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

Please do not mis-understand me. I have the very highest regard for Arthur Lydiard as fully expressed in Lore of Running. My point was that we do not necessarily know that, if coaching today, he would be able to produce athletes who could compete with the Kenyans and Ethiopians. Elite performances in the sport have clearly move on and it would be helpful to know if the most successful (Kenyan and Ethiopian) coaches of today use exclusively Lydiard techniques or if they have discovered additional refinements that Lydiard did not use. It seems to me that the ability to speed up in the middle of races (ie before the endspurt) seems to have become a more popular racing technique than it might have been in Lydiard's day. But this might be an incorrect impression.

Realted post and ensuing series on this topic:

http://scienceofsport.blogspot.com/2008/04/fatigue-series-introduction.html

Point 1: With respect, I am not sure which papers of our work you have read and which you have not read. It would be very helpful for you to quote exactly which of these papers provides no evidence to support our theory. Recall that all these published papers have had to go through a process in which they are reviewed by other scientists who do not necessarily agree with our ideas. If there was any reason not to publish those papers - if there was the slightest doubt that they did not support the theory that we claim they support - I can assure you that they would not have had the slightest chance of being published. (This is because there is a strong publishing bias towards studies which support the conventional dogma). So if you are correct, then it is clear that the review process has failed in these cases. I am sure that the editors of the journals that published those articles that you feel do not support what we claim they support, would welcome your reasons for believing that. In fact you are welcome to write letters to those editors which they would then publish.

And we would have the opportunity to answer your criticisms. That is the correct scientific approach. It is really not appropriate to make grandiose statements on this blog without providing the supporting evidence for your view. Facts are always better evidence than opinions (which as I have stated before are determined principally by what you already believe).

With respect, the theory is not negated because no one has yet located a specific brain site for the Central Governor. In fact we are actively looking with various colleagues around the world who have access to the sophisticated equipment that we lack. It is quite interest that these scientists should think it worthwhile to put their money behind these costly experiments. Clearly these brain specialists have more faith in the theory than do you.

Perhaps you are also unaware that the relevant brain scanning techniques cannot be used during whole body exercise, the type of exercise in which we speculate that the central governor is most active. So it is rather difficult to look for a brain region that is meant to be active only during exercise when the current techniques do not allow us to perform those experiments.

But then perhaps you have some advice on how we can proceed and so get round this rather large obstacle.

The strongest (but not the only) evidence supporting the central governor theory is that when they are allowed to pace themselves during exercise in different experimental conditions, humans modify their behavior BEFORE they run into trouble. This is the precise opposite of the Hill model which predicts that the athlete is powerless to change his exercise behavior until there has already been a catastrophic breakdown in metabolism causing "peripheral fatigue". Thus we have shown that on exposure to heat (which they can obviously detect consciously) or an increased or reduced oxygen partial pressure in the air (which they can detect consciously much less easily), athletes modify their behavior (by slowing down in the heat or when there is less oxygen or speeding up in the cold or when there is more oxygen in the inhailed air). Now we can argue whether or not this is a conscious or a subconscious decision. But in my view that is irrelevant. What it clearly shows is that the brain is causing the behavior to be altered "in anticipation" in a way that the Hill model because it does not allow for any intervention by the brain, does not sanction. Thus to the extent that we have shown the presence of this anticipatory control, we have advanced the understanding of how the body behaves during exercise. Whether or not this information is immediately helpful to coaches is not the reason why we undertake such research. Nor have we ever claimed that this information is of great value to coaches.

Interestingly we have also shown that during exercise in cool, hot and warm conditions, the athlete chooses a pace that produces EXACTLY the same rate of heat accumulation within the body. Now you might say that this is done consciously but I could equally claim that this is impossible - How can you consciously judge how quickly you are heating up when your skin temperature (which is the main feedback telling your conscious brain how hot you are) is very different in the different experiments. So we have concluded that the pace setting under these conditions is done subconsciously by a complex regulator and is not simply a conscious decision.

Point 2: Our model does not exclude the role of the conscious brain and the desire to win. In fact it embraces the concept and has made it defendable on physiological grounds. Instead the Hill model predicts that the desire to win can play no part since once the muscles develop "peripheral fatigue", they are unable to go faster whatever the brain might want of them. The analogy of beating a dead horse comes to mind.

In fact, since the central governor model puts the conscious controller of exercise performance as the rate at which the rating of perceived exertion (RPE) rises during exercise and since we know that the RPE is not regulated purely by physiological events in the body but must be influenced by conscious and subconscious factors as well, it becomes rather easier to understand how self-belief, motivation, the desire to win and all other psychological factors can modify performance (by changing the rate at which the RPE rises during exercise). In contrast I am not sure how the "will to win" can have any effect on performance according to the Hill model.

Interestingly when athletes are told that through their CONSCIOUS beliefs they can alter the rate at which they perceive they are becoming tired, they seem to perform better. This was one of the interventions that helped the South African rugby team (in a small way) win the 2007 Rugby World Cup and two South African rowers to win the 2008 Trans-Atlantic Rowing race.

Telling them that they have no control over their feelings of fatigue since these feelings are determined purely by their failing muscles (according to the Hill Model) is not only wrong but it does not allow them to control their destiny in a way that the central governor model does.

Point 3: I am not a non-athlete. During my life I have run more than 45 marathons and 25 ultra-marathons including seven 90km Comrades Marathons, a few ultra-triathlons and about 10 long distance cycling events. That has caused me a great deal of pain and given me much time to ponder these ideas. If I had not been a runner I would never have experienced any doubts with the Hill model. Instead this experience convinced me that there was more to human exercise physiology than was (and is) in the popular textbooks.

TheRunningMan wrote:

Realted post and ensuing series on this topic:

http://scienceofsport.blogspot.com/2008/04/fatigue-series-introduction.html

I tend see a lot of statements such as 'they couldn't speed up earlier'. This is false. They can speed up earlier.

