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

I can appreciate the difficulty in determining causation for anything related to our heads. The necessity of pushing limits, tolerating discomfort and simply believing something can be achieved isn't exactly something new. I'm sure your work can identify the patterns although I'm not convinced it necessary to classify the instigator of these patterns as something like a CG. Unless you can apply very distinct and firmly defined characteristics to the CG then I see little value in the term.

As for limits, there are physiological markers that help identify these, and that's one area where lactate threshold is of value. There is a tight correlation between LT and performance. Coyle showed this correlation isn't dependant on abilities, it applies to runners of all ability levels. As others here already pointed out, a person off the street can't just run a 4 minute mile, they still need to develop themselves physically before any notion of psychology can push them to that goal. You need to be in the ball park before you can take a swing. In the same way, someone who only does 3 mile runs at 12 minutes a mile a few days a week won't be setting marathon records anytime soon. The mind cannot make the body do things it's simply not capable of doing.

depends how your define spirituality i guess Fred. Sure as i age i become softer in my way which is akin to developing the spirit i guess. I'm becoming more cooperative instead of compeititive. Coaching children is an excellent activity to practise this. Proabably having ones own children would be even better for this purpose. Diminish one's own ego for the sake of another.

There is hard-line spirituality such as Zen meditition which can easily become monastic (24/7) but i've tried this way and it is not for me. When i was younger i was a competitive athlete and i was good at the competition side of it all. You said competitive activities are not spirituality and in the ultimate sense this is true. Yet for me competition was a prelude to the spirit. It refined me in many ways so that when i cam across meditation it just fit in. I has focus and concentration and a high degree of physical fitness with which to 'sit' with. As a result i was able to find the mind that is able to 'let go' quite quickly.

So whilst running long distance and finding peace with thyself is a step in the direction of the spirit, i would also argue, for most men anyway, that competition acitivites are part of this spiritual path.

Who is to say that competition and good spirit between competitors cannot go hand in hand. I was a decathlete and we tend to help each other through those 2 days. Maybe decathlon is already heading in the right direction :)

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I am not certain how this distinguishes between the two models. In our 1990 paper we studied a larger sample of runners with a greater range of performances than did Ed Coyle in his 1979 paper with Peter Farrell and came to an almost identical conclusions - the running velocity at the lactate turnpoint explained about 91% of the variance in the 10 and 42km performances of these athletes. But this does not help explain the mechanism since in the marathon, athletes run at quite low blood lactate concentrations so that it is the avoidance of lactate accumulation rather than its accumulation which is associated with superior performance. Whereas perhaps in the 10km the accumulation of lactate is much greater.

I would have thought that your other points are obvious. Certainly I have never suggested that they are otherwise. Perhaps the question is: Why can you not will yourself to run as fast as you might want? In my view because the system is regulated by the brain to insure that you can never damage yourself. But what sets the "limits" in this system?

My point is that the evidence suggests that you can will yourself to run just a little faster than you might believe possible; that the best athletes do this regularly (and so they adapt their belief system to a new reality) and that the best coaches make us run faster in part because they know how to make us all believe that we are slightly better than we originally believed. A peripherally regulated system does not allow this to happen since fatigue is always absolute and cannot be overridden.

Of course this is the other side of the argument that the CG is ultimately there to see that you do not damage yourself and is therefore also the ultimate regulator of what you can achieve. Even the mentally strongest athletes like Peter Snell and Herb Elliott did not run so fast that they died.

Tim,

I was wondering if we would ever get here. We've been dancing around this point for a couple weeks now. From the collective work of Coyle including his work in Dave Costil's lab until his work with Project 96 in cyclists, he has repeatedly shown that the physiological factors that determine endurance performance are those constellation of factors that contribute to LT (however you want to determine it). In particular, Type I fiber composition, mitochondrial content, and ATPase efficiency. Of course, you are well aware of these factors, but for some reason feel one can will themselves to overcome them. I'm not sure how that is, efficiency is a rate of fuel utilization issue, and therefore something not under central control.

