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A new theory concerning the significance of pedalling style.

Moderator: Tonton

A new theory concerning the significance of pedalling style.

16 Jul 2013 16:12

Hi folks,

We often see the 'experts' shouting down any suggestion that pedalling style is important, referring to those experimental studies that failed to find a link between style and gross efficiency. Without going through that debate again, I think that it is significant that, despite what the 'experts' say, many riders are convinced that a 'good' style helps them to delay the onset of fatigue and so forth and most professionals do have a very 'smooth' pedalling style. This makes me suspect that the 'experts', who after all not that long ago were telling everyone that elevated levels of blood lactate 'caused' fatigue, are missing something.

I recently read the following paper:

Fatigue is a brain-derived emotion that regulates the exercise behavior to ensure the protection of whole body homeostasis

http://www.frontiersin.org/striated_muscle_physiology/10.3389/fphys.2012.00082/abstract

This paper essentially argues that fatigue is not a physical state at all, rather a neural 'Central Governor', acting on multiple cues, triggers a feeling of fatigue in order to maintain homeostasis and prevent damage. In reality, in a trained person at least, the body is actually capable of much higher levels of work, if only this 'Central Governor' could somehow be over-ridden. (Which is exactly what drugs like amphetamine and caffeine do.)

Relating this to the old 'pedalling efficiency / style debate, it strikes me that one factor that might contribute to the 'emotion' of fatigue is how well a rider is able to maintain a 'smooth', 'coordinated' pedalling style. (Or perhaps, whatever style feels the 'best' for them.)

Studies show that, when riding at the limit, the style of even the best rider tends to break down. It seems quite possible that this break-down in style would create neuro-muscular cues that the 'Central Governor' would, along with multiple other cues, interpret as signalling a high-workload, and in turn the potential onset of a state where homeostasis is threatened. It also seems possible that the longer a rider is able to maintain a smooth and coordinated pedalling style, the longer they would be able to suppress these cues.

In short, it seems possible that you feel fatigued, at least in part, because of a failure in the ability to maintain a 'smooth' pedalling style, not because this directly influences gross efficiency but because of the influence this has on the functioning of the 'Central Governor'. To look at this a slightly different way, when your pedalling becomes 'ragged' due to having to maintain high work load, an awareness of this contributes to a feeling of 'fatigue'.

Doubtless the 'experts' would cling to the old view that it is the fatigue that is the limiting factor here and the breakdown in style is just a symptom of this. However, as that paper above argues, fatigue as a genuine physical state may only occur at a level of work way beyond the point where the rider actually feels fatigued.

Just an idea!
Robert21
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16 Jul 2013 16:56

Here is the main problems that I see with Noakes theory.

1. He doesn't theorize a mechanism.
2. His theory is untestable, as I understand it. It is simply a black box theory in which the CNS is the black box taking unknown inputs from the body that then processes them and then puts out unknown outputs to limit physical performance.

There are probably others.

While it is clear that the CNS can alter performance and effort (after all we decide to exercise easier or harder all the time) I simply see no hard evidence that the CNS is the ultimate limiter to performance and the source of fatigue.
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FrankDay
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16 Jul 2013 17:20

FrankDay wrote:While it is clear that the CNS can alter performance and effort (after all we decide to exercise easier or harder all the time) I simply see no hard evidence that the CNS is the ultimate limiter to performance and the source of fatigue.


So, if I exercise to 'exhaustion' and produce a certain workload and then, after recovery, repeat the exercise after taking a 'heroic' dose of CNS stimulants, and this time the point of exhaustion comes after sustaining a higher workload, what limited my performance the first time around, if not the control systems of the CNS?

If stimulants facilitate a higher workload, then the 'fatigue' that limits one's performance when not using those stimulants can hardly be the 'ultimate' determinant of performance, can it?

Obviously, a well-trained physiology is still a requirement and, in my experience, until one has a pretty high level of fitness psychological / CNS factors are unlikely to play a primary role as the level of work one can sustain is so low. However, at the point where one is fit enough to really 'hammer' oneself, it does seem that CNS related factors are likely to be far more significant.
Robert21
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16 Jul 2013 17:33

FrankDay wrote:Here is the main problems that I see with Noakes theory.