This is a tactical issue. The goal is to outpace the opponent(s) to the end and has to be timed to ensure you can maintain this pace to the finish, or at least maintain it better than your opponent(s).

Point 1: With respect, I am not sure which papers of our work you have read and which you have not read. It would be very helpful for you to quote exactly which of these papers provides no evidence to support our theory. Recall that all these published papers have had to go through a process in which they are reviewed by other scientists who do not necessarily agree with our ideas. If there was any reason not to publish those papers - if there was the slightest doubt that they did not support the theory that we claim they support - I can assure you that they would not have had the slightest chance of being published. (This is because there is a strong publishing bias towards studies which support the conventional dogma). So if you are correct, then it is clear that the review process has failed in these cases. I am sure that the editors of the journals that published those articles that you feel do not support what we claim they support, would welcome your reasons for believing that. In fact you are welcome to write letters to those editors which they would then publish.

And we would have the opportunity to answer your criticisms. That is the correct scientific approach. It is really not appropriate to make grandiose statements on this blog without providing the supporting evidence for your view. Facts are always better evidence than opinions (which as I have stated before are determined principally by what you already believe).

With respect, the theory is not negated because no one has yet located a specific brain site for the Central Governor. In fact we are actively looking with various colleagues around the world who have access to the sophisticated equipment that we lack. It is quite interest that these scientists should think it worthwhile to put their money behind these costly experiments. Clearly these brain specialists have more faith in the theory than do you.

Perhaps you are also unaware that the relevant brain scanning techniques cannot be used during whole body exercise, the type of exercise in which we speculate that the central governor is most active. So it is rather difficult to look for a brain region that is meant to be active only during exercise when the current techniques do not allow us to perform those experiments.

But then perhaps you have some advice on how we can proceed and so get round this rather large obstacle.

The strongest (but not the only) evidence supporting the central governor theory is that when they are allowed to pace themselves during exercise in different experimental conditions, humans modify their behavior BEFORE they run into trouble. This is the precise opposite of the Hill model which predicts that the athlete is powerless to change his exercise behavior until there has already been a catastrophic breakdown in metabolism causing "peripheral fatigue". Thus we have shown that on exposure to heat (which they can obviously detect consciously) or an increased or reduced oxygen partial pressure in the air (which they can detect consciously much less easily), athletes modify their behavior (by slowing down in the heat or when there is less oxygen or speeding up in the cold or when there is more oxygen in the inhailed air). Now we can argue whether or not this is a conscious or a subconscious decision. But in my view that is irrelevant. What it clearly shows is that the brain is causing the behavior to be altered "in anticipation" in a way that the Hill model because it does not allow for any intervention by the brain, does not sanction. Thus to the extent that we have shown the presence of this anticipatory control, we have advanced the understanding of how the body behaves during exercise. Whether or not this information is immediately helpful to coaches is not the reason why we undertake such research. Nor have we ever claimed that this information is of great value to coaches.

Interestingly we have also shown that during exercise in cool, hot and warm conditions, the athlete chooses a pace that produces EXACTLY the same rate of heat accumulation within the body. Now you might say that this is done consciously but I could equally claim that this is impossible - How can you consciously judge how quickly you are heating up when your skin temperature (which is the main feedback telling your conscious brain how hot you are) is very different in the different experiments. So we have concluded that the pace setting under these conditions is done subconsciously by a complex regulator and is not simply a conscious decision.

Point 2: Our model does not exclude the role of the conscious brain and the desire to win. In fact it embraces the concept and has made it defendable on physiological grounds. Instead the Hill model predicts that the desire to win can play no part since once the muscles develop "peripheral fatigue", they are unable to go faster whatever the brain might want of them. The analogy of beating a dead horse comes to mind.

In fact, since the central governor model puts the conscious controller of exercise performance as the rate at which the rating of perceived exertion (RPE) rises during exercise and since we know that the RPE is not regulated purely by physiological events in the body but must be influenced by conscious and subconscious factors as well, it becomes rather easier to understand how self-belief, motivation, the desire to win and all other psychological factors can modify performance (by changing the rate at which the RPE rises during exercise). In contrast I am not sure how the "will to win" can have any effect on performance according to the Hill model.

Interestingly when athletes are told that through their CONSCIOUS beliefs they can alter the rate at which they perceive they are becoming tired, they seem to perform better. This was one of the interventions that helped the South African rugby team (in a small way) win the 2007 Rugby World Cup and two South African rowers to win the 2008 Trans-Atlantic Rowing race.

Telling them that they have no control over their feelings of fatigue since these feelings are determined purely by their failing muscles (according to the Hill Model) is not only wrong but it does not allow them to control their destiny in a way that the central governor model does.

Point 3: I am not a non-athlete. During my life I have run more than 45 marathons and 25 ultra-marathons including seven 90km Comrades Marathons, a few ultra-triathlons and about 10 long distance cycling events. That has caused me a great deal of pain and given me much time to ponder these ideas. If I had not been a runner I would never have experienced any doubts with the Hill model. Instead this experience convinced me that there was more to human exercise physiology than was (and is) in the popular textbooks.

Point 1: With respect, I am not sure which papers of our work you have read and which you have not read. It would be very helpful for you to quote exactly which of these papers provides no evidence to support our theory. Recall that all these published papers have had to go through a process in which they are reviewed by other scientists who do not necessarily agree with our ideas. If there was any reason not to publish those papers - if there was the slightest doubt that they did not support the theory that we claim they support - I can assure you that they would not have had the slightest chance of being published. (This is because there is a strong publishing bias towards studies which support the conventional dogma). So if you are correct, then it is clear that the review process has failed in these cases. I am sure that the editors of the journals that published those articles that you feel do not support what we claim they support, would welcome your reasons for believing that. In fact you are welcome to write letters to those editors which they would then publish.