Your point:

"But this does not help explain the mechanism since in the marathon, athletes run at quite low blood lactate concentrations so that it is the avoidance of lactate accumulation rather than its accumulation which is associated with superior performance. Whereas perhaps in the 10km the accumulation of lactate is much greater"

Is easily explained by the availability of glycogen, and the rate limitations of ATP provision in the absence of glycogen. Are you saying the individual can run at 80% of VO2max in the glycogen depleted state? Of course not, that's why running at a pace that spares glycogen for the distance of the race is important. This is not necessarily the reason for the pacing/fatigue relationship at shorter distances (e.g. 5 km) but for 42 km, it is. Run out of glycogen and certainly a strong willed person can continue, but fast? No. This is the thermodynamics of performance and we all must obey the laws of physics, correct?

Why is it that for all out efforts, our maximal speed declines with time, in inverse proportion to lactate? It's not that lactate is the poisonous metabolite you refernced previously, but that glycogen metabolism is directly related to lactate appearance, and glycogen metabolism is refractory with time. The instance you start using glycogen the rate of glycgen utilization slows down.

Is this a protective mechanism? Maybe. Is it centrally controlled, almost certainly not.

So, isn't it possible that if one exhibits an "endspurt" in the marathon, for example, it's likely the individual chose a pacing strategy that left enough glycgen in the tank to suppor the spurt. This would depend on the length of the spurt though. For shorter spurts, it may be that they simply didn't recruit all of their fast fibers (an argument you have made), but these last recruited fibers do not have the capacity to support extended efforts becasuet they are not oxidative enough. Therefore, they can support that last effort on some glycogen and ATP-PC. So, an experienced runner might choose a conservative strategy that would leave them with enough energy to give it full gas in the last little bit. OTOH, what about the runner who is trying to hang with the leaders, and cracks at 5 k to go mark, and has nothing left. Are you saying if they were simply of stronger will they could overcome the rate limitation of metabolism and stay with the leaders? Would this individual still exhibit an endspurt?

Steve

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Thanks Steve for this response and for the one you have just sent. I will get to the next one tomorrow but don't have time now to do it justice (it is evening here in Darkest Africa). There is some overlap so all I will say here is:

When students are exposed to all the facts, mass hysteria sometimes results. The key is that we show them the information about muscle recruitment during exercise. Then the picture becomes much clearer. If they receive only the metabolic data, then of course the Hill model looks fantastic. But when you add the recruitment information, then the picture changes.

What is interesting is that when people started measuring EMG during dynamic exercise, the EMG experts said that the information could not be interpreted since EMG only measured the extent of recruitment during isometric contractions. So initially it was very difficult to have the recruitment side of the argument heard. Fortunately Prof Jerry Dempsey from Wisconsin who might originally have been considered a supporter of the traditional (Hill) model started to evaluate the alternate model and had his senior students including Markus Amann do some really exciting studies in which they used EMG activity as a measure of muscle recruitment. This has rather silenced the argument - as a result it now seems that we can use EMG data to argue the extent of muscle activation during dynamic exercise. Once this is accepted, then it becomes possible to present the CG model more effectively. But unless the data on recruitment are considered, it is impossible effectively to argue the CG model and to expose the weaknesses of the traditional model.

But more on this tomorrow.

Thanks again for always asking the right questions in the appropriate manner.

Best wishes,

Tim Noakes.

Is running out of glycogen dangerous? How about when compared to the accumulation of the negative aspects of the lactate system?

We can't even get close to really hurting ourselves. Well i can't. If i run to exhaustion over about 400m i'm really quite safe even though i am exhuasted. The same when i am really low on glycogen except i'm just really tired. I think i would fall asleep well before i was in mortal danger.

Over protective central governor or prevented by peripheral factors. We eat when our blood sugar is low and we can't concentrate properly. Is hunger the mechanism the central governor stimulates?