1. He doesn't theorize a mechanism.

2. His theory is untestable, as I understand it. It is simply a black box theory in which the CNS is the black box taking unknown inputs from the body that then processes them and then puts out unknown outputs to limit physical performance.


Fifty years ago one could have said much the same about all the cognitive processes (such as 'short term memory' and so forth) about which so much has been discovered in the last few decades. Surely, it is the job of science to discover how such a 'mechanism' might function, and how it is embodied in the biology of the brain and CNS?
Robert21
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16 Jul 2013 20:24

Robert21 wrote:So, if I exercise to 'exhaustion' and produce a certain workload and then, after recovery, repeat the exercise after taking a 'heroic' dose of CNS stimulants, and this time the point of exhaustion comes after sustaining a higher workload, what limited my performance the first time around, if not the control systems of the CNS?

If stimulants facilitate a higher workload, then the 'fatigue' that limits one's performance when not using those stimulants can hardly be the 'ultimate' determinant of performance, can it?

Obviously, a well-trained physiology is still a requirement and, in my experience, until one has a pretty high level of fitness psychological / CNS factors are unlikely to play a primary role as the level of work one can sustain is so low. However, at the point where one is fit enough to really 'hammer' oneself, it does seem that CNS related factors are likely to be far more significant.
I guess one needs to define what one means by fatigue. Is it the sense of fatigue? Or, a measurable reduction in output after a period of use. All biological systems "fatigue" with use including nerve cells. Anyhow, Noakes theorizes it is some unknown central processor that somehow senses peripheral work and then somehow turns around and limits that same work. One central mechanism that actually does that is called learning from experience but that isn't what he is talking about. I guess it is possible but, IMHO, the evidence in support of such a primary limiter is scanty at best. What is the purpose of such a limiter? To prevent injury? If so, it doesn't do a very good job there. What other evolutionary purpose could have caused this mechanism to evolve? None that I can think of.
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FrankDay
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16 Jul 2013 20:28

Robert21 wrote:Fifty years ago one could have said much the same about all the cognitive processes (such as 'short term memory' and so forth) about which so much has been discovered in the last few decades. Surely, it is the job of science to discover how such a 'mechanism' might function, and how it is embodied in the biology of the brain and CNS?
Science doesn't "discover" anything without there being a hypothesis that can be tested. Noakes doesn't put forth a testable hypothesis AFAIK. Therefore, he can never be proven wrong.
Life is short, both reading my posts and training with PowerCranks will make it seem longer
FrankDay
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16 Jul 2013 20:55

FrankDay wrote:I guess one needs to define what one means by fatigue.


We might say that the 'traditional' models conceives 'fatigue' to be 'that which limits performance'. As such, a simple measure of performance should also stand as an acceptable measure of fatigue. So, let a rider complete a set course as fast as they can within the limits set by 'fatigue'. Next, repeat the exercise after taking CNS stimulants. If the two performances are identical, then there is no need to suggest that the CNS plays a role. If there is a difference, which I think there would be, then there is more to 'fatigue' than the traditional model allows.
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16 Jul 2013 20:58

FrankDay wrote: Noakes theorizes it is some unknown central processor that somehow senses peripheral work and then somehow turns around and limits that same work.


But the body employs a whole range of homeostatic 'mechanisms', so the general principle is hardly novel. Perhaps you are taking the concept of a 'central processor' too literally.
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16 Jul 2013 21:10

Robert21 wrote:But the body employs a whole range of homeostatic 'mechanisms', so the general principle is hardly novel. Perhaps you are taking the concept of a 'central processor' too literally.
Noakes is the one putting forth the idea of a "central governor" that limits exercise intensity, not I. Most exercise scientists believe fatigue to be peripherally mediated (although still not well understood). He has also put forth the reason for this is to prevent injury (although there is zero evidence it does this effectively). It is up to him to better define a mechanism for same and put it into a form that could possibly be tested if he expects anyone to take this theory seriously. He has yet to do so, AFAIK.
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FrankDay
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17 Jul 2013 02:47

FrankDay wrote:Noakes is the one putting forth the idea of a "central governor" that limits exercise intensity, not I. Most exercise scientists believe fatigue to be peripherally mediated (although still not well understood). He has also put forth the reason for this is to prevent injury (although there is zero evidence it does this effectively). It is up to him to better define a mechanism for same and put it into a form that could possibly be tested if he expects anyone to take this theory seriously. He has yet to do so, AFAIK.


