I have only just started reading the book and was going to write about it after I finished it, but I came across an article in Running Times magazine that excerpts Chapter 2 of Noakes' book. You can read the article in Running Times here, but I think this is really important so I am posting the Chapter 2 excerpt from Running Times:
Drink to Thirst
An Excerpt From Tim Noakes' New Book WaterloggedBy Tim NoakesEDITOR'S NOTE: Tim Noakes, author of Lore of Running, has a new book out that will surprise many readers and perhaps even offend some. In writing Waterlogged, Noakes pored over seemingly every bit of research ever conducted on hydration and performance and concluded that much of what we've been told on the topic is wrong. Noakes says we've been sold a "dehydration myth." In the following excerpt from Chapter 2 of Waterlogged, Noakes explains the physiology of dehydration and how research on the topic often contradicts conventional wisdom.
As featured in the July 2012 issue of Running Times Magazine
"Dehydration" is a physiological term indicating a reduction in the total-body water content. Once the reduction in body water causes the solute concentration, especially the sodium concentration (actually the osmolality), of the blood to rise, the brain detects the change and develops the symptom of thirst. This is a normal biological response that has evolved in all creatures to ensure that they maintain a constant body water content at least once each day, usually after the evening meal.
When fluid is lost from the body, either in sweat as a result of exercise or from the gastrointestinal tract in diseases like cholera or typhoid, the concentration of solutes, especially sodium in the blood, rises, causing the blood osmolality to increase. This rise stimulates receptors in a special part of the brain, the hypothalamus, which in turn interact with three other nuclei, which increase secretion of the hormone AVP/ADH (arginine vasopressin, also known as antidiuretic hormone), whose function is to increase water reabsorption by the kidney. In response to the action of AVP/ADH, the kidney reduces the amount of fluid secreted. As a result, urine flow into the bladder is reduced. Nucleus 5 also stimulates the cells in another part of the brain, the cingulate gyrus, which increases thirst. As a result, the desire to drink is increased and water (and sodium through the action of aldosterone) is reabsorbed by the kidneys. The result is that the blood osmolality returns to its homeostatically regulated value, switching off the desire to drink.
Thus the only symptom of dehydration is thirst. If, however, the thirst cannot be quenched because fluid is unavailable, as occurs in those stranded in the desert, then the body activates a series of emergency adaptations that prolong life for a period but ultimately cause death when all the major bodily organs fail, leading probably to cardiovascular collapse.
The remarkable achievement of the sports drink industry was that it convinced recent generations that these control mechanisms do not exist. Instead, we've been told, all athletes must drink to ensure that they do not lose any body weight during exercise. But there are no known receptors that regulate thirst by monitoring the extent of the body weight lost or gained. In addition, this myth also convinced exercisers that they could become dangerously dehydrated not just when lost in the desert for more than 48 hours but when running for a few minutes in, for example, a big-city marathon, during which they have unrestricted access to as much fluid as they might wish. I am unaware of any other human activity in which so much fluid is freely available as in a modern big-city marathon. How is it possible under these circumstances to become dehydrated except according to a definition that has no proper biological basis?
In response to the body's pure fluid loss, the usual human living in a Western society with easy access to fluid will develop the sensation of thirst and will usually drink fluid as a result. Receptors in the back of the mouth and the esophagus, but particularly in the stomach, then detect how much fluid has been ingested. Once the stomach is filled, the desire to drink is temporarily curtailed but resumes as the stomach empties, especially if food is eaten at the same time. Eventually enough fluid (and sodium) has been ingested to return the solute concentration of the extracellular fluid (ECF) back to the normal range. Since the ECF (and hence whole body) osmolality is then within the homeostatically regulated range, the symptom of thirst is switched off; as a result, most people will stop drinking.
SYMPTOMS OF INADEQUATE FLUID INGESTION
When athletes sweat during exercise, they lose both water and electrolytes, especially sodium, in varying amounts. Because sodium is the dominant solute lost in sweat, and since the sweat sodium concentration is always less than its concentration in the ECF, sweating will always cause a greater loss of water than solute from the ECF. As a result, in the absence of any fluid ingestion, sweating must cause the ECF solute concentration to rise. Ultimately this will change enough to stimulate thirst in everyone.