Again we fall back on what it is the CG is protecting you against. Two runners of very different levels of conditioning, maybe they both can 'will' themselves to run faster than they thought they could, but still it's within a limitation. Whatever that 'danger' point is, it won't be the same for these runners as it's dependant on their individual conditioning. Our primary concern is training our bodies to be capable of running fast, so we can achieve higher levels of performance before the theoricial CG kicks in to pressure us back.

Tim,

Thank you for the reply. I correspond often with athletes and coaches in SA, and so, am quite familiar (moreso than I'd like actually) with the time difference issue.

I look forward to your further comments.

In fact, you're probably up and around as I wander off to bed.

Steve

sim wrote:

Is running out of glycogen dangerous? How about when compared to the accumulation of the negative aspects of the lactate system?

We can't even get close to really hurting ourselves. Well i can't. If i run to exhaustion over about 400m i'm really quite safe even though i am exhuasted. The same when i am really low on glycogen except i'm just really tired. I think i would fall asleep well before i was in mortal danger.

Over protective central governor or prevented by peripheral factors. We eat when our blood sugar is low and we can't concentrate properly. Is hunger the mechanism the central governor stimulates?

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Sim,

As you know hypoglycemia (second to liver glycogen depletion) exaggerates the symptoms of fatigue and causes the sudden reduction in exercise performance known as the bonk. Since this can be completely reversed within about 7-10 minutes with ingestion of 50 or more grams of carbohydrate, it is very likely a centrally regulated phenomenon. I wrote about my personal experiences with hypoglycemia in Lore of Running and why I interpret these effects as evidence for central regulation. The bonk was much more common in the 70's and 80's before athletes began to eat and drink more carbohydrates during marathon and longer races.

Muscle glycogen depletion reduces the capacity to produce ATP and must therefore cause the muscle to run out ATP if there is no nervous control. ATP depletion causes the muscle to go into rigor (irreversible contraction). Since rigor has yet to be described in healthy people during exercise and since muscle ATP concentration remain within the normal range even when the muscle has (almost completely) depleted its glycogen stores, so there must be a regulation, either within the muscle or via the nervous system, to insure that ATP concentrations do not fall too low. This control has to link the extent of muscle recruitment to the muscles' continuing capacity to generate enough ATP from glycogen as the glycogen stores fall. This is analogous to the problem faced by the cheetah as she speeds up to 100 km per hour within seconds of starting her chase. Unless her pace is regulated through a link between the extent to which she is able to recruit her muscles and her capacity to generate ATP within those muscles, she will stop running with her muscles in rigor. Since this does not happen one must assume that such a control exists.

Timothy Noakes wrote:

Of course this is the other side of the argument that the CG is ultimately there to see that you do not damage yourself and is therefore also the ultimate regulator of what you can achieve. Even the mentally strongest athletes like Peter Snell and Herb Elliott did not run so fast that they died.

Ron Clarke has claimed (or his doctor, I am not sure) that his collapse after the 10km final at the Olympics in Mexico resulted in permanent damage to his heart.

Tim would you care to comment on that? I believe that was debated heavily in the past. And BTW thank you again for your contribution to this thread. It's been a privilege for me to be able to read your thoughts/arguments and interact with you.

Tim, forgive me, but I must interject on this point:

Your statement:

"Muscle glycogen depletion reduces the capacity to produce ATP and must therefore cause the muscle to run out ATP if there is no nervous control."

Does not necessarily lead to your next statement:

" ATP depletion causes the muscle to go into rigor (irreversible contraction)."

As I stated in my response, glycogen depletion certainly reduces the capacity to produce ATP at a high rate, but glygocen depletion does no necessarily result in "rigor". McArdle's patients do just fine at activities of daily living, and actually, the "second wind" phenomenon appears to alleviate the rigor or contracture if you will, to a very large extent. So, as I pointed out, glycgoen depletion simply means that rate of ATP provision is limited.

Further, this statement:

"Since rigor has yet to be described in healthy people during exercise and since muscle ATP concentration remain within the normal range even when the muscle has (almost completely) depleted its glycogen stores, so there must be a regulation, either within the muscle or via the nervous system, to insure that ATP concentrations do not fall too low."