And we would have the opportunity to answer your criticisms. That is the correct scientific approach. It is really not appropriate to make grandiose statements on this blog without providing the supporting evidence for your view. Facts are always better evidence than opinions (which as I have stated before are determined principally by what you already believe).

With respect, the theory is not negated because no one has yet located a specific brain site for the Central Governor. In fact we are actively looking with various colleagues around the world who have access to the sophisticated equipment that we lack. It is quite interest that these scientists should think it worthwhile to put their money behind these costly experiments. Clearly these brain specialists have more faith in the theory than do you.

Perhaps you are also unaware that the relevant brain scanning techniques cannot be used during whole body exercise, the type of exercise in which we speculate that the central governor is most active. So it is rather difficult to look for a brain region that is meant to be active only during exercise when the current techniques do not allow us to perform those experiments.

But then perhaps you have some advice on how we can proceed and so get round this rather large obstacle.

The strongest (but not the only) evidence supporting the central governor theory is that when they are allowed to pace themselves during exercise in different experimental conditions, humans modify their behavior BEFORE they run into trouble. This is the precise opposite of the Hill model which predicts that the athlete is powerless to change his exercise behavior until there has already been a catastrophic breakdown in metabolism causing "peripheral fatigue". Thus we have shown that on exposure to heat (which they can obviously detect consciously) or an increased or reduced oxygen partial pressure in the air (which they can detect consciously much less easily), athletes modify their behavior (by slowing down in the heat or when there is less oxygen or speeding up in the cold or when there is more oxygen in the inhailed air). Now we can argue whether or not this is a conscious or a subconscious decision. But in my view that is irrelevant. What it clearly shows is that the brain is causing the behavior to be altered "in anticipation" in a way that the Hill model because it does not allow for any intervention by the brain, does not sanction. Thus to the extent that we have shown the presence of this anticipatory control, we have advanced the understanding of how the body behaves during exercise. Whether or not this information is immediately helpful to coaches is not the reason why we undertake such research. Nor have we ever claimed that this information is of great value to coaches.

Interestingly we have also shown that during exercise in cool, hot and warm conditions, the athlete chooses a pace that produces EXACTLY the same rate of heat accumulation within the body. Now you might say that this is done consciously but I could equally claim that this is impossible - How can you consciously judge how quickly you are heating up when your skin temperature (which is the main feedback telling your conscious brain how hot you are) is very different in the different experiments. So we have concluded that the pace setting under these conditions is done subconsciously by a complex regulator and is not simply a conscious decision.

Point 2: Our model does not exclude the role of the conscious brain and the desire to win. In fact it embraces the concept and has made it defendable on physiological grounds. Instead the Hill model predicts that the desire to win can play no part since once the muscles develop "peripheral fatigue", they are unable to go faster whatever the brain might want of them. The analogy of beating a dead horse comes to mind.

In fact, since the central governor model puts the conscious controller of exercise performance as the rate at which the rating of perceived exertion (RPE) rises during exercise and since we know that the RPE is not regulated purely by physiological events in the body but must be influenced by conscious and subconscious factors as well, it becomes rather easier to understand how self-belief, motivation, the desire to win and all other psychological factors can modify performance (by changing the rate at which the RPE rises during exercise). In contrast I am not sure how the "will to win" can have any effect on performance according to the Hill model.

Interestingly when athletes are told that through their CONSCIOUS beliefs they can alter the rate at which they perceive they are becoming tired, they seem to perform better. This was one of the interventions that helped the South African rugby team (in a small way) win the 2007 Rugby World Cup and two South African rowers to win the 2008 Trans-Atlantic Rowing race.

Telling them that they have no control over their feelings of fatigue since these feelings are determined purely by their failing muscles (according to the Hill Model) is not only wrong but it does not allow them to control their destiny in a way that the central governor model does.

Point 3: I am not a non-athlete. During my life I have run more than 45 marathons and 25 ultra-marathons including seven 90km Comrades Marathons, a few ultra-triathlons and about 10 long distance cycling events. That has caused me a great deal of pain and given me much time to ponder these ideas. If I had not been a runner I would never have experienced any doubts with the Hill model. Instead this experience convinced me that there was more to human exercise physiology than was (and is) in the popular textbooks.

So American universities would achieve better results by recruiting Kenyan coaches rather than Kenyan athletes?

Lasse Viren ran 13:55 when he had been training only one year.Guess how much was his mileage that year?

1830!! That is about 35m/week.

Why the hell he would need blood transfers to run 13:16,3?

Timothy Noakes wrote:

The strongest (but not the only) evidence supporting the central governor theory is that when they are allowed to pace themselves during exercise in different experimental conditions, humans modify their behavior BEFORE they run into trouble.

I don't see this as evidence of a central governor. I see it as a result of experience and learning. They choose an effort level they know they can sustain for a given workout base on previous experience, and they can interpolate/extrapolate to a new unfamiliar situation accordingly.

By what reasoning do you determine this behavior is related to what you call the 'central governor' and not some other factor(s)?

I will not contest anything you have written. However the problem you have inherited from the Hill model is that you want to put the cart before the horse so to speak. My point has always been that muscles do not contract because they are supplied with oxygen etc. They contract because they are activated by the brain. Once they are activated they are then free to increase their metabolism and to produce or not to produce lactate etc. But without activation, nothing happens regardless of how much energy and oxygen the muscle is receiving and how well trained are its mitochondria.

So the reason why athletes run faster is not because they have altered their lactate turnpoints etc. They run faster because they recruit more muscle fibres (or, less likely, that they utilize the same number of muscle fibres but get more power from each fibre – so called increased “contractility”). Why the best athletes are able to increase their muscle recruitment more than slightly less good athletes especially at the end of races, is the key question for exercise physiologists to explain and ultimately for coaches to exploit.