However, this response is highly individualized--some athletes will become thirsty at quite low levels of weight loss, whereas the thirst of others allows them to lose up to 12 percent of body weight during ultra-endurance exercise, as in the Ironman Triathlon, without developing any more severe symptoms of homeostatic failure. To understand the real symptoms that develop when people drink less than their thirst dictates, we need to look at those studies in which participants are forced to exercise for prolonged periods while they have access to less fluid than their thirst dictates. These people develop both an unquenched thirst and additional symptoms caused by a progressive biological failure due to a falling total-body water content. One of the original studies to define these symptoms was performed in the Nevada Desert during the early years of World War II.
The Nevada Desert study reported the sequence in which symptoms of unreplaced water losses, since conveniently termed "dehydration," developed. Of course, one can equally argue that some of these symptoms are due to an absence of drinking and the knowledge that drinking will be allowed only when the activity is completed. We now appreciate that the brain responds not just to biological stimuli but also to what it anticipates will happen in the future. Knowing that a demanding activity must be performed without fluid replacement will cause all symptoms to be experienced more intensively.
The head of the Nevada Desert study wrote, "The order of appearance of the signs and symptoms is particularly characteristic. Thirst is noticeable very early, but does not increase much in intensity as the water deficit continues to increase. Vague discomfort, not experienced by controls who drank water, gradually becomes defined in the flushing of the skin, heat oppression, weariness, sleepiness, impatience, anorexia and dizziness. At about the time that the walking pace can no longer be maintained, dyspnea, tingling and cyanosis, as well as a suggestion of tetany, appear. Still later, a man cannot stand alone, either because of impaired coordination or fainting." The Nevada researchers also recognized that the inability to stand was due to the development of a low blood pressure, postural hypotension: "The inability to continue muscular work (exhaustion) seems to be a consequence of circulatory inadequacy. Temporarily, the movements themselves help in some degree to improve the return of blood to the heart. When the movements stop, failure is suddenly imminent; some persons faint at this point. Lying down promptly relieves the circulation and the symptoms."
Another Nevada Desert researcher described his experiences: "Aside from thirst, the symptoms of dehydration were in large part indications of impending collapse. A vague, generalized discomfort and a feeling of restlessness followed closely the stage of 'mouth thirst.' There was a great desire to sit or lie down. Drowsiness was often noted. A feeling of heat oppression was a frequent complaint; it was often more serious than thirst. Muscular tiredness grew more acute progressively, although manual coordination was not measurably altered. Among the signs of approaching collapse, the most reliable were a rising pulse rate and a rising rectal temperature. Sometimes there was a noticeable dyspnea. Frequently, the subject was cyanotic and his face became flushed. In the exhausted state, tingling in hands, arms and feet occurred in some cases."
So described are the real symptoms that develop when people exercise in extremely hot conditions without any chance to replace their fluid losses appropriately. Of course this is not what happens in modern marathon races in which athletes exercise usually for relatively short periods of a few hours in much cooler conditions while they have access to unlimited amounts of fluid.The extensive research of the Nevada Desert research group established a range of findings that subsequent research has not contradicted. Not all these findings have received equal exposure over the years. Those findings that dehydration may not be quite as dangerous as the dehydration myth proposes have not been as widely propagated as those supporting the value of fluid ingestion during exercise. The principal findings were as follows:
1. Even when given free access to adequate fluids, people drank less than they lost in sweat or urine. Hence they developed "voluntary dehydration," which was corrected only after exercise and when food was eaten, especially at the evening meal.
2. In the experiments in which groups of soldiers either drank freely or not at all during day-long marches in desert heat, a much greater percentage of those who did not drink during exercise were likely to terminate the exercise bout prematurely.