May or may not be true. Again, if by "rigor" you mean contracture or "cramps", then they are observed in healthy people all the time, and typically attributed to electrolyte imbalance. It is quite likely that a certain proportion of "cramps" that are observed in exercising individuals may be attributed to insufficient ATP provision for release of the cross bridges. Of course, there is no evidence of this, but there is also no evidence against it, so, in the context of this discussion, it seems to be appropriate to include.

I will agree with this part though:

" so there must be a regulation, either within the muscle or via the nervous system, to insure that ATP concentrations do not fall too low."

Finally, the Cheetah argument again appears to be a red herring. Why not use a human example? In fact, didn't you use the Cheetah as an example of thermoregulation and the "CG"? If we put the argument in the context of physiology we are all more familiar with, the 100 m sprinter "fatigues" within a few seconds, if not immediately. Some may go into rigor, some may not, but they don't become glycogen depleted, so, why not? If the pacing strategy is intended for them to complete the bout with energy reserves, why dont' they just run twice as fast and run out of glycogen? Of course, in part it's because ATP utilization is limited by myosin ATPase, and SERCA. It's also because ATP provision is rate limited and as PC stores become depleted, ATP is provided in a much slower fashion. These factors are regulated peripherally, not centrally.

Sorry to barge in, but I felt compelled;)

Steve

GeorgeY wrote:

Timothy Noakes wrote:

Of course this is the other side of the argument that the CG is ultimately there to see that you do not damage yourself and is therefore also the ultimate regulator of what you can achieve. Even the mentally strongest athletes like Peter Snell and Herb Elliott did not run so fast that they died.

Ron Clarke has claimed (or his doctor, I am not sure) that his collapse after the 10km final at the Olympics in Mexico resulted in permanent damage to his heart.

Tim would you care to comment on that? I believe that was debated heavily in the past. And BTW thank you again for your contribution to this thread. It's been a privilege for me to be able to read your thoughts/arguments and interact with you.

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Dear George,

Thanks for your kind comments which are much appreciated.

Clarke was clearly unconscious for some time after the 10 000m in Mexico City and this is not normal. The unconsciousness in his case (since one does not have to consider other possibilities) means an inadequate blood supply to the brain usually due to a low blood pressure. Usually lying down corrects this but he was unconscious when lying down and when given oxygen. The low blood pressure results either from an inability of his heart to pump enough blood (either due to damage to the heart muscle or heart valves or to an abnormal heart rhythm) or due to a failure to constrict the blood vessels that have been dilated during exercise, or perhaps to a combination.

If Clarke had irreversibly damaged his heart muscle as a result of that race, then he would have known about it immediately. It would not have taken 40 years to disclose itself.

I would guess that he had an abnormal heart rhythm that slowly reverted to normal. The abnormal heart rhythm could have been caused either by a direct effect of hypoxia on the heart itself or perhaps in the brain.

Interestingly we know that if you develop an abnormal heart rhythm during exercise, you instantly become too weak to exercise. Clarke took more than 80 seconds to run the last lap of that race so that his rhythm disturbance might have started during the race.

Clarke really adapted himself well for running at altitude - he lived and trained at quite a high altitude in France for some months before the Games. Being so well adapted allowed him to push himself closer to his limits, perhaps.

Many years later Clarke had surgery to replace a leaking heart valve. It is difficult to think that a single run at altitude could have caused either that or other irreversible heart damage. I would argue that he suffered an abnormal heart rhythm (mechanism unknown) but probably related to the profound stress of running so fast for so long at altitude in someone accustomed to running at sea level. The leaking heart valve would then be caused by unrelated factors including some sort of genetic predisposition, perhaps exacerbated by all the running he did in his life (this is speculative of course).

I am currently following up some cases in which very serious, potentially fatal abnormal heart rhythms developed in runners the instant they stopped running in competitive events. All had normal hearts when tested subsequently (or in one case at autopsy). Thus there is something other than structural heart disease that can cause apparently normal hearts very suddenly to develop very serious abnormal heart rhythms during or after exercise. Perhaps Clarke had a non-fatal variant of this (unknown) condition.