Perhaps the best athletes are able to increase their recruitment near the end of races because of an altered lactate metabolism. But it could be due to many other factors as well. For example (as you know) there are receptors in muscle (mechanoreceptors) that inform the brain of how hard the each muscle is working. These then activate respiratory and cardiovascular changes. Thus whilst lactate is (almost certainly) a chemical that produces sensory feedback to the brain (and to many other organs including probably the heart), it is most certainly not the only candidate that can provide sensory feedback to the brain and to the rest of the body about how hard the athlete is exercising.

But to continue along this line, I believe that running is best understood as a series of jumps in which the runner jumps from one foot to the other. In a sense the better the jumper, the better the runner. Now jumping is a complex neuromuscular phenomenon. This contrasts with the Hill model which reduces the runner to just an engine in which the more petrol you provide, the faster the machine goes. Because the Hill model does not integrate the biomechanics of running into performance, so it is more applicable to sports like cycling in which the same mechanical factors do not apply as in running or jumping.

Now if you consider runners as jumpers, you can begin to understand the mechanics of how runners are able to speed up in the endspurt or conversely to slow down when fatigued and this explanation does not initially have to include considerations of lactate metabolism or oxygen delivery (those are refinements that can be added to the model at a later stage). To run faster the runner has to reduce the time his foot is on the ground and to increase the time he is off the ground in the air. This requires that he must produce more force more quickly when the foot is on the ground. This is achieved in part by the process known as pre-activation in which the brain causes certain muscles in the lower limb to contract BEFORE the foot touches the ground. This turns the limb into a more rigid but still very springy structure that more effectively returns the energy of landing into forward movement.

But pre-activation alone does not explain this phenomenon. To speed up, whilst his foot is on the ground, the runner must recruit more muscle fibres so that they produce more force in a shorter time (ie the muscles must produce more power) whilst the foot is on the ground. I suspect that the best athletes have muscle fibres that are better able to produce power; ie their muscles have greater contractility (as proposed on this blog by Richard – The Muscle Power Model). But to my knowledge this has not really ever been properly studied in human athletes. (Interestingly this is true for Thoroughbred race horses. Besides having superior cardiovascular function compared to Percherons (huge horses designed to pull heavy loads slowly), the muscle fibres of Thoroughbreds have much superior contractility).

In contrast when athletes slow down, they begin to stick to the ground – their ground contact time increases; their flight time is reduced and they are in the air for a shorter time. This will be seen as a reduced stride length. Together with our colleagues in Finland (Dr Ari Nummela in Jyvaskyla) we have shown that when this occurs, the level of pre-activation in the muscle goes down. Since pre-activation is a brain function that is not controlled consciously, this indicates that the brain has “decided” to slow the runner down. Logically (but not yet properly shown) when the runner slows down, the extent of muscle activation when the foot is on the ground should also be reduced or the contractility of the lower limb muscles may be impaired (in which case “peripheral fatigue” has also contributed to the slowing. But because not all the muscle fibres are activated at this point, the brain could still override the “peripheral fatigue” by recruiting more fibres and so maintaining or increasing the pace. Thus even if there is “peripheral fatigue” at this stage, the brain has still chosen not to override it for some reason).

The evidence that slowing down during short distance track races can be at least partially explained by these factors comes from an unlikely source. Oscar Pistorius who runs on 2 artificial limbs has become the only athlete ever in the history of athletics not to slow down in the third 100m (compared to time over the first 100m) of the 400m race. This is because he does not need pre-activation to keep his legs “springing” – that effect is provided by his artificial limbs. Similarly I recently observed that the only athlete still running after 15h of a recent Ironman triathlon shown on television was an athlete with two artificial limbs. Again, since he does not need to pre-activate his calf muscles when running, so he does not develop one form of fatigue that seems to be “limit” the performance of the less well conditioned and less competitive Ironman triathletes.

The point is that these effects appear to be centrally-regulated in response to sensory information received by the brain. Exactly what sensory information is involved would seem to be uncertain at this time but could include any or all of the factors that you mention.

Interestingly a new theory that is rapidly gaining credence judging by the number of publications on this topic in the past few months, is that the oxygenation of the brain is impaired during high intensity exercise and that this then causes brain (“central”) fatigue that “limits” exercise performance.

The logic behind this belief is that when athletes run at higher exercise intensities (ie above the “lactate turnpoint”), they begin to hyperventilate. In this way, there may indeed be a link between lactate metabolism and exercise performance in that whenever you exercise sufficiently hard to cause a progressive increase in blood lactate concentrations, then you will also be exercising with a high rate of ventilation. This then causes carbon dioxide (CO2) to be exhaled in increasing amounts causing the partial pressure of CO2 in the blood to fall. This is important because the falling partial pressure of CO2 in the brain reduces brain blood flow by causing constriction of the blood vessels supplying the brain with blood (as you also know). Thus the latest theory is that it is not an inadequate blood supply to the muscles that limits exercise performance (as predicted by the Hill model) but rather an inadequate blood flow to certain areas of the brain.

It is then held that this reduction in brain blood flow to critical brain areas reduces the ability of the brain to recruit more muscle fibres causing a reduced muscle recruitment and a slowing of pace. In this way it would be possible to explain a link (not necessarily causal) between lactate metabolism in the muscles, brain blood flow, the extent of muscle recruitment and hence running speed, and the development of fatigue.

Training could then impact on any or all of these physiological factors and so improve running performance by multiple different mechanisms as is almost certainly the case since the body is a complex organism that cannot be understood simply by studying one biological system in isolation.