Hmmm ... this seems similar to certain theories put forward on crank length. Wonder why we don't take you seriously, Frank?
"If you're going through hell, keep going." - Winston Churchill
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17 Jul 2013 02:57

elapid wrote:Hmmm ... this seems similar to certain theories put forward on crank length. Wonder why we don't take you seriously, Frank?
Not quite. I can and have, at least, put forth a testable hypothesis for my theory.
Life is short, both reading my posts and training with PowerCranks will make it seem longer
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17 Jul 2013 04:49

FrankDay wrote:It is up to him to better define a mechanism for same and put it into a form that could possibly be tested if he expects anyone to take this theory seriously.


Whilst I would agree that the use of a quasi mechanistic term such as 'Central governor' can only ever be a starting point for further research, I would argue that you are demanding much more than is necessary at this stage. Again, there are many parallels to be found in the world of cognitive psychology, for example, Chomsky's conception of an innate 'Language acquisition device'. Such terminology can only ever really be a collective, high level functional description for a range of processes and structures that are implemented at the biological level. This does not mean to say that such a high level description is useless or untestable though.

The basic hypothesis here is that the ultimate mediator of performance is the CNS, and that when a rider experiences 'exhaustion', they are actually capable of a much higher and / or more extended work load. I would say that the influence of CNS stimulants offers both a way to test, and a conformation, of this basic hypothesis. The next stage would be to identify possible 'cues' and to manipulate them to see if this has the predicted effect on performance.

This basic hypothesis also provides an explanation for a range of phenomenon that the 'traditional' model cannot account for, or even runs counter to. For example. the observation that:

fatigue in all forms of exercise develops before there is complete skeletal muscle recruitment. Indeed only between 35 and 50% of the active muscle mass is recruited during prolonged exercise (Tucker etal.,2004; Amann et al.,2006); during maximal exercise this increases to only about 60% (Sloniger etal.,1997a,b; Albertus, 2008).


Then there is the phenomenon of the pain and 'suffering' that is associated with intense exercise. If the mediating role of the CNS is rejected, then what reason could there be for the pain of exercise? This especially so given that pain is generally understood to be an adaptive mechanism designed to protect the organism from damage.

Why did not the body adapt to make intense and prolonged exercise emotionally neutral or even pleasant, especially given that in many circumstances having to 'force' the body to perform would seem to be a maladaptation? Surely, it would be better to be able to chase prey, or run away from a predator, without this being associated with a whole set of emotional, affective cues telling the individual to stop?
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17 Jul 2013 15:50

Robert21 wrote:Whilst I would agree that the use of a quasi mechanistic term such as 'Central governor' can only ever be a starting point for further research, I would argue that you are demanding much more than is necessary at this stage. Again, there are many parallels to be found in the world of cognitive psychology, for example, Chomsky's conception of an innate 'Language acquisition device'. Such terminology can only ever really be a collective, high level functional description for a range of processes and structures that are implemented at the biological level. This does not mean to say that such a high level description is useless or untestable though.
I am only putting forth what I see are weaknesses and flaws in the theory. If someone else wants to pursure this line and come up with the evidence to support the truth of it they are welcome to do so. They would be on a fools errand IMHO but I have been wrong about many things before, and I will probably be wrong about different things again.

The basic hypothesis here is that the ultimate mediator of performance is the CNS, and that when a rider experiences 'exhaustion', they are actually capable of a much higher and / or more extended work load. I would say that the influence of CNS stimulants offers both a way to test, and a conformation, of this basic hypothesis. The next stage would be to identify possible 'cues' and to manipulate them to see if this has the predicted effect on performance.
Can you name one CNS stimulant that doesn't also have a peripheral effect? The fact that a CNS stimulant drug can affect performance is not, by itself, particularly compelling evidence that there is a central governor. How on earth does the central governor theory explain the performance benefits of a drug like EPO? Certainly no CNS stimulant effects there yet the benefits are clearly demonstrable.