This does not answer your question but it does offer a range of possibilites.

Sincerely,

Tim Noakes.

I'm also confused about this statement by Dr. Noakes:

"Muscle glycogen depletion reduces the capacity to produce ATP and must therefore cause the muscle to run out ATP if there is no nervous control."

The body will replenish stores on the fly. It's not like the body is at a set level and can only run down to zero. Ironman triathletes and ultrarunners will eat actually during exercise. We're rarely in such a 'dry' state that there's no active recovery happening. The body will even autolize tissue if it has to.

Running out of ATP is theoretically possible but I think it would be extremely difficult for this to actually take place.

All good Steve

i have this query regarding the myosin ATPase. Does it act as a limiter so only a certain amount of ATP can be synthesized at any one moment?

If there is a limiter possibly it is to limit the energy release so that it is in sync with other systems such as the muscular system or the motor control system even.

There is that book 'Zen and the art of motorcycle maintenance' and i started reading it to see if i could save money and service my own car. The book basically describes the motorbike as a set of independent systems that need to become dependent on one another so as its function can be fulfilled ie drive.

In running it is the body's function to run and the systems all interact and are dependent upon one another in order to facilitate this.

In a bike if one system is functioning sub maximally then the overall performance is limited even if the other systems could increase that performance.

In a body i would assume the same and so far this supports peripheral control.

Yet, in modern bikes there are computers which have some regulatory function on the bike such as fuel injectors. Further forward in time came ABS. There are lots of examples where a central computer has slowly been taking the control function for a specific role from the the peripheral factors. I get annoyed when this happens to me because of the government :) or the athletics 'government'.

Eventually we can see (and there are prototypes) that bikes (cars) can be run almost automatically. Does this mean total central control?

Almost. but just because the central governor is able to limit things and control things does not mean it isn't bound to what is happening in the periphery. If muscle glycogen falls to certain levels then the CG must step in or else we won't even be able to walk home afterwards unless someone comes along and squeezes a gel into the side of our mouth. I'm not sure about this rigor because you have contended it Steve so i ask this question. Is the cause of rigormortis in a dead person total depletion of glycogen. Is it timed with totally running out? Is it the causative factor?

sim

In speculating about heart damage following the Mexico City race, Clarke says that he never again was able to run as well as he'd done before. His performances after Mexico City support that statement. Do you think there is any connection between his difficulties in Mexico City and his subsequent loss of form?

Dear Steve,

Here are my comments:

YOU WROTE: "We've been dancing around this point for a couple weeks now. From the collective work of Coyle including his work in Dave Costil's lab until his work with Project 96 in cyclists, he has repeatedly shown that the physiological factors that determine endurance performance are those constellation of factors that contribute to LT (however you want to determine it). In particular, Type I fiber composition, mitochondrial content, and ATPase efficiency. Of course, you are well aware of these factors, but for some reason feel one can will themselves to overcome them. I'm not sure how that is, efficiency is a rate of fuel utilization issue, and therefore something not under central control."

MY ANSWER:

I have only one problem with this conclusion. It is entirely model dependent. If you believe that oxygen and lactate determine performance then you will believe that this work PROVES that these variables DETERMINE performance.

But the only way to PROVE this statement is to change only those variables and none other and then to see if performance changes. But it is not possible to do this in a training study since whenever you train you change your self-belief; you alter your neuromuscular function etc, etc. So it is not possible to change only the metabolic and muscular variables without changing at the same time the other variables which the CG model predicts are important for changing exercise performance.

Thus what you conclude and what you believe will always be model dependent. That is why I said earlier that the only way really to differentiate between the two models is to use an pharmacological intervention that changes only the metabolic variables. Then you have to show that the effect occurs WITHOUT ANY CHANGE IN NEUROMUSCULAR FUNCTION. Because if the neuromuscular function changes then I would argue that the peripheral adaptation is acting by altering feedforward from the brain (not simply by making the muscles work better).