"Point 1: With respect, I am not sure which papers of our work you have read and which you have not read. It would be very helpful for you to quote exactly which of these papers provides no evidence to support our theory"

Point taken, but sorry, I don't have time to go looking these up. You didn't quote exactly where your conclusions below were published so let's just agree that we have read what we have read and move forward. I agree with you but it is not practical.

"Recall that all these published papers have had to go through a process in which they are reviewed by other scientists who do not necessarily agree with our ideas. If there was any reason not to publish those papers - if there was the slightest doubt that they did not support the theory that we claim they support - I can assure you that they would not have had the slightest chance of being published. (This is because there is a strong publishing bias towards studies which support the conventional dogma)."

I agree with you that there is such a bias. But to say that the peer review process would kick out any paper where the author's conclusions and theories during discussion were not fully supported by the data provided is unrealistically optimistic. You are allowed to theorize in your conclusions, and peer review is not as perfect as you pretend it to be (I deal with it every day).

"Facts are always better evidence than opinions (which as I have stated before are determined principally by what you already believe)."

I agree. Yet you have provided to biological or physical evidence showing the existence of a Central Governor, or the biological manifestation of it. And continue to talk like it is a fact of some sort. The fact that current techniques do not allow you to do the proper experiments does not allow you to escape the need to provide evidence before pretending this theoretical governor actually exists.

"With respect, the theory is not negated because no one has yet located a specific brain site for the Central Governor."

I agree. But the caveat is that, without this, you have no support either. It is just another vague theory that doesn't even do so far as to give us an idea what biological mechanisms are at work. It's the Dark Matter of exercise physiology -- no direct evidence but take our word for it.

"Perhaps you are also unaware that the relevant brain scanning techniques cannot be used during whole body exercise, the type of exercise in which we speculate that the central governor is most active. So it is rather difficult to look for a brain region that is meant to be active only during exercise when the current techniques do not allow us to perform those experiments."

I understand the limitation (try to run while immobilized in a PET scanner) but again, this is a burden for you to find a way around and I sympathize. However it doesn't remove the burden of evidence to prove your point.

"But then perhaps you have some advice on how we can proceed and so get round this rather large obstacle."

No, but it doesn't remove the need for the evidence.

"The strongest (but not the only) evidence supporting the central governor theory is that when they are allowed to pace themselves during exercise in different experimental conditions, humans modify their behavior BEFORE they run into trouble. This is the precise opposite of the Hill model which predicts that the athlete is powerless to change his exercise behavior until there has already been a catastrophic breakdown in metabolism causing "peripheral fatigue"."

Now this is the part where, with all due respect, you step out of the real world. The real world is not a model. If you could ask Hill if he believed the mind was not connected to the runner and the runner was not at all capable of pacing themselve and just went as hard as it could until it collapsed, he'd say NO. It's just idiotic to propose such a thing. Proposing that an athlete could actually think to pace themselves, or take in feedback through their senses and modify their effort, is nothing new and requires no new Central Governor model. What you are saying is that the athlete has a brain and that, amazingly enough, they use it. Wow.

"Now we can argue whether or not this is a conscious or a subconscious decision. But in my view that is irrelevant."

Now this is just silly. Deciding to do something and your body unconsciously overriding your decisions or will are two very different things.

"What it clearly shows is that the brain is causing the behavior to be altered "in anticipation" in a way that the Hill model because it does not allow for any intervention by the brain, does not sanction."

Again, just silly. Step away from the academics and take a look at the real world here. Who cares if Hill's model included the conscious decision or not; all models are simplifications of real life that exclude some variables. We all know that the mind works during exercise otherwise pacing would not be in our lexicon. Pretending that you need some now Central Governor theory for this is silly.

"Thus to the extent that we have shown the presence of this anticipatory control, we have advanced the understanding of how the body behaves during exercise. "

Did anyone here not realize you don't start a marathon at a dead sprint and only slow down when exhaustion causes you to? If so, you are the only ones learning from this.

" So we have concluded that the pace setting under these conditions is done subconsciously by a complex regulator and is not simply a conscious decision."

Again, what is the nature of this regulator, how does it work? You have no idea and have presented no evidence. You can't explain something, so you create some new regulatory mechanism and give it a name and say that the evidence supporting it is simply that we don't know how something else works. This is not evidence in support at all -- do you not understand the difference?

In molecular biology, you can't get published by simply showing something you don't fully understand and naming some hypothetical protein that may do that function. You have to identify the protein, sequence the gene, knock it out in a mouse model and characterize its function. To complete the analogy, you would have to show some sort of physical evidence showing us the physical nature or location of the Governor and give us an idea how it regulates exercise. But you haven't.

"Instead the Hill model predicts that the desire to win can play no part since once the muscles develop "peripheral fatigue", they are unable to go faster whatever the brain might want of them. The analogy of beating a dead horse comes to mind."

Now I thought the Central Governor was supposed to defend against us causing irreversible damage to our heart -- now you say it can overcome signals to slow down and keep us pushing. So which way is it?

"Telling them that they have no control over their feelings of fatigue since these feelings are determined purely by their failing muscles (according to the Hill Model) is not only wrong but it does not allow them to control their destiny in a way that the central governor model does."

I can save you some work. I doubt anyone, including Hill, actually believed(s) that the mind plays no part in exercise. Otherwise we'd do nothing but sprint to exhaustion. This is a totally academic and useless exercise if this is your point.

"I am not a non-athlete."

I actually knew this, yet you make some conclusions that no athlete with any experience would make and I'm curious where they come from.

"Now if you consider runners as jumpers, you can begin to understand the mechanics of how runners are able to speed up in the endspurt or conversely to slow down when fatigued and this explanation does not initially have to include considerations of lactate metabolism or oxygen delivery (those are refinements that can be added to the model at a later stage). To run faster the runner has to reduce the time his foot is on the ground and to increase the time he is off the ground in the air. This requires that he must produce more force more quickly when the foot is on the ground. This is achieved in part by the process known as pre-activation in which the brain causes certain muscles in the lower limb to contract BEFORE the foot touches the ground. This turns the limb into a more rigid but still very springy structure that more effectively returns the energy of landing into forward movement."