This basic hypothesis also provides an explanation for a range of phenomenon that the 'traditional' model cannot account for, or even runs counter to. For example. the observation that:
fatigue in all forms of exercise develops before there is complete skeletal muscle recruitment. Indeed only between 35 and 50% of the active muscle mass is recruited during prolonged exercise (Tucker etal.,2004; Amann et al.,2006); during maximal exercise this increases to only about 60% (Sloniger etal.,1997a,b; Albertus, 2008).


actually, it is easy to explain why fatigue develops before all the active muscle mass is recruited. It has to do with the balance between muscle mass and capillary density. The more blood vessels there are the less room there is for contracting muscle mass and the energy required to maintain such vessels is inefficient when they would be used so infrequently. The body somehow magically is capable of balancing the needs of the various exercise components based upon the demands it regularly sees. It is why sprinters have big muscles and few capillaries and endurance runners have smaller muscles and more capillaries. Using just some of the muscles for an endurance event allows time for recently used contractile elements to recover why "fresh ones" are doing the work demanded until they need to pass off the job to other sarcomeres. It is a way of dividing and sharing the load. But, there is zero evidence this is a CNS controlled phenomenon but, rather, is a local homeostatic mechanism.



Then there is the phenomenon of the pain and 'suffering' that is associated with intense exercise. If the mediating role of the CNS is rejected, then what reason could there be for the pain of exercise? This especially so given that pain is generally understood to be an adaptive mechanism designed to protect the organism from damage.
Well, pain and suffering associated with exercise can just as well be a learned phenomenon. Watch little kids run, it is usually either 100% or nothing. Over time they will learn to pace themselves if they want to run further. And, they will learn the concept that researchers call "perceived exertion" that they use to moderate their effort. But, such limits are learned and not due to an innate central governor present to prevent injury.

Why did not the body adapt to make intense and prolonged exercise emotionally neutral or even pleasant, especially given that in many circumstances having to 'force' the body to perform would seem to be a maladaptation? Surely, it would be better to be able to chase prey, or run away from a predator, without this being associated with a whole set of emotional, affective cues telling the individual to stop?
??? Something tells the body to stop. The question is whether it is a central governor or peripheral mechanisms or something else. The evidence is overwhelmingly against a central governor, IMHO.
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FrankDay
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17 Jul 2013 17:40

FrankDay wrote:The fact that a CNS stimulant drug can affect performance is not, by itself, particularly compelling evidence that there is a central governor.

Once again, you are (willfully?) failing to consider that a term such as 'Central governor' is effectively a high-level functional description of lower level biological processes.

FrankDay wrote:How on earth does the central governor theory explain the performance benefits of a drug like EPO?

Why would it need to? Noakes, nor anyone else, have tried to claim that performance is entirely due to CNS mechanisms, and that no energy production systems are needed at all!

FrankDay wrote:Using just some of the muscles for an endurance event allows time for recently used contractile elements to recover...there is zero evidence this is a CNS controlled phenomenon but, rather, is a local homeostatic mechanism.


Are you saying that 'local homeostasis' somehow is maintained entirely independently of those CNS systems that control homeostasis at the level of the organism? Any references you have to support this claim would be welcome. This certainly does not seem to be the case for other homeostatic systems. For example:

There is considerable evidence that the central nervous system (CNS) is significantly involved in potassium homeostasis

http://www.ncbi.nlm.nih.gov/pubmed/8477870


FrankDay wrote:Well, pain and suffering associated with exercise can just as well be a learned phenomenon.


What are you saying here? That those sensations are somehow not intrinsically unpleasant at all? Why not say the same about all sensations of 'pain and suffering'? Somehow I doubt that the way dental work without anesthetic or serious burns are regarded as being intrinsically unpleasant can be written off as nothing more than a 'learned response'.

P.s. Earlier you said:

FrankDay wrote:the evidence in support of such a primary limiter is scanty at best. What is the purpose of such a limiter? To prevent injury? If so, it doesn't do a very good job there.


In reality, given how sensitive muscle cells are to damage in response to exercise, it could be argued that not only is some sort of central control system necessary, it actually seems to work rather well. For example:

Side effects of excessive physical exercise are the production of reactive oxygen species (ROS) and the mechanical damage of mitochondria... For these reasons, a highly dynamic tissue such as skeletal muscle requires a rapid and efficient system for the removal of altered organelles, the elimination of protein aggregates, and the disposal of toxic products that may lead to cell death.

Cells 2012, 1, 325-345; doi:10.3390/cells1030325
Robert21
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17 Jul 2013 18:56

Robert21 wrote:Once again, you are (willfully?) failing to consider that a term such as 'Central governor' is effectively a high-level functional description of lower level biological processes.