YOUR NEXT WROTE:

Your point:

"But this does not help explain the mechanism since in the marathon, athletes run at quite low blood lactate concentrations so that it is the avoidance of lactate accumulation rather than its accumulation which is associated with superior performance. Whereas perhaps in the 10km the accumulation of lactate is much greater"

Is easily explained by the availability of glycogen, and the rate limitations of ATP provision in the absence of glycogen. Are you saying the individual can run at 80% of VO2max in the glycogen depleted state? Of course not, that's why running at a pace that spares glycogen for the distance of the race is important. This is not necessarily the reason for the pacing/fatigue relationship at shorter distances (e.g. 5 km) but for 42 km, it is. Run out of glycogen and certainly a strong willed person can continue, but fast? No. This is the thermodynamics of performance and we all must obey the laws of physics, correct?

MY ANSWER:

Mark Allen ran a ~ 2:39 marathon during the Ironman after 180 km and 4 and a half hours on the bike which would have depleted his muscle glycogen content. We made some calculations that this would have been possible if he was burning about 1.3g of fat every minute on the run - this is about 30% higher than rates we measured in the laboratory. Improbable yes, but not impossible. It seems that some unique humans can run remarkably well on little glycogen. But this is not really your point.

Perhaps your point is that these variables could predict performance because the higher the running speed at the lactate turnpoint, the faster you can run whilst burning less glycogen thus you can go further, faster. This sounds entirely logical but it is also a very convenient explanation (as you would argue are my explanations for the CG model).

But I am not sure how this disagrees with the CG model which appears to anticipate what is possible in terms of glycogen availability and so to chose the appropriate pace early on in exercise (if allowed to).

YOU WROTE:

Why is it that for all out efforts, our maximal speed declines with time, in inverse proportion to lactate? It's not that lactate is the poisonous metabolite you refernced previously, but that glycogen metabolism is directly related to lactate appearance, and glycogen metabolism is refractory with time. The instance you start using glycogen the rate of glycgen utilization slows down.

Is this a protective mechanism? Maybe. Is it centrally controlled, almost certainly not.

MY ANSWER:

I don't know of any event in which humans voluntarily choose this form of exercise. So I am not sure that humans would have evolved the proper control mechanisms for this type of exercise. Even then there is pretty good evidence that performance in the Wingate test is centrally regulated - cadence comes down and glycolytic ATP is increased in hypoxic exercise showing that in normoxia, more work could have been done if needed if it had been possible to activate more glycolytic ATP production. But the brain chooses not to. This is more fully argued in our BJSM paper entitled Logical limitations etc.

YOU WROTE:

So, isn't it possible that if one exhibits an "endspurt" in the marathon, for example, it's likely the individual chose a pacing strategy that left enough glycgen in the tank to suppor the spurt. This would depend on the length of the spurt though. For shorter spurts, it may be that they simply didn't recruit all of their fast fibers (an argument you have made), but these last recruited fibers do not have the capacity to support extended efforts becasuet they are not oxidative enough. Therefore, they can support that last effort on some glycogen and ATP-PC. So, an experienced runner might choose a conservative strategy that would leave them with enough energy to give it full gas in the last little bit.

MY ANSWER:

Of course this is entirely possible that this is voluntarily chosen and we cannot yet design an experiment to disprove that theory (as far as I can think at the moment). But in a general sense, consciously or subconsciously chosen, the brain is in control. My point is that we have shown that there are some controls which clearly work subconsciously (oxygen and heat) and that these come into play long before the catastrophe develops.

In your model as I see it the athlete somehow consciously knows how to avoid the catastrophe or to delay the catastrophe so that it happens only the instance he crosses the finish line. But how would he consciously know this other than through (subconscious) feedback to his brain (about the changes in the variables that are about to cause the catastrophe - the "catastrophe molecules") which he follows and then thinks he did it consciously?

There is a saying - if you cannot measure it you cannot control it. Without measuring the "catastrophe molecules", the runner cannot regulate his performance to leave enough energy for the endspurt and still to avoid the catastrophe. Which brings us back to the CG model.

