BionicMan wrote:
Spoke wrote:
Noakes argues the sodium content of drinks makes little difference but that it is the amount you drink that matters. Drink too much and sodium levels drop. He advises drinking to thirst.
http://sweatscience.com/...-noakes-vs-gatorade/
First off, are you Noakes? I just want to understand since it's not clear and you have posted his information many times. Almost seems like a sales pitch.
Secondly, if you drink to thirst, it's too late, unless you are really slow at the event/effort. If I wait until I'm thirsty, I'm screwed. Period.
I have encountered the situation where I drank too much water leading to a 70.3 race without supplementing electrolytes. I got to into a hyponatremic state (or at least darn near it). Ended up in the med tent for over an hour. My caretakers even brought over the rookie caretakers to see what could happen to people when they were severely undernourished.
I received fantastic care (Racine 70.3) and 6 weeks later fixed my nutrition/hydration issues at IMKY when the temps were 92 during the run. I modified my full IM race based on what happened in Racine and I know it helped in IMKY.
Believe what you want but some of us have our own physical experiences to confirm the science.
No I'm not Noakes.
Here is a rather long post he made on this forum some years ago. I quote him because I remember the years before energy drinks. No one had any problems, people drank when thirsty, just plain water worked fine.
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Tim Noakes
Apr 21, 09 23:42
Post #6 of 231 (11948 views)
Re: Tim Noakes: we need you back for a moment [Slowman] [In reply to] Quote | Reply
Basic Physiology 1.
The textbooks say that sodium is the principal electrolyte in the extracellular fluid (ECF) which is a volume of 10-14 L depending on body mass. There is apparently little sodium inside cells. The measured concentration inside cells is about 5mmol/L versus 140mmol/L in the ECF. Indeed 40% of the energy we expend at rest is spent on pumping sodium to the outside of our cells. The amount of sodium in the ECF determines the ECF volume. This is because the body homeostatically regulates the osmolality of the body fluids so that there is a constant osmolality which produces a blood sodium concentration of about 140mmol/L in an ECF volume of 10-14 L. What the usual textbooks do not say is that whilst this relationship can well explain the ECF osmolality, it cannot explain the whole body osmolality. Thus in 1957 Edelman discovered that to explain the osmolality of the total body water (TBW - a volume of 35-42 L) there has to be substantially more sodium in the body than that measured in the ECF. But where is it since we “know” it is not in the cells (which are actively pumping sodium from the cells into the ECF to insure that the measureable intracellular sodium (Na+) concentration is very low)? Edelman used a radioactive sodium tracer and showed that the “sodium space” into which the tracer dilutes is much greater than the ECF sodium “space”. He called this new, previously undiscovered amount of sodium the “exchangeable sodium”. It constitutes about 50% more sodium than that present only in the ECF.
The next interesting observation is that in the 1950’s McCance produced a true state of sodium deficiency in humans. To my knowledge this is the only study in the published literature showing that a true sodium deficit can be produced in humans under experimental conditions. He had to go to inordinate lengths to achieve this. Three of the four subjects for his study had to live in his house whilst Mrs McCance fed them a sodium-free diet. Each day they sat in a hot room which produced prodigious sweating for 2 hours a day. By the fifth day they began to show evidence for a salt deficiency. The fourth subject a medical student at Oxford, a Miss Edwards, chose not to live in the McCance residence. A state of sodium deficiency could not be produced in her. Probably she was sneaking some extra salt in her diet.
The evidence for the salt deficiency was a set of symptoms that the subjects developed – absolute lethargy was a key factor – and a fall in blood sodium concentrations (hyponatremia). But the interesting observation was that to recover, the subjects needed to ingest far more sodium than the amount that would have been predicted on the grounds of the fall in their blood (and ECF) sodium concentrations. Thus it were as if something was preventing the fall in ECF sodium concentrations which should have fallen to much lower values based on how much salt the subjects had lost in their urine and sweat during the experiment. It were as if there was a store of sodium that had been called upon to maintain the ECF sodium at a higher concentration than in should have been if all the sodium in the body was only in the the ECF.
