Is Noakes wrong?

actually H diffusion doesnt always require energy, malate aspartate exchange, glycerol phosphate. passive diffusion across the sarcolemma

JP2 wrote:

otter, the "fatigue" to which Noakes refers in his central governor theory is quite different from muscular fatigue. Noakes is talking about a general feeling of lethargy (that limits your maximal performance); muscular fatigue is the cumulative effect of prolonged exercise that limits endurance performance.

The bicarbonate supplementation would affect the second concept, not the first - that is, if the individual can get over the raging bout of diarrhea caused by the *huge* amount of sodium bicarbonate that he/she must consume to actually see an effect.

I understand it better now. I guess I better read over the Naokes chapter again because I must of misinterpreted what he was saying. I thought he was casting the muscular fatigue theory aside in favor of the central governor theory. I didn't realize he had separated the two. In that case I've side tracked the conversation.

First, Im astounded anyone might consider a physiology conversation inapproriate for a running website. As if

suggesting 140 miles/week isnt a physiology discussion...

I think the main point of Noakes' alternate theory is that

the old model is incomplete. The primary question to ask is, are there limits in endurance exercise which are clearly unrelated to oxygen delivery and fuel utilation?

yes, of course there are.

1. the central fatigue data is very clear: change your brain chemistry, limit or enhance your endurance capability.

2. VO2 drift / VO2 slow component data suggest variable VO2 uptake options for any velocity/power requirement.

3. increases in peak power/ motor unit synergy via neurological adaptations as occur with interval or power training, each altering "running economy", by extending fatigue resistance without altering VO2peak. Contractility issues.

4. peaking/tapering data, which suggests a dissociation betwen oxdiative enzyme levels in the active muscle, and endurance performance.

5. various studies indicating that fatigue resistance can often be enhanced/ RPE reduced despite a higher oxygen cost to the exercise. Reminds me of the Olympic Training Center physiologists who told a young Lance Armstrong to lower his cycling RPM to save oxygen cost! It is not just about oxygen.

I could list several more examples, but if you cant get past these few, you havent really got a model.

Is it really that big of a step to suggest some control mechanism oversee the numerous active cooperating subsystems in exercise? Or that evolutionary considerations like survival, maximizing adapation to exercise, minimizing/distributing stresses across the various working systems might supercede oxygen delivery considerations?

I don't see how sodium bicarbonate loading can possibly work. As well as the enourmous upset to the digestive system which is reported from this silly practice, any buffering advantage would surely be negated by the weight gain of ingesting large amounts of sodium.

So you either get the shits and become dehyrated, or you have a raging thirst and gain several pounds of water retention.

Scientician wrote:

I don't see how sodium bicarbonate loading can possibly work. As well as the enourmous upset to the digestive system which is reported from this silly practice, any buffering advantage would surely be negated by the weight gain of ingesting large amounts of sodium.

So you either get the shits and become dehyrated, or you have a raging thirst and gain several pounds of water retention.

Well, numerous studies show bicarb loading works. Usually for short distance events say 800m. Go to PubMed and you will see variations of bicarb loading.

Peter Snell just published a paper in MSSE taking on the central governor hypothesis. Snell's paper shows that the central governor cannot be correct.

luv2run wrote:

Scientician wrote:

I don't see how sodium bicarbonate loading can possibly work. As well as the enourmous upset to the digestive system which is reported from this silly practice, any buffering advantage would surely be negated by the weight gain of ingesting large amounts of sodium.

So you either get the shits and become dehyrated, or you have a raging thirst and gain several pounds of water retention.

Well, numerous studies show bicarb loading works. Usually for short distance events say 800m. Go to PubMed and you will see variations of bicarb loading.

I should add that many studies show that things like sodium citrate also work in this capacity leading the thinking that it might be the sodium playing a large role. Makes some sense because Na is a + ion.

I do not think the debate between the supporters of "classical" theory and Noakes' theory is something that will be resolved with one/a few papers - there are just too many questions that need to be answered by creative individuals with new ways of observing the cardiorespiratory system.

Moreover, regardless of the outcome, Noakes' theory has pushed academics to re-examine a model that they took for Truth, and that's always a good thing.

For anyone who has read the full Snell paper - did they use 52 or 156 for their "n" when computing statistical significance? It appears from reading only the abstract that the statistics were run treating each of the different participant trials as a separate data point. I'm not sure if I agree with this methodology, since the lack of a plateau has been argued to be attributable to individuals, not trials.

Robergs et al have answered your question thus:

"We are indebted to the prior work of Lindinger et al. (8) for teaching us to recognize the importance of the strong ion difference (SID) in understanding proton balance and activity. Nevertheless, we feel that it is important to clarify an underlying message contained in this editorial.