Incidentally I would not be surprised if humans subconsciously monitor a much wider range of sensory inputs than we currently conceive. We clearly have a very good clock that can measure the time that has passed during exercise. We were able to show that this clock could predict between exercise lasting 30 or 33 seconds. Also I guess that humans monitor either distance or speed since the really good athletes know exactly how fast they are running repetitions without being told the time. Since ants have the ability to measure distance by counting their steps (subconsciously - note), there is no reason why humans cannot do the same (if it has survival value).

YOU WROTE:

OTOH, what about the runner who is trying to hang with the leaders, and cracks at 5 k to go mark, and has nothing left. Are you saying if they were simply of stronger will they could overcome the rate limitation of metabolism and stay with the leaders? Would this individual still exhibit an endspurt?

MY ANSWER:

No. At this point his RPE is 19 or 20 and he cannot speed up. His RPE was telling him to slow down all along but he chose to override it. But once the RPE reaches 19 or 20, that is it. No endspurt.

A great example would be Paula Radcliffe in the Athens Olympic marathon. Our interpretation is that she overheated because she was trying to win the race and so ran faster than her heat losing mechanisms could accommodate. Her brain was shouting in her ears to slow down (she said she felt uncomfortable the whole way) but she willed herself to run with the lighter Japanese runner who was not as affected by the heat as she was 12 kg lighter (and thus producing much less heat when running at the same speed).

But when her RPE reached 19 and her core temperature 41.5 degrees C, the CG said - so far and no further or you will die from heatstroke.

Again - all arguments are model dependent. The goal of science is to keep researching the models to see which one can survive.

Warm regards,

Tim Noakes

HRE,

i saw Ron Clarke a couple of years ago at his Track and Field center on the Gold Coast. He is a driven man, head down, pushing onward. He also has a reasonable limp. He is wealthy though and now Mayor of the Gold Coast as well.

I personally had an athletic misadventure. In Atlanta 96 i fouled 3 times in the long jump. Looking back this was the beginning of my sensitivity and the end of my true competitivenss.

sim

I have a theory too wrote:

I'm also confused about this statement by Dr. Noakes:

"Muscle glycogen depletion reduces the capacity to produce ATP and must therefore cause the muscle to run out ATP if there is no nervous control."

The body will replenish stores on the fly. It's not like the body is at a set level and can only run down to zero. Ironman triathletes and ultrarunners will eat actually during exercise. We're rarely in such a 'dry' state that there's no active recovery happening. The body will even autolize tissue if it has to.

Running out of ATP is theoretically possible but I think it would be extremely difficult for this to actually take place.

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Theoretically this is correct. The muscles do re-synthesize glycogen during exercise, probably in the muscle fibers that are inactive. But the effect is tiny and the main effect on glycogen metabolism during prolonged exercise is net breakdown especially in the Ironman. The carbohydrate that you eat are burned directly by the muscles as fuel or perhaps stored in the liver. But you cannot eat enough carbohydrate during exercise (at competitive pace) to match what you are burning. So there is a net loss of glycogen and quite low levels are always present at the end of race in competitive athletes.

But they are never zero. Again something stops you short of completely depleting your stores.

HRE wrote:

In speculating about heart damage following the Mexico City race, Clarke says that he never again was able to run as well as he'd done before. His performances after Mexico City support that statement. Do you think there is any connection between his difficulties in Mexico City and his subsequent loss of form?

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Dick Beardsley said the same after his race with Salazar at Boston. I think he said that something had gone out of him and he could never push himself as hard again.

If Clarke believed that he had almost died at Mexico City then surely that would have had a (brain) effect that would have made it difficult for him ever to push himself to the same level again.

But if he had suffered heart damage, I would have expected a LARGE change in his performance - say from 28 minutes for the 10 000m to 40-45 minutes. If his performances fell a little say from 28 to 29 minutes, I would not think that that could be due to serious heart damage.

But this is a guess based on changes in performance that I have seen in athletes who develop heart conditions. Going from being the worlds-best to top 10 in the world would not be due to serious heart damage (for example)