Why would it need to? Noakes, nor anyone else, have tried to claim that performance is entirely due to CNS mechanisms, and that no energy production systems are needed at all!
Noakes is trying to say that exercise is limited by the CNS. That is what the term central governor means. That is the issue under discussion.



Are you saying that 'local homeostasis' somehow is maintained entirely independently of those CNS systems that control homeostasis at the level of the organism? Any references you have to support this claim would be welcome. This certainly does not seem to be the case for other homeostatic systems. For example:
Most homeostatic mechanisms are local. One example is blood flow to the tissues is locally regulated to need to maintain a constant end capillary oxygen concentration. An obvious exception might be skin flow which can have a separate regulation to help control temperature but blood flow for exercise need is generally locally controlled. Anyhow, we are discussing exercise limitation, not potassium regulation or any other potential CNS regulation. The CNS has a role in a lot of stuff. The question here is whether there is a CNS central governor that limits exercise with the presumed goal of preventing injury. That is Noakes theory. That is what is being discussed.





What are you saying here? That those sensations are somehow not intrinsically unpleasant at all? Why not say the same about all sensations of 'pain and suffering'? Somehow I doubt that the way dental work without anesthetic or serious burns are regarded as being intrinsically unpleasant can be written off as nothing more than a 'learned response'.
It doesn't matter if they are unpleasant or not, we learn what different efforts feel like. It is learned and we use that information to moderate our activity. That is different than there being a central governor. voluntarily restricting exercise intensity because it becomes unpleasant is not the same as a central governor.

P.s. Earlier you said:



In reality, given how sensitive muscle cells are to damage in response to exercise, it could be argued that not only is some sort of central control system necessary, it actually seems to work rather well. For example:
Side effects of excessive physical exercise are the production of reactive oxygen species (ROS) and the mechanical damage of mitochondria... For these reasons, a highly dynamic tissue such as skeletal muscle requires a rapid and efficient system for the removal of altered organelles, the elimination of protein aggregates, and the disposal of toxic products that may lead to cell death.

Cells 2012, 1, 325-345; doi:10.3390/cells1030325
???what does that example have to do with the central governor theory. The fact that some things are under some or complete central control (breathing, for example) doesn't mean everything is under a central limitation. In general, biological systems evolve to have simple mechanisms, not complex mechanisms. The central governor theory limiting exercise involves a much more complex system than local mechanisms such as local oxygen levels, fuel availability, electrolyte changes, and pH changes that can occur an all can limit exercise intensity and require no central control. Even changes in HR associated with normal exercise are almost entirely local.

The fact that it makes sense to you that there should be a central governor is not evidence that one actually exists. Any theory, to be correct, must explain all circumstances and to understand it we must understand the mechanism. The central governor theory simply cannot explain the changes in exercise limitations associated with changes in hemoglobin concentrations and a multitude of other things, IMHO, nor does Noakes put forth any proposed mechanisms that might explain how this is supposed to work. Noakes has been putting this out for many many years and so far he (and some of the people he has trained) are about the only ones who believe it.
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FrankDay
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18 Jul 2013 13:18

Frank, sorry but I feel that you are almost being perverse in your refusal to recognise what is actually being argued here. OK, so you don't understand how high-level functional theories, often adopting quasi-mechanistic or computational metaphors, can help to guide research and lead to a fuller understanding of the brain and CNS. The huge progress made in cognitive neuroscience and cognitive psychology in recent decades show just how productive such an approach can be. That is your loss.

Your refusal to recognise that understanding how any CNS control system might function and understanding of how cells produce energy, or how Epo can aid that process, poses two very different sets of questions is particularly baffling. Again, your loss.

Once more, why on Earth should the functioning of any central control system operate without also engaging the conscious intervention of the individual? Just consider thirst and the way homeostatic mechanisms actively prompt the individual to act in a certain way. In this case taking a drink in order to restore homeostatic balance.