3. Subjects in the groups who did not drink during these marches usually stopped when they had lost 7 to 10 percent of their starting body weights. In this state they experienced postural hypotension (EAPH), but after they experienced the symptoms of fainting caused by EAPH, they recovered rapidly within minutes of lying down and ingesting fluid.
4. Dehydration reduced neither the sweat rate, nor the rate of urine production during exercise. However, the rectal temperature and heart rate rose as linear functions of the level of dehydration. The body temperature rose about 0.2 to 0.3 degrees C for each 1 percent level of dehydration.
5. There were no immediate health risks associated with the level of dehydration of 7 to 10 percent present at the termination of exercise in those who did not ingest any fluids during exercise. The authors considered that only at very high levels of dehydration (15 to 20 percent) was there a serious risk of organ failure.These studies, which clearly established the value of fluid ingestion during exercise, had little impact on the athletic community. Instead, for at least the first two decades after the publication in 1947 of the book describing these studies, athletes continued to be advised not to drink at all during exercise. Only after the development of Gatorade and the publication of relevant studies was proper attention finally paid to the use of fluid ingestion during exercise.
Another set of U.S. Army studies occurred soon after American troops began to fight in jungle heat in Burma during World War II. It soon became apparent that on first exposure to conditions of high temperatures and suffocating humidity (caused by the transpiration of water from the leaves of the jungle vegetation), soldiers were essentially incapacitated but began to adapt within a few days. To study the special physiological challenges posed by jungle heat, a special research group was established at Fort Knox, Ky., where a "hot room" was built in which the environmental conditions present in either the desert or the jungle could be reproduced.
These studies showed that the major cause for incapacitation on first exposure to both desert and jungle heat was the development of EAPH, beginning the moment the exercise bout terminated. This disappeared within a few days of repeated heat exposures. An important contribution of these studies was to establish the condition of EAPH as a cause of post-exercise collapse and to show that this condition was not simply due to dehydration, as would become the industry-driven mantra after the 1980s.
These researchers were also interested in the psychological effects of exercising in the heat without fluid replacement. Thus they wrote the following: "An important change which the chart does not show was the actual condition of the men, their low morale and lack of vigor, their glassy eyes, their apathetic, torpid appearance, their 'don't-give-a-damn-for-anything' attitude, their uncoordinated stumbling, shuffling gait. Some were incapable of sustained purposeful action and were not fit for work. All they wanted to do was rest and drink." This shows that the symptoms of dehydration are largely of a psychological nature, the goal of which is to stop the athletes from continuing to exercise. It's a built-in mechanism to prevent bodily damage.
Scientists at the United States Army Research Institute of Environmental Medicine have conducted a study to evaluate the influence of unreplaced fluid losses on the development of various symptoms. The study used fluid restriction and exercise to produce four levels of loss of body weight (0 percent, 3 percent, 5 percent, and 7 percent) and showed that the intensity of sensations of thirst, tiredness, weakness, lightheadedness, weariness and dizziness increased linearly with increasing levels of weight loss. But thirst was the symptom that was felt with the greatest intensity.
The study is important for two reasons. First, it shows that thirst is the symptom that best indicates the presence of a fluid deficit caused by exercise and fluid restriction. This conflicts with the myth developed in the 1990s that thirst is an inadequate guide to the fluid needs of the body. Rather, in this study, a weight loss of 7 percent produced near-maximal thirst sensations.
Second, during competition, some athletes develop levels of weight loss in excess of 7 percent without developing the same intensity of symptoms experienced by the participants in this study. This shows the individuality of the thirst response. Athletes who lose substantial amounts of weight during exercise without becoming as thirsty either prevent a large increase in the solute content of their ECF (as a result of internal relocation of body sodium stores) or because their brains are less sensitive to any large changes in ECF solute concentrations.
These individuals are, in fact, dehydrated because they have lost total-body water; however, this water loss is easily replaced by drinking normally, often with a meal, after the race. It does not lead to myriad ill effects, as the sports drink industry would like us to believe. In fact, the best endurance athletes in the world are typically those who lose the most weight during exercise, who have the least thirst and who run the fastest when they are quite markedly dehydrated, perhaps because the weight loss is beneficial to performance, just as the avoidance of thirst must have been an advantage to early hominid persistence hunters.