This is all well and good if you are a sprinter. Most of us are not sprinters on the website. We are operating at a rate of contraction far below what we are capable of at any point. Running faster, for us, entails not increased turnover but longer strides as we're always at roughly 180 strides per minute. It's not that we can't take longer strides at any moment, but that we can't sustain that effort. I'm with you for sprinters, but this has no application to distance runners. Any decent high schooler can beat me over 400m but at 5k and above they'll be several minutes behind me. The principles that govern long distance running are not the same as for sprinting. To liken a marathoner to jumping from foot to foot for a few minutes is not a valid comparison.

Possibly. But the action is not through the muscles but through the brain. That is all we claim. The Hill model puts the regulation of exercise in the muscles.

Interestingly we took the name governor from Hill's own work. In his model the actual limitor of exercise was the development of an inadequate blood supply (ischemia) to the heart. But already in 1923 Hill knew that if the heart became ischemic it would be damaged. So he postulated the existence of a governor in either the heart or the brain, the function of which was to slow the working of the heart (NOTE - not the exercising muscles) and so protect the heart for that period whilst the muscles were rapidly becoming "anaerobic" and so fatigued. In this way the muscles would rapidly fatigue and would stop working before the heart became damaged.

We simply modified the model by saying that the governor would be much more effective if it were to stop the working of the muscles since that is the best way to protect the heart. We called it a central governor, not a heart or muscle governor to indicate that it is most probably sited somewhere in the central nervous system.

Whilst it seems that the governor does indeed have the final say in regulating the exercise performance, this does not mean that it is not influenced by what is happening in all of the organs in the body, or that it is not modified by the adaptations that occur with training or that it cannot be influenced by conscious thoughts. The governor is there to insure that exercise (almost) always terminates before the body damages itself.

spaniel--

It would be easier to take your objections seriously if you weren't intent on objecting to every single thing that Dr. Noakes has said.

Also, the field of exercise physiology and the field of molecular biology have different ways of understanding the use and verification of concepts and the level of precision that is necessary to establish the usefulness of a hypothesis. It's not fair or helpful to ask exercise physiology to conduct itself according to the methods or molecular biology. The concepts that are generated in each field are generated for different purposes, and if you do not reference the purposes for which a concept might be used, then you have no frame of reference for objecting to the concept's truth value. It's your unwillingness to see the relation between truth and purpose that makes you say that the concept of "Central Governor" is not empirically verifiable. The empirical effects that Dr. Noakes is interested in are not proteins. They are improvements in performance. These effects are measurable, just not in a bio lab.

Thanks for including me. Of course your presence has stirred up quite a hornets nest, so, I appreciate the fact you're taking the time to continue the discussion. (my responses in Bold-- well bold didn't work, so, **)

Noakes said:

"I will not contest anything you have written. However the problem you have inherited from the Hill model is that you want to put the cart before the horse so to speak. My point has always been that muscles do not contract because they are supplied with oxygen etc. They contract because they are activated by the brain. Once they are activated they are then free to increase their metabolism and to produce or not to produce lactate etc. But without activation, nothing happens regardless of how much energy and oxygen the muscle is receiving and how well trained are its mitochondria."

**I have you at a bit of an advantage since you really don't have much notion of what I "believe", so, please don't try to pigeon hole me into this dogmatic notion you have of the field. I have no misconception about the fact that a muscle will not contract without stimulation. Again, these points are self evident, so, I'm not putting any cart before a horse. My 95 year old grandmother can contract her muscles through neurological stimulation, but I am fairly confident she will not win the Olympic marathon this summer, not even the 1500 (she doesn't like the heat). So, we both agree that the muscle is dependent upon neurological stimulation, but a very important factor in performance are the things that contribute to the LT, primarily fiber type comp, mitochondrial content, FABP contentl etc. But if I give my grandma 100% O2, she still won't win the Olympic marathon, but similarly, you can activate Martin Lel's muscles all you like, but if they aren't getting enough O2, or utilizing it in the mitochondria, he will not do anything at London either. So, a bit of a red herring, I think.

Noakes said:

"So the reason why athletes run faster is not because they have altered their lactate turnpoints etc. They run faster because they recruit more muscle fibres (or, less likely, that they utilize the same number of muscle fibres but get more power from each fibre – so called increased “contractility”). Why the best athletes are able to increase their muscle recruitment more than slightly less good athletes especially at the end of races, is the key question for exercise physiologists to explain and ultimately for coaches to exploit. "

**Hmm.. I would call increased power from each fiber increased efficiency, which would lead to increased economy, not "contractility." I might side with Coyle on this that increased "efficiency" of the myosin ATPase would result in increased efficiency of the fibers. This is not dogma being perpetuated from 1929, this is data that has repeatedly been shown by his group (and others) over the last 20-25 yrs.

**From your data though, I can seen where you would argue it is not an efficiency/economy issue, because you have not seen it (difference in economy), but it is often observed by others in other populations and animals such as the model I cited previously.

Noakes said:

"Perhaps the best athletes are able to increase their recruitment near the end of races because of an altered lactate metabolism. But it could be due to many other factors as well. For example (as you know) there are receptors in muscle (mechanoreceptors) that inform the brain of how hard the each muscle is working. These then activate respiratory and cardiovascular changes. Thus whilst lactate is (almost certainly) a chemical that produces sensory feedback to the brain (and to many other organs including probably the heart), it is most certainly not the only candidate that can provide sensory feedback to the brain and to the rest of the body about how hard the athlete is exercising."