The question crucial to the main purpose of our original manuscript is "Where do the protons come from?" Clearly, protons do not come from the lactate dehydrogenase reaction and therefore the production of lactate. However, the Lindinger et al. (8) presentation of the physical chemistry pertaining to the acid-base balance of aqueous solutions indirectly argues that there is no evidence for proton consumption and release from chemical reactions and that changes in cellular or blood pH are caused predominantly by changes in strong ions (their Eq. 7). We do not agree.

Despite the solid basic science foundation of the SID concept, we feel that it alone does not answer the question of where do the protons come from. If it did, then the answer is water, and this opposes what we know of the organic chemistry of the reactions of intermediary metabolism. Certainly, the SID approach can explain the final aqueous solution pH when given component changes for a given proton release condition of cellular metabolism. Thus we feel that to best comprehend the acid-base changes associated with intense exercise, you need a combination of a stoichiometric approach fine tuned by the SID method. For example, given the metabolic proton release conditions of intense exercise, the SID computations would predict the final muscle pH. Such a scenario is presented in our Fig. 17 (9; p. R513), where the final pH resulting from this imbalance in proton release and consumption would adhere to the SID concept."

luv2run, do you really take these studies showing improvements from excess sodium ingestion seriuously?

Don't you think that the best 800m runners are able to store the optiumum level of sodium from their normal diet?

Seb Coe's World Record lasted 16 years. Wilson Kipketer's World Record is nearly 10 years old.

You forget that Coe was taking EPO before it was even invented.

I just want to point out the volume of sodium bicarbonate we're talking about here. I'm not encouraging or discouraging the use of sodium bicarbonate, but I think a mental picture here would be useful.

Study: Effects of sodium bicarbonate ingestion on prolonged intermittent exercise.

Authors: Price M, Moss P, Rance S.

Findings (copied from abstract): Peak power expressed relative to sprint 1 demonstrated a significant main effect between trials (P < 0.05). Sprint 2 increased by 11.5 +/- 5% and 1.8 +/- 9.5% for NaHCO(3) and NaCl, respectively. During NaHCO(3), sprint 8 remained similar to sprint 1 (0.2 +/- 17%), whereas a decrease was observed during NaCl (-10.0 +/- 16.0%). CONCLUSION: The results of this study suggest that ingestion of NaHCO(3) improves sprint performance during prolonged intermittent cycling.

AMOUNT OF SODIUM BICARBONATE CONSUMED: 0.3 g/kg

I weigh roughly 79 kg.

79kg *0.3g/kg ~ 24g of sodium bicarbonate

Say sodium bicarbonate comes in 650mg tablets (a cursory search showed tablets ranging from 300-650mg). That's 37 tablets.

no it is the bicarbonate that is loosely binding with the H+ ions; which then break down into water & carbon dioxide, which I believe is breathed off at the lung. correct me if I am wrong..

otter wrote:

gf79 wrote:

Otter

contrary to what most think about sodium bicarbonate buffering, it is actually the sodium that is providing the buffer, the sodium is a cation, which in turn raises SID, reducing H concentration in the cellbut like JP2 said, local fatigue and central fatigue are 2 different stories.

So is it the sodium that is nuetralizing the Hydrogen Ion in the muscle cells? Do I have that right?

Acid Base regulation is not completely understood, i am not saying i am right and thats it, but the Peter Stewart model approaches acid base much different that the traditional view. Bicarbonate loading isnt going to do much, the amount of bicarbonate in the body is so large that any addition will not improve the buffering capacity. I can not tell you in one sentence the answer to this hypothesis, but reading the Stewart approach to acid base will help understand this approach. The idea is that H, OH, Bicarbonate, and Carbonate are dependent variables that cant change with out another independent variable changing. The independent variables are the SID, PCO2, and total weak acids in the body (mainly proteins and phosphates), when these 3 things change within a system it is responsible for changes in the dependent variables. from this perspective, the addition of stong acids will alter SID and change H concentration. There is much work to be done to truly understand acid base.

Letsrun.com I wanted to add this note that Tim Noakes wanted posted to the site. Below is a copy & paste of his Email to me:

Dear John,

Perhaps you could add the following comments to the site.

I really appreciate the attention that has been spent on the Central

Governor Model. It is however clear that very few have read the full

exposition of the model in a series of articles in the British Journal

of Sports Medicine in 2004 and 2005. Some of those articles can be

accessed for free and it might be helpful if any one who believes he or

she is an expert on the Central Governor Model to first read those

articles. To base an opinon on a brief description in a book that was

written 5 years ago does not seem a good idea. Ideas evolve and my

understanding of the Central Governor Model is very different today from

what it was in 2001 and 2002.

The statement is frequently made that there is no evidence for this

model. This is quite incorrect. There are now a host of studies which

can only be interpreted according to the Central Governor Model and

which absolutely are incompatible with the traditional peripheral

fatigue model. There are 2 crucial findings. First that any exercise

performance is regulated "in anticipation" so that the brain adjust the

behaviour during exercise (usually by slowing down) well before harm

develops. It is clear that only an intelligent complex system is able to

modify behaviour in a predictable way in anticipation of what might

happen if no such behaviour change were to occur. So the brain does

not allow the body simply to continue to exercise until some catastrophe

(exhaustion or extreme fatigue) occurs. Your readers might wish to read

our recent (2006) paper in the Journal of Physiology, authored by Ross

Tucker. This study clearly shows that the perception of fatigue is used

by the brain to modify exercise behavior specifically to insure that

harm does not occur sometime in the future (of the exercise bout).

