Is Noakes wrong?

weeeee wrote:

One question that I do not remember him touching on is the fact that the blood goes through the heart first. Maybe that is why the heart can keep up aerobically and other muscles cannot. there may not be enough oxygen left. The body redirects blood flow to working muscles well the heart is the most important muscle and the body does a great job protecting vital organs in times of need. What effects would anaerobic actions have on the brain? if the brain and heart are not supplied with enough oxygen during exercise to what extent is it to much that it would do damage to them.

If I am understanding your question correctly, you are asking whether coronary tissue (the heart) takes enough of the cardiac output during high-intensity exercise that it compromises oxygen delivery to the muscles? If I got that right, I believe the answer is no. Ditto for blood flow to the brain. In the case of the heart, it does require more blood flow as intensity increases, but it is a small enough mass that the effect on total cardiac output is negligible. In the case of the brain, the demand for blood flow doesn't increase during exercise, so the relative amount of flow decreases (while the absolute amount stays the same).

However, Jerome Dempsey's lab has done some interesting work suggesting that the diaphragm might require enough blood flow at intensities close to VO2max that it effectively does limit blood flow to working muscle. This "stealing" of cardiac output can occur with this tissue because it is a large muscle mass that vasodilates in proportion to exercise intensity. One final note is that this has only been shown to be true in elite/sub-elites at or near max.

Most of what some might call controversial is supported by strong evidence, which Noakes is careful to cite. At this point the central governor is theory yes, not fact, and Noakes presents it as such. There are some obvious and even glaring problems with the oxygen delivery paradigm of old which cant be overlooked. Central fatigue is a reality; and yes, running can come to a halt even when there is plenty of oxygen and fuel left in the active muscle. To think running is just about heart rates and lungs, getting oxygen to mitochondria is these days akin to thinking the earth is flat.

Scientician

i guess he states that, but the point is that the same concept is occuring, but it is in the form of lactate and a proton rather than in the acid form of HLa. His methodolgy is flawed, he chases the protons that are occuring during ATP hydrolysis, he states that lactate actually diminishes acidosis by forming, but he fails to recognize the law of electrical neutrality, when the Lactate forms, the strong ion difference becomes more negative which causes a flux of Hydrogen from one system to another system in this case extracellular to intracellular, if there is a flux of H into the cell in order to make up for the negative H ion, then there is an efflux of OH out of the cell at the same time leading to greater acidosis. So while lactate may not directly cause acidosis (according to Robergs), we cannot merely look at metabolism and try to quantify one reaction creating a proton and one taking away a proton to determine acidosis or alkalosis. The entire system must be considered, one proton is like spitting in the ocean.

correction on the OH leaving the cell, the Lactate formed is negative ion which in turn causes flux of positive H into the cell to maintain electrical neutrality

who cares!!!! i am tired of master and phd students spouting off on this message board about exercise physiology. if you want to talk exercise physiology ad nauseam go to sportsci.org or the ACSM conference in New Orleans...Thank YOU

If you don't want to read it....don't click on the thread.

I'd much rather have this than the typical bashing of runners or "Top 10 hottest runners in Big 12 indoor DMR races" threads.

this is a runners message board not exercise physiology board. this is not a place to post or learn about exercise physiology. It is a anonymous runners message board!

The central governor was not elected by popular vote.

Neither is Noakes hot.

1) Most researchers (Bengt Saltin, others) agree that it is *not* the accumulation of H+ (and certainly not lactate) that limits maximal oxygen consumption. Instead, the #1 \"suspect\" is cardiac output, or how \"fast\" you can deliver metabolites to working muscle.

2) That said, there are any number of steps that could limit maximal oxygen uptake (lung surface area, diffusion rates across the alveoli/cell membrane, others). Certain highly \"selected\" organisms (racehorses) are limited more by \"hardware\" limitations (such as lung surface area) - humans do not.

3) Noakes\' theory, while compelling, has little formal evidence to support it. This is the major arguement put forth in academic journals to counter Noakes\' theory.

4) Noakes\' theory is interesting because in his model, maximal VO2 is a by-product of the mechanical work that your body (due to muscle properties, e.g.) can accomplish, not the major determinant of the mechanical work that your body can accomplish.

5) It is important to distinguish those factors that contribute to maximal oxygen uptake (VO2) from those factors that contribute to muscular fatigue. Factors such as H+ (derived from lactic acid dissociation and other sources) contribute to fatigue, but not to maximal oxygen uptake.

true that wrote:

I wonder what the lydiard group (Nobby, HRE and others) would think of the topic?

Here's a guess. The types of training changes that take place primarily in the muscles, lungs, blood, connective tissues, etc. are the aerobic-type base training, and to a much lesser extent the hill training. There's huge room for improvement in these areas. The results of anaerobic training take place primarily in the central nervous system, and you can only get so much improvement out of them. This is why you need a lot of the first and much less of the latter.

It's interesting how some 800 - 1500 meter runners attempt to buffer the acid levels in their blood with sodium bicarbonate to delay fatigue. If the central governor was the only limiting factor then that would not work.

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.

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.

1: J Appl Physiol. 2007 Feb;102(2):781-6. Epub 2006 Oct 26.Click here to read Links

Maximal oxygen uptake is not limited by a central nervous system governor.

* Brink-Elfegoun T,

* Kaijser L,

* Gustafsson T,

* Ekblom B.

Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.

We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (VO2 max). We measured cardiac output (Q) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting VO2 max. Eight well-trained men (age 24.4 +/- 2.8 yr, weight 81.3 +/- 7.8 kg, and VO2 max 59.1 +/- 2.0 ml x min(-1) x kg(-1)) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured VO2 max, maximal Q, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently VO2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.

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?

statistically this whole study is flawed. did you use nonparametric statistics on such a small sample? there is no way you met the criteria for a normal distribution with 8 well trained subjects....how can you infer from such a small sample anyways...we know VO2max is quite variable due to genetic variation...

what about the numerous H+ pumps within the cell between the mitochondria & cytoplasm and cell membrane & interstitial fluid? did you take that in effect? also are you talking about cell H+ concentation or blood H+ concentration or interstitial H+ concentration?

well a few of the strong ions in the body are sodium, potassium, and calcium (all cations+), then there is chloride and Lactate for instance (anions -), well within a system there must be electrical neutrality, so that means all anions=cations. well when lactate is formed for instance, you increase the number of anions in the system (being the cell), as the ion difference becomes more negative than there is and influx of H (cation) in order to satisfy this law. to get to your question, as you load more sodium (cation), you increase the SID (strong ion difference) ion difference more positive, so H is effluxed to maintain a more basic pH.

but H efflux is a process which requires energy and therefore does not just magically happens...we know the H efflux can be altered with training but we don't now exactly how?