**I'm not really arguing for or against the finishing "kick" if you will as an indication of anything. A badly paced race can contain a kick in the middle, but the race is over for the kicker. Depending on the race though, *on average* the race will be run at a given relationship to the LT/CV and as the LT/CV improves the ave pace of the race will be faster, but the kick will be based on the pace of the race. That kick doesn't necessarily NEED to happen at the end. Again, as I have stated previously in this thread, I'm not actually attributing much significance to lactate per se at all. Simply that the point where lactate accumulates without compensation is a point where many pertubations to homeostasis are occuring (primarily glycogenolysis/glycolysis) and as a result, one cannot exercise for very long (depending on the relationship to that point of accumulation). To me, the LT is again, just a conceptual point where homeostasis can no longer be maintained. As such, lactate serves as a fairly easy to assay indicator of that point, but so does performance for given durations (e.g. 1 hr).

Noakes said:

"But to continue along this line, I believe that running is best understood as a series of jumps in which the runner jumps from one foot to the other. In a sense the better the jumper, the better the runner. Now jumping is a complex neuromuscular phenomenon. This contrasts with the Hill model which reduces the runner to just an engine in which the more petrol you provide, the faster the machine goes. Because the Hill model does not integrate the biomechanics of running into performance, so it is more applicable to sports like cycling in which the same mechanical factors do not apply as in running or jumping."

**Ahh... yes, this is the crux of the matter isn't it. Running is not cycling. Cycling is fairly simple to figure out, whereas running has that biomechanical component. You will note in all of my discussions that I have not entirely discounted the biomechanical aspect of running. In fact, I have held it up as an example where there is a "gray" area in comparison to other aerobic sports. That being said, the biomechanical aspects of running are, overall, less imporatant than the metabolic, and further, don't really relate to the CGM, I don't believe. At this point though, I may have forgotten where we started;) Regardless, metabolism certainly contributes to fatigue in cycling as it does in running, just maybe to a different extent. Again though, if you take an untrained runner with a *really big engine* and have him run a 5 km against a trained runner with a *small engine*, the bigger engine may win, despite the biomechanical issue. Again though, I'm not sure of the relevance to the CGM.

Noakes said:

Now if you consider runners as jumpers, you can begin to understand the mechanics of how runners are able to speed up in the endspurt or conversely to slow down when fatigued and this explanation does not initially have to include considerations of lactate metabolism or oxygen delivery (those are refinements that can be added to the model at a later stage). To run faster the runner has to reduce the time his foot is on the ground and to increase the time he is off the ground in the air. This requires that he must produce more force more quickly when the foot is on the ground. This is achieved in part by the process known as pre-activation in which the brain causes certain muscles in the lower limb to contract BEFORE the foot touches the ground. This turns the limb into a more rigid but still very springy structure that more effectively returns the energy of landing into forward movement. “

**Of course I’m familiar with the spring model of running.

Noakes said:

But pre-activation alone does not explain this phenomenon. To speed up, whilst his foot is on the ground, the runner must recruit more muscle fibres so that they produce more force in a shorter time (ie the muscles must produce more power) whilst the foot is on the ground. “

**OK, yes this would be contractility. I didn’t see where you were going earlier (silly me;).

Noakes said:

“I suspect that the best athletes have muscle fibres that are better able to produce power; ie their muscles have greater contractility (as proposed on this blog by Richard – The Muscle Power Model). But to my knowledge this has not really ever been properly studied in human athletes. (Interestingly this is true for Thoroughbred race horses. Besides having superior cardiovascular function compared to Percherons (huge horses designed to pull heavy loads slowly), the muscle fibres of Thoroughbreds have much superior contractility). “

**Well, if you are going to ACSM this year, maybe you should come to my student’s talk. The talk will not be directly relevant to this point of contractility, but it will give you a glimpse of how we plan(are) looking at this *exact* issue.

In contrast when athletes slow down, they begin to stick to the ground – their ground contact time increases; their flight time is reduced and they are in the air for a shorter time. This will be seen as a reduced stride length. Together with our colleagues in Finland (Dr Ari Nummela in Jyvaskyla) we have shown that when this occurs, the level of pre-activation in the muscle goes down. Since pre-activation is a brain function that is not controlled consciously, this indicates that the brain has “decided” to slow the runner down. Logically (but not yet properly shown) when the runner slows down, the extent of muscle activation when the foot is on the ground should also be reduced or the contractility of the lower limb muscles may be impaired (in which case “peripheral fatigue” has also contributed to the slowing. But because not all the muscle fibres are activated at this point, the brain could still override the “peripheral fatigue” by recruiting more fibres and so maintaining or increasing the pace. Thus even if there is “peripheral fatigue” at this stage, the brain has still chosen not to override it for some reason).”

**I have to see the data. Sorry. On this point in particular though, the fact that the brain “should” be able to override the peripheral fatigue but doesn’t, again, isn’t necessarily confirmation of your model I don’t believe. I really don’t want to get contentious on this point, but I think this really lies at the heart of why the model is not generally accepted.

“The evidence that slowing down during short distance track races can be at least partially explained by these factors comes from an unlikely source. Oscar Pistorius who runs on 2 artificial limbs has become the only athlete ever in the history of athletics not to slow down in the third 100m (compared to time over the first 100m) of the 400m race. This is because he does not need pre-activation to keep his legs “springing” – that effect is provided by his artificial limbs. Similarly I recently observed that the only athlete still running after 15h of a recent Ironman triathlon shown on television was an athlete with two artificial limbs. Again, since he does not need to pre-activate his calf muscles when running, so he does not develop one form of fatigue that seems to be “limit” the performance of the less well conditioned and less competitive Ironman triathletes. “

**In the case of Pistorius, I’m honestly not that familiar with his physiology, but I might surmise, as the USOC probably has, that the artificial limbs provide an energetic advantage whereby he may not be working as hard? Therefore, does not fatigue? In the case of the Ironman, if they were similar limbs to those used by Pistorius, I would surmise that the “cushioning” effect reduces the impact forces of repeated foot strikes and attenuates the loss of economy that would occur during the marathon. It would be analogous to the athlete who does an evenly paced bike leg and produces the same power at the end as the beginning. The primary difference in something like a marathon, especially at the end of an Ironman would be the tremendous impact forces causing injury to the muscle and loss of economy. Remove that and the run becomes essentially an extension of the bike without the aerodynamics. To be truthful though, I can’t discount your supposition either since neither of us has hard evidence either way.