The second point that is not compatible with the traditional model is

the finding that not all the muscle fibers are ever active during any

form of exercise. If not all the fibers are active during exercise, then

the brain regulates the exercise performance (as fully argued in the

BJSM articles). For if peripheral fatigue was the regulator, why does

the brain not simply activate more muscle as so continue to exercise

until all the muscle fibers were exhausted? The answer is that if this

were to occur, no one would survive a single exercise bout.

Those who focus only on the VO2max and oxygen delivery to muscle as

evidence for against this model ignore all the evidence from other

studies showing that the traditional model simply does not explain

enough to be considered a realistic explanation of what happens during

exercise and the nature of the controls that determine our exercise

behaviours.

The Central Governor Model is not perfect but it is currently the only

model that can reasonably explain so many of the most obvious features

of running including the fact that we start at different paces when we

run races of different distances; why we can produce an end-spurt when

we are the most exhausted (near the end of a race); why drugs like

amphetamines can improve performance remarkably even though they do not

act to prevent "peripheral fatigue" - Amphetamines clearly show that we

all run with a biological reserve that can be (very easily) accessed

when we interfere with the higher brain control mechanisms; and why

fatigue is never absolute. Even the most exhausted marathon runner can

still walk to his car etc.

I remain astonished that some can believe that the control of exercise

performance lies with the heart and the muscles and that the brain can

play no part. That seems far more unrealistic than anything I have ever

proposed.

Best wishes and keep the debate going,

Tim Noakes.

Dear John wrote:

The Central Governor Model is not perfect but it is currently the only model that can reasonably explain so many of the most obvious features of running including the fact that we start at different paces when we run races of different distances;

This is a PERFECT example of how silly some of Noakes; reasoning is. My model is the ONLY one that can explain things!

Hey Tim, would you like to know why we start at different paces when we run races of different distances? Because we're not IDIOTS, that's why. We've actually done this stuff before. When we were kids and we ran our first 5k race, we all took off at sprint speed, only to be slowed down by the inevitable fatigue in our bodies. Why didn't our Central governor stop us then? Now that we've learned a few things, we start off at a speed we might actually be able to hold.

Why can we sprint when we're tired at the end of the race? For the same reason we could sprint when we hit the midway point of the race. Because we have the energy in us. The only reason that we don't do it during the middle of the race is that, once again, we're not idiots

But not to Tim. It's not a conscious decision to him. Nope, the mysterious "Central Governor" is dictating our every action. A nice, somewhat reasonable model made to sound ridiculous by its creator's insistence that it is the "one true way"

Average_Joe wrote:

When we were kids and we ran our first 5k race, we all took off at sprint speed, only to be slowed down by the inevitable fatigue in our bodies. Why didn't our Central governor stop us then? Now that we've learned a few things, we start off at a speed we might actually be able to hold.

Why can we sprint when we're tired at the end of the race? For the same reason we could sprint when we hit the midway point of the race. Because we have the energy in us. The only reason that we don't do it during the middle of the race is that, once again, we're not idiots

Noakes would argue that the central governor did stop us as kids, hence why we slowed down. Were we tired? Yes, but that is also because our bodies dont have as many muscle fibers. I dont think his argument is bad at all, he raises many valid points. And his argument makes perfect sense for the end of a race. Most people, myself included, feel that we might not make it to the end, and yet, with one lap, one mile etc... left we can lay out another gear. His model makes way more sense than you saying that we save it for the end. Sure we know how to pace better, but when you see someone add that extra gear at the end, it makes sense to me to assume something has to be going on.

More accurate for me to have asked, "Why didn't our central governor prevent us from starting off too fast then"?

It was in response to this

"including the fact that we start at different paces"

I don't come on here to say that there is no central governor or that Noakes is "wrong", just that his reasoning for supporting it is often quite silly. Perhaps he's just not able to express himself correctly sometimes.

But the reason that we start at different paces in races of different lengths is that we have experience. I start off a marathon at 6:xx per mile pace (and do NOT try to run a 60 second first 400 meters) because I know it's not an 800 meter race, not because my "Central Governor" is making me.

It sounds like you don't really disagree with the "Central Governor" model, just with what the Central Governor is. Noakes has a lot of solid evidence undermining the peripheral fatigue theory, but there is little to support his assertion that the central governor is unconcious. In every study he interprets he makes the assumption that every volunteer put out a truly maximal effort in every trial. That is unreasonable. To say that subjects push themselves just as hard when there are 5 trials left as they do on the last one seems naive.