More recent studies further confirm that the sensations of thirst are always sufficient to ensure proper hydration both before and during exercise. Participants who began exercise in a dehydrated state (-3.4 percent BW) drank 5.3 times as much fluid during 90 minutes of exercise than when they started exercise normally hydrated such that, provided they were able to drink during exercise, it made no difference whether subjects began exercise dehydrated or normally hydrated; by the end of exercise their core body temperatures, heart rates, blood osmolalities and thirst ratings were the same.
You can get the book from Amazon.com:Copyright © 2012 Running Times Magazine - All Rights Reserved.FLUID LOSS AND PERFORMANCE
If fluid loss leads to thirst, why do some of the best competitors finish endurance races in quite advanced states of fluid loss? Time and again, studies, even those by researchers expecting different outcomes, have shown that the runners who are the most dehydrated, as measured by percentage of body weight loss, run the fastest. Two examples that valdiate this conclusion are the results of the 2000 and 2001 South African Ironman triathlons and the 2004 New Zealand Ironman Triathlon.
The largest body weight loss in these studies was 12 percent in an athlete who finished the race in ~720 minutes. The five fastest finishers in the South African Ironman all finished in less than 9 hours and all lost 6 to 8 percent of their body weights during the race. Three years later, this relationship was confirmed in finishers in the 2004 New Zealand Ironman Triathlon.
Why would the fastest endurance performers exhibit the highest percentages of body weight loss during their winning performances? Perhaps clues exist in the phenomenon that has been termed voluntary dehydration. Exercising humans do not drink to maintain a constant body weight every moment of the day. Rather, we develop a water deficit termed voluntary dehydration by drinking less than the amount of weight (assumed to be due entirely to water loss) that we lose as sweat during exercise. Only at mealtimes do humans increase water intakes and so correct exactly the fluid loss developed in the hours between meals.
There are a number of probable explanations for this phenomenon. First, not all the weight lost during exercise is fluid that needs to be replaced immediately. For example, there is an inevitable loss of weight caused by the fuel, either fat or carbohydrate, that must be burned in order to provide the energy needed for the exercise. The analogy would be the fuel in a motor car that is burned as the car travels--the result is that, until it is again filled with fuel, the car loses weight in direct proportion to how far it travels.
An additional factor is not covered by this car analogy. It is that the carbohydrate that is burned during exercise may be stored in the muscle and liver in a complex that includes a substantial mass of bound water. It has been argued for some years that each gram of carbohydrate used during exercise releases up to 3 grams of water. This water acts as a fluid reserve that is restored only when the body's carbohydrate stores are again filled 12 to 36 hours after exercise. Because the body can store 500 grams of carbohydrate (with an associated 1,500 grams of water), this would explain why humans might lose at least 2,000 grams of weight during exercise without any real water loss. Indeed, studies of this problem have shown that exercising humans can lose at least 1,000 grams without a measureable change in their total-body water content.
Thus the term "voluntary dehydration" may not accurately describe what happens in athletes who lose less than 1 kg during exercise because they may not have lost any body water and hence are not dehydrated. But athletes who lose more than 3 kg during prolonged exercise probably do show a reduction in total-body water content and hence are likely to be voluntarily dehydrated to varying degrees. The explanation for this phenomenon is that already given--either they prevent a large change in ECF solute concentration in response to quite large changes in body water content or their brains are less sensitive to a normal increase in ECF osmolality (solute concentration). But either way, the fact that athletes with the greatest levels of weight loss are usually the fastest finishers in endurance events shows that the response of their brains to body water loss has been entirely appropriate, perhaps optimal.
There is no direct evidence that exercise performance is impaired in those who lose weight during exercise, provided they drink to the dictates of thirst and do not become thirsty. In fact, evidence that the best marathon runners have a remarkable capacity to resist high levels of fluid loss has been provided in countless races around the world.