Dear Steve,
Here are my comments:
YOU WROTE: "We've been dancing around this point for a couple weeks now. From the collective work of Coyle including his work in Dave Costil's lab until his work with Project 96 in cyclists, he has repeatedly shown that the physiological factors that determine endurance performance are those constellation of factors that contribute to LT (however you want to determine it). In particular, Type I fiber composition, mitochondrial content, and ATPase efficiency. Of course, you are well aware of these factors, but for some reason feel one can will themselves to overcome them. I'm not sure how that is, efficiency is a rate of fuel utilization issue, and therefore something not under central control."
MY ANSWER:
I have only one problem with this conclusion. It is entirely model dependent. If you believe that oxygen and lactate determine performance then you will believe that this work PROVES that these variables DETERMINE performance.
But the only way to PROVE this statement is to change only those variables and none other and then to see if performance changes. But it is not possible to do this in a training study since whenever you train you change your self-belief; you alter your neuromuscular function etc, etc. So it is not possible to change only the metabolic and muscular variables without changing at the same time the other variables which the CG model predicts are important for changing exercise performance.
Thus what you conclude and what you believe will always be model dependent. That is why I said earlier that the only way really to differentiate between the two models is to use an pharmacological intervention that changes only the metabolic variables. Then you have to show that the effect occurs WITHOUT ANY CHANGE IN NEUROMUSCULAR FUNCTION. Because if the neuromuscular function changes then I would argue that the peripheral adaptation is acting by altering feedforward from the brain (not simply by making the muscles work better).
YOUR NEXT WROTE:
Your point:
"But this does not help explain the mechanism since in the marathon, athletes run at quite low blood lactate concentrations so that it is the avoidance of lactate accumulation rather than its accumulation which is associated with superior performance. Whereas perhaps in the 10km the accumulation of lactate is much greater"
Is easily explained by the availability of glycogen, and the rate limitations of ATP provision in the absence of glycogen. Are you saying the individual can run at 80% of VO2max in the glycogen depleted state? Of course not, that's why running at a pace that spares glycogen for the distance of the race is important. This is not necessarily the reason for the pacing/fatigue relationship at shorter distances (e.g. 5 km) but for 42 km, it is. Run out of glycogen and certainly a strong willed person can continue, but fast? No. This is the thermodynamics of performance and we all must obey the laws of physics, correct?
MY ANSWER:
Mark Allen ran a ~ 2:39 marathon during the Ironman after 180 km and 4 and a half hours on the bike which would have depleted his muscle glycogen content. We made some calculations that this would have been possible if he was burning about 1.3g of fat every minute on the run - this is about 30% higher than rates we measured in the laboratory. Improbable yes, but not impossible. It seems that some unique humans can run remarkably well on little glycogen. But this is not really your point.
Perhaps your point is that these variables could predict performance because the higher the running speed at the lactate turnpoint, the faster you can run whilst burning less glycogen thus you can go further, faster. This sounds entirely logical but it is also a very convenient explanation (as you would argue are my explanations for the CG model).
But I am not sure how this disagrees with the CG model which appears to anticipate what is possible in terms of glycogen availability and so to chose the appropriate pace early on in exercise (if allowed to).
YOU WROTE:
Why is it that for all out efforts, our maximal speed declines with time, in inverse proportion to lactate? It's not that lactate is the poisonous metabolite you refernced previously, but that glycogen metabolism is directly related to lactate appearance, and glycogen metabolism is refractory with time. The instance you start using glycogen the rate of glycgen utilization slows down.
Is this a protective mechanism? Maybe. Is it centrally controlled, almost certainly not.
MY ANSWER:
I don't know of any event in which humans voluntarily choose this form of exercise. So I am not sure that humans would have evolved the proper control mechanisms for this type of exercise. Even then there is pretty good evidence that performance in the Wingate test is centrally regulated - cadence comes down and glycolytic ATP is increased in hypoxic exercise showing that in normoxia, more work could have been done if needed if it had been possible to activate more glycolytic ATP production. But the brain chooses not to. This is more fully argued in our BJSM paper entitled Logical limitations etc.
YOU WROTE:
So, isn't it possible that if one exhibits an "endspurt" in the marathon, for example, it's likely the individual chose a pacing strategy that left enough glycgen in the tank to suppor the spurt. This would depend on the length of the spurt though. For shorter spurts, it may be that they simply didn't recruit all of their fast fibers (an argument you have made), but these last recruited fibers do not have the capacity to support extended efforts becasuet they are not oxidative enough. Therefore, they can support that last effort on some glycogen and ATP-PC. So, an experienced runner might choose a conservative strategy that would leave them with enough energy to give it full gas in the last little bit.
MY ANSWER:
Of course this is entirely possible that this is voluntarily chosen and we cannot yet design an experiment to disprove that theory (as far as I can think at the moment). But in a general sense, consciously or subconsciously chosen, the brain is in control. My point is that we have shown that there are some controls which clearly work subconsciously (oxygen and heat) and that these come into play long before the catastrophe develops.
In your model as I see it the athlete somehow consciously knows how to avoid the catastrophe or to delay the catastrophe so that it happens only the instance he crosses the finish line. But how would he consciously know this other than through (subconscious) feedback to his brain (about the changes in the variables that are about to cause the catastrophe - the "catastrophe molecules") which he follows and then thinks he did it consciously?
There is a saying - if you cannot measure it you cannot control it. Without measuring the "catastrophe molecules", the runner cannot regulate his performance to leave enough energy for the endspurt and still to avoid the catastrophe. Which brings us back to the CG model.
Incidentally I would not be surprised if humans subconsciously monitor a much wider range of sensory inputs than we currently conceive. We clearly have a very good clock that can measure the time that has passed during exercise. We were able to show that this clock could predict between exercise lasting 30 or 33 seconds. Also I guess that humans monitor either distance or speed since the really good athletes know exactly how fast they are running repetitions without being told the time. Since ants have the ability to measure distance by counting their steps (subconsciously - note), there is no reason why humans cannot do the same (if it has survival value).
YOU WROTE:
OTOH, what about the runner who is trying to hang with the leaders, and cracks at 5 k to go mark, and has nothing left. Are you saying if they were simply of stronger will they could overcome the rate limitation of metabolism and stay with the leaders? Would this individual still exhibit an endspurt?
MY ANSWER:
No. At this point his RPE is 19 or 20 and he cannot speed up. His RPE was telling him to slow down all along but he chose to override it. But once the RPE reaches 19 or 20, that is it. No endspurt.
A great example would be Paula Radcliffe in the Athens Olympic marathon. Our interpretation is that she overheated because she was trying to win the race and so ran faster than her heat losing mechanisms could accommodate. Her brain was shouting in her ears to slow down (she said she felt uncomfortable the whole way) but she willed herself to run with the lighter Japanese runner who was not as affected by the heat as she was 12 kg lighter (and thus producing much less heat when running at the same speed).
But when her RPE reached 19 and her core temperature 41.5 degrees C, the CG said - so far and no further or you will die from heatstroke.
Again - all arguments are model dependent. The goal of science is to keep researching the models to see which one can survive.
Warm regards,
Tim Noakes