your knowledge of physiology is laughable. You must be joking right?

Having observed you amateurish attempts to muddle through the concepts (there's that tricky word again!) here, I'm not particularly concerned with your low opinion.

Richard,

Couldn't you make an argument that the logical application of the muscle factor model is race-pace training at race distance? That way you would be recruiting and fatiguing fibers in the exact durations and proportions that you do in your event. Actually, looking at your list that almost seems to be what you're recommending.

Maybe I should have asked: How would you assign percentages to these training zones to target, say, a 5k?

non sequiter wrote:

Richard,

Couldn't you make an argument that the logical application of the muscle factor model is race-pace training at race distance? That way you would be recruiting and fatiguing fibers in the exact durations and proportions that you do in your event. Actually, looking at your list that almost seems to be what you're recommending.

Agreed. Logically one would need to practice race pace to train the strongest active fibers that are specific to race pace.

However, you also have to train at a wide variety of slower paces in order to overload those weaker fibers that are active at race pace but are sub-optimally trained at race pace due to a too-short training duration.

And you would need to train those stronger fibers not recruited at race pace so that they adapt and are trained for during-race surges and end-of-race sprints.

Classic Richard. He's backed into a corner, so now fatigue doesn't matter, he just closes his eyes and pretends nothing except muscle fibers exist. After all, blood vessels, cardiac output, myoglobin transfer rate, etc etc can't attack his pet model if he just pretends they don't exist!

Let me tell you something about a good model in science, Richard. It includes as many of the important variables as possible while at the same time standardizing those that are less important and thereby making the model easier to manipulate/predict than whatever the model is serving as a surrogate for (in this case, the human body).

Your silly little model, in which you simply ignore the things you are too stupid to integrate into the model, is akin to trying to predict the performance of a car by testing only the pistons.

Your problem, wellnow, is that you latch onto a single study and start pretending it is fact. The fact is, myself and now Tinman have provided you with references that contradict your position. If you were actually a scientist with knowledge in the area, you'd know that there is much more current evidence supporting my position than yours.

Isn't wellnow Jon Orange? Jon has no background at all in the sciences you know.

Spaniel i see no point in continuing. Those two guys won't listen to what you are saying to them so there is no possibility of you changing their mind and therefore no possibility of them seeing sense.

I propose a new thread which they don't participate in.

Dear Letsrunners,

Below is a email from Dr Noakes.

I have had some contact with him with regard to several bits & bobs over the past few years. He has a paper coming out, which I am not allowed to share with the public dealing with the CG, I promised Noakes.

I have asked him to comment twice or three times in the last few weeks while this debate has raged. Below is some of his response.

Enjoy

___________________________________________________________

Dear XXXXX,

Thanks for this. I will respond more fully in due course after our paper is published. In the meantime you might want to add this piece:

I have read with interest all the debate that has been going on in this blog. May I be allowed to make a few points:

First, the legacy of Hill's model is that it produced a reductionist model of what determines exercise performance - ie there is a single factor that determines or limits exercise performance. In this case that it is lactic acid alone that causes fatigue. The existence of this thread nearly 90 years later attests to the continuing strength of his influence.

The real question that requires to be answered is this: What is the evidence that exercise performance can ever be reduced to a single factor, lactic acid or something else for example calcium leakage as recently proposed?

Second, the key prediction of the central governor (CG) theory is that exercise is a behavior regulated in the brain, not to produce a maximal exercise performance regardless of cost, but to insure that exercise terminates BEFORE there is irreversible fatigue or organ damage. In contrast the Hill model predicts that exercise ends only AFTER there has been a failure of organ function causing fatigue or the termination of exercise. (Note that such a strategy would have had little survival value if as now seems clear, humans developed as hunters able to run down prey on the hot African savannah. Without a central regulator that set the pace we would simply have sprinted after our prey which would have had no difficulty outsprinting us. As a biologist you have to consider the evolutionary value of what you study).

Indeed one of the assumptions of the blog is that when exercise terminates, marked muscle fatigue is already present. If so, why is it that elite athletes competing at the distances of interest to the readers of this blog (3000m to 21km and sometimes up to 42km) speed up and run the last section of the race faster than any previous section? How can they run the fastest when they are the most tired? This is compatible with a model in which the brain anticipates what the body can do (or the brain will allow) BEFORE the race starts and chooses the optimum pacing strategy that allows the athlete to complete the event BEFORE catastrophic fatigue develops. Certainly the presence of the endspurt cannot be explained by a model in which fatigue is determined only by the development of a chemically-induced peripheral muscle fatigue. Indeed when you come to the final analysis, the best athlete is always the one with the fastest endspurt. So if you want to understand what makes great athletes, a good start would be to understand the physiology of the endspurt. I suspect that this involves more than the VO2max and the maximum lactate steady state.

The single most important finding on which the CG theory rests is the finding that exercise always terminates whilst there is still muscle reserve - in other words exercise terminates before all the available muscle fibers in the active limbs have been activated. This has to be reasonably obvious. The difference between the speed at which we sprint and at which we can run a marathon is determined by the number of muscle fibers we recruit in our active limbs, not by the amount of oxygen or ATP we can use. These are secondary effects, determined by the number of muscle fibers that are active. Importantly recruitment comes before metabolism and oxygen delivery - muscles that are not activated do not metabolize and utilize oxygen (above resting values) or produce lactic acid (above resting values) or other purportedly harmful chemicals until the fibers become active after they have been recruited by the brain.

Thus if you finish a race at a pace less than your peak sprinting speed, then that is because you were unable to activate all the available muscle fibers in your active limbs. (Why this is so is the mystery that the CG theory seeks to answer).

The main effect of Hill's theory was that it caused generations of exercise physiologists to forget this simple fact - without muscle recruitment there cannot be any movement. And if exercise terminates when a large (~ 60% in a marathon) proportion of the muscle fibers in the active limbs are inactive, then the only reasonable conclusion is that the brain is regulating the exercise performance (by insuring that only a certain number of muscle fibers are allowed to be activated under different conditions).

Finally it is often said that there is no strong scientific support for the CG theory. One of our studies that can be explained only by the CG model (which predicts that the brain can modify the exercise behavior IN ANTICIPATION and before catastrophic fatigue develops) and not by Hill's model has been published in one of more influential scientific publications and can be downloaded from this address: Enjoy it:

http://jp.physoc.org/cgi/reprint/574/3/905

Timothy Noakes

I just don't know about all of that!

Is nobody willing to touch this? Clearly there are errors of thinking.

sim wrote:

Is nobody willing to touch this? Clearly there are errors of thinking.

It's just Richard posting under new names. Is there a reason to bother responding to him?

sim wrote:

Is nobody willing to touch this? Clearly there are errors of thinking.

Perhaps you should touch it. What errors do you think Prof Noakes has made?