(For the purposes of this discussion we can ignore the fact that in the first few days of the experiment the blood sodium concentration was protected by the usual contraction of the ECF that occurs whenever there is an acute sodium loss from the ECF. But after day 4 the ECF began to expand despite an ongoing whole body sodium loss. This caused the blood sodium concentration to fall more sharply thereafter).
More recently there has been increased interest in this “hidden” sodium store. Balance studies of humans fed a very high salt diet showed that they were storing sodium in a site other than the ECF. Thus they did not simply excrete (in urine and sweat) the excess sodium in the diet; nor was it stored in the ECF causing an expansion of the ECF. It had gone somewhere else.
The authors proposed that the extra sodium is stored in the body in an “osmotically-inactive but exchangeable” form (Na) in which it is not measureable as ionic sodium (Na+) but where its presence can be detected by radioactive dilution techniques of the type undertaken by Edelman.
According to this theory there is a store of osmotically-inactive sodium (Na) in the body which can produce osmotically-active sodium (Na+) when it is required. Alternatively when the ECF Na+ concentration rises too high, there can theoretically be osmotic-inactivation of circulating Na+ which is then stored inside cells in the osmotically-inactive form (Na) to be returned to the ECF when it is required.
There are a number of modern observations that support McCance and Edelman’s findings that there must be more sodium in the body than is accounted for by the measured Na+ in the ECF.
For example, if subjects ingest less sodium and water than they lose in sweat during exercise, their blood sodium concentrations ALWAYS rise. This of course is not a fact that the sports drink industry wants you to know. Instead over the past 15 years that industry and its funded scientists have consistently argued that if you don’t replace all the sodium and water that you lose during exercise you will develop exercise-associated hyponatremia (EAH) (which can therefore only be prevented by ingesting a sports drink containing sodium (at low concentrations)). But this is simply not true. The blood sodium concentration ALWAYS rises under these conditions because sweat contains less sodium than does blood (and as I hope we will discuss in due course can contain essentially NO sodium in people living on a very low salt diet) so that more water is lost that salt. As a result the ECF contracts causing the blood sodium concentration to rise. Of course in a perfectly homeostatically regulated system this rise should not be more than a few mmoles/L but in some athletes in competition it can be up to 10-12mmol/L which is surprising and presently unexplained (although it might be explained by individual differences in the ability to osmotically-inactivate ECF Na+ as discussed below).
However we have shown that the change in blood sodium concentrations during exercise is highly individualized and cannot (probably) be explained purely by sodium losses in sweat and urine and changes in the ECF volume. Rather in our paper published in the Proceedings of the National Academy of Sciences in 2005 (and available for free from their website) we proposed that some of this variation must be explained by individual differences in the movement of sodium between the osmotically-active and inactive stores during and after exercise.
Interestingly the ability to deactivate Na+ during prolonged exercise and store it would delay the onset of thirst (which is stimulated by a rising ECF sodium concentration). Thus the presence of this store could have been a way in which our hominin ancestors were able to delay their thirst during long, hot, water-less hunts (see the thread on Why cannot scientists ever agree on anything?).
A tragic case supports this contention that there must be this internal sodium store. When Cynthia Lucero died after the 2002 Boston marathon because she had drunk too much of a sports drink (and retained that fluid excess within her body because she was also excreting too much anti-diuretic hormone – ADH), our calculations show that she simply could not have drunk sufficient to drop her blood sodium concentration as low as the value measured when she was admitted to hospital. Instead something else must have happened and one possibility is that she had also osmotically-inactivated some of her ECF Na+ at the same time transporting it into her cells causing her hyponatremia to be exacerbated. When we performed calculations on the data of fluid and sodium balance on patients treated by either ourselves or Dr Speedy in New Zealand for EAH, we came to the conclusion that some may have inactivated Na+ during the races in which they developed EAH with subsequent osmotic re-activation during recovery. But since we did not actually measure the process we cannot be sure.