Noakes said:

The point is that these effects appear to be centrally-regulated in response to sensory information received by the brain. Exactly what sensory information is involved would seem to be uncertain at this time but could include any or all of the factors that you mention.

**Agreed

Noakes said:

Interestingly a new theory that is rapidly gaining credence judging by the number of publications on this topic in the past few months, is that the oxygenation of the brain is impaired during high intensity exercise and that this then causes brain (“central”) fatigue that “limits” exercise performance.

The logic behind this belief is that when athletes run at higher exercise intensities (ie above the “lactate turnpoint”), they begin to hyperventilate. In this way, there may indeed be a link between lactate metabolism and exercise performance in that whenever you exercise sufficiently hard to cause a progressive increase in blood lactate concentrations, then you will also be exercising with a high rate of ventilation. This then causes carbon dioxide (CO2) to be exhaled in increasing amounts causing the partial pressure of CO2 in the blood to fall. This is important because the falling partial pressure of CO2 in the brain reduces brain blood flow by causing constriction of the blood vessels supplying the brain with blood (as you also know). Thus the latest theory is that it is not an inadequate blood supply to the muscles that limits exercise performance (as predicted by the Hill model) but rather an inadequate blood flow to certain areas of the brain.”

**I don’t think many informed physiologists think that lack of blood flow causes fatigue, regardless of the model. It is clear though that if you can increase blood flow to a region of the body, that region will increase it’s performance (e.g. maximal work capacity of one legged vs two legged exercise). Thanks though for emphasizing the importance of knowing the lactate turnpoint for an athlete;))

“It is then held that this reduction in brain blood flow to critical brain areas reduces the ability of the brain to recruit more muscle fibres causing a reduced muscle recruitment and a slowing of pace. In this way it would be possible to explain a link (not necessarily causal) between lactate metabolism in the muscles, brain blood flow, the extent of muscle recruitment and hence running speed, and the development of fatigue.

Training could then impact on any or all of these physiological factors and so improve running performance by multiple different mechanisms as is almost certainly the case since the body is a complex organism that cannot be understood simply by studying one biological system in isolation.”

**Agreed.

Thanks again.

Steve

So you diminish the relevence of learning and experience by branding it a 'possibility'. In the context used it is certainly much more than a possibility.

Also, as indicated by the other segments of your response (below), I would certainly say it is much more than just claiming actions are controlled through the brain. The main point of contention as I see it is not on whether the brain plays a role, but how. It seems to be a level of hand waving to blur the lines between what a 'central governor' forces and what cognitive skills resolve to. You cannot expicitly rule out the role of experience when a runner chooses an effort level in a workout as you seem to be doing.

Steve McGregor wrote:

Well, of course there are still less fatiguable motor units available for recruitment, and certainly you can continue contracting them, but I'm not sure how continuing to run at a slower pace is going to help you win. I guess I don't see your point.

Steve

Steve,

The point is this - muscle fibers fatigue at different rates. This fact has significant training consequences.

The principle of overload applies to individual muscle fibers. If a muscle fiber is not overloaded it won't adapt. Activating a fiber is not, by itself, sufficient to cause a fiber to adapt. A fiber has to be overloaded, not just activated, and the way to overload a fiber is to train it fairly intensely - i.e. train it to a reasonable level of fatigue.

Since fibers fatigue at widely varying rates, this means training must be of widely varying durations in order to overload as many fibers as is practical.

Those non-fatigued fibers used in the example were contracting and producing force the entire time the runner ran his race. But, since they weren't particularly fatigued at the end of the race, as evidenced by their ability to easily continue to contract, they were not optimally overloaded.

I suggest the above facts - which I call the muscle factor model - explain why multi-paced training works and answers many previously unanswered questions about why particular training methods work or don't work.

Timothy Noakes wrote:

Please do not mis-understand me. I have the very highest regard for Arthur Lydiard as fully expressed in Lore of Running. My point was that we do not necessarily know that, if coaching today, he would be able to produce athletes who could compete with the Kenyans and Ethiopians. Elite performances in the sport have clearly move on and it would be helpful to know if the most successful (Kenyan and Ethiopian) coaches of today use exclusively Lydiard techniques or if they have discovered additional refinements that Lydiard did not use. It seems to me that the ability to speed up in the middle of races (ie before the endspurt) seems to have become a more popular racing technique than it might have been in Lydiard's day. But this might be an incorrect impression.

Last night i had a supra natural meet with Lydiard ghost. He apeares in front of me. i was scared. But he said to me that if he wikll have the oportunity to coach Bekele or Gebrelassie he will make them winners as he did inn the 60s and 70s.

Well, we really don't *know* which fibers are being recruited in humans due to ethics and subject availability, but most of the evidence indicates that around 75% VO2 max (depending on the fitness of the subject) one will recruit most, if not all of their Type I and IIa fibers, which leaves the highly fatiguable IIx. So, one might argue an effective way to overload the IIxs would be to ran at approximately 75% (the LT?... Hmm) for a very long time in order to slowly recruit the highly fatiguable IIxs, or to run faster for a shorter amount of time, to recruit them faster. No magic formulas are likely needed though. Run at or above the LT/MLSS, but below the VO2max and you're good.

Steve