In order to sidestep all the above issues, I think what I have said could be put in a rather different way, whilst effectively saying the same thing. That is, it seems possible that so many riders feel that having a 'smooth' pedalling style helps them to delay the onset of fatigue, despite the minimal evidence showing that this leads to an increase in GE, is because of the way having such a 'smooth' style is strongly associated with coasting along whilst not been under any pressure, whilst becoming 'ragged' is associated with being 'on the limit'. Consequently, the longer a rider can maintain a 'smooth' style, the longer they are able to convince themselves that they are not on the limit, with this helping them to keep on pushing for longer than they otherwise would.
Robert21
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18 Jul 2013 15:27

Robert21 wrote:Frank, sorry but I feel that you are almost being perverse in your refusal to recognise what is actually being argued here. OK, so you don't understand how high-level functional theories, often adopting quasi-mechanistic or computational metaphors, can help to guide research and lead to a fuller understanding of the brain and CNS. The huge progress made in cognitive neuroscience and cognitive psychology in recent decades show just how productive such an approach can be. That is your loss.

Your refusal to recognise that understanding how any CNS control system might function and understanding of how cells produce energy, or how Epo can aid that process, poses two very different sets of questions is particularly baffling. Again, your loss.

Once more, why on Earth should the functioning of any central control system operate without also engaging the conscious intervention of the individual? Just consider thirst and the way homeostatic mechanisms actively prompt the individual to act in a certain way. In this case taking a drink in order to restore homeostatic balance.

In order to sidestep all the above issues, I think what I have said could be put in a rather different way, whilst effectively saying the same thing. That is, it seems possible that so many riders feel that having a 'smooth' pedalling style helps them to delay the onset of fatigue, despite the minimal evidence showing that this leads to an increase in GE, is because of the way having such a 'smooth' style is strongly associated with coasting along whilst not been under any pressure, whilst becoming 'ragged' is associated with being 'on the limit'. Consequently, the longer a rider can maintain a 'smooth' style, the longer they are able to convince themselves that they are not on the limit, with this helping them to keep on pushing for longer than they otherwise would.
Look, here is what Noakes writes in his abstract:
The model predicts that attempts to understand fatigue and to explain superior human athletic performance purely on the basis of the body’s known physiological and metabolic responses to exercise must fail since subconscious and conscious mental decisions made by winners and losers, in both training and competition, are the ultimate determinants of both fatigue and athletic performance.
He basically states here that his model is right and other (physical) biological models are wrong because, well because, his model is right. I mean, where on earth is the experimental support for the statement in bold above? From my own experience, when I used to commute by running to work sometimes after a 14 hour day I was so fatigued and wasted I could barely imagine getting the shoes on and running home but a mile down the road I started to feel great and had a great and invigorating run. While it is possible that some feelings of fatigue are purely psychological (CNS based) it is by no means proven that they all are. In fact, the evidence that fatigue and performance are related to purely physical/peripheral systems (the effect of EPO, for example) is overwhelming. That evidence, in and of itself, is enough to disprove the above statement by Noakes in bold.

Edit: another little "problem" for Noakes theory is the issue of observed muscle fatigue in isolated, in vitro, muscle preparations, where there is no central nervous system. How does Noakes theory explain that observation?
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FrankDay
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18 Jul 2013 20:49

Robert21 wrote:...
is because of the way having such a 'smooth' style is strongly associated with coasting along whilst not been under any pressure, whilst becoming 'ragged' is associated with being 'on the limit'. Consequently, the longer a rider can maintain a 'smooth' style, the longer they are able to convince themselves that they are not on the limit, with this helping them to keep on pushing for longer than they otherwise would.

------

Do you think that this actually happens?
Especially the part about
"with this helping them to keep on pushing for longer than they otherwise would".

Jay Kosta
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19 Jul 2013 10:00

JayKosta wrote:Do you think that this actually happens? Especially the part about "with this helping them to keep on pushing for longer than they otherwise would".


I am certain that mental attitude is big part of racing, and whilst there are doubtlessly many factors that contribute to a rider deciding that they have had enough, they are truly cooked, and that break can ride away if it wants to, I feel that how a rider perceives the way they are pedalling could well be one of them.
Robert21
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19 Jul 2013 13:31

Robert21 wrote:I am certain that mental attitude is big part of racing,
...
I feel that how a rider perceives the way they are pedalling could well be one of them.

------
Thank you, and I fully agree that mental attitude is very important.
Perhaps in a 'race situation' where there is a 'reward' available, mental attitude plays a bigger role than in laboratory 'controlled testing'.
Testing with animals typically involves some type of reward for achievement, perhaps doing that with people would provide meaningful information.

Jay Kosta
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