What might this all mean. To return to the evolutionary perspective. It would make sense for humans evolving in a relatively salt-free environment to have an internal sodium store that could be filled in times of plenty and depleted in times of scarcity. Since salt is the most important regulator of the ECF volume and since if we cannot regulate the ECF volume accurately we die very quickly it makes sense to de-link regulation of the ECF volume from the daily sodium intake. How could we have survived if our lives depended on finding just enough salt each day in an environment in which salt was in scarce supply? Those who developed an internal sodium store under these conditions would be the most likely to survive.
If this store exists it might explain, in part, why it is so difficult to cause a true state of sodium deficiency in humans.
But more importantly, how does one measure a state of sodium deficiency in athletic humans? This is important since many contributors to this forum as do you yourself, believe that you develop cramps (or impaired performance) because of a sodium-deficit caused by large sodium losses in sweat. (Note that the model you use to explain this is catastrophic and non-homeostatic. It is based on the belief that the body has no ability to homeostatically regulate its losses and so will just continue to exercise until there is a catastrophic failure of function, in this case muscle cramps. But does it not make more sense to believe that evolution would have weeded out all these obvious system failures so that your problem is not likely caused by a system that is known to be homeostatically regulated and essential for life not just during exercise and the failure of which would have killed you long before you developed muscle cramps? Should we not look elsewhere for a better explanation than in a system that if it did not work perfectly we would not survive? Of course this is not how industry sees it. They want us all to believe that humans are weak and on the verge of a catastrophic biological failure that can only be prevented by the ingestion of their products, be they pharmaceutical products, sports drinks or other nutritional supplements).
The usual way to measure a sodium deficiency is by measuring the blood sodium concentration. But this is not fool proof since we know that the main cause of a low sodium concentration is a large increase in the ECF (and TBW) volume as occurs in EAH. Thus to prove a sodium deficiency you need to measure a low blood sodium concentration WITHOUT any increase in ECF volume. But this would not necessarily tell you what is the state of your internal sodium stores. The problem might be in the ability to activate intracellular osmotically-inactive Na.
But we can prove when a sodium-deficit does NOT explain your symptoms. Thus if you have symptoms and your blood sodium concentration is normal then BY DEFINITION your symptoms cannot be due to a sodium-deficit. Of course this is not something that you will hear from the sports scientists who acts as spokespersons for the sports drink industry. I recall hearing one well know (notorious?) such speaker for the industry say at a meeting in Australia that the presence of muscle cramps proved that the athlete had a sodium deficit even though the blood sodium concentration was normal. Of course this is not what we were taught in medical school. But then why cannot industry develop its own brand of physiology? Especially if it can find sufficient “scientists” to promote this novel brand of knowledge.
So the short answer to your question is the following: What was your blood sodium concentration at the time you developed your muscle cramps? If it was normal then the ingestion of salt either before or during exercise does not cure or prevent the condition by preventing the development of a sodium deficit. Rather it is acting in some other way that we currently do not understand.
That is enough for today. More on anther occasion. ""
http://forum.slowtwitch.com/...r_a_moment_P2297723/
And later in the same thread,
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Re: Tim Noakes: we need you back for a moment [Tom A.] [In reply to]Quote |Reply
No. What you are trying to do is to maximize your performance. All the published evidence shows that if you drink to thirst you will maximize that performance. If you want to maintain your ECF volume during exercise you have to drink way beyond thirst and ingest a large amount of salt, much more than is present in sports drinks. So you can't do it by just drinking a sports drink. We showed this years ago - published in the European Journal of Applied Physiology (B. Sanders et al).
So clearly the body does not need to maintain its ECF volume in order to maximize performance. Again the evidence is that the very best athletes are able to sustain large fluid losses during exercise (presumably with quite large drops in ECF volume) without any apparent impact on their performances.
More later.
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