Fast, Furious and Deadly - Carbohydrates for Endurance Sports

Fast, Furious and Deadly – Carbohydrates for Endurance Sports

Nutrition for Cycling Part 1: Carbohydrates

I want to start with three examples that have stuck with me and really got me thinking. How do wild animals know what and how much to eat and yet are never fat or chronically ill? How can african hunters run for hours in the midday desert heat chasing antelopes until the animals are exhausted (not the humans!) and accomplish that without breaks for food and water (antelopes are fast). Finally no matter what the advertising has to say, the Tour de France, Ultra mega giga Ironmans are not even close to some of the feats our ancestors performed usually with only survival in mind rather than fame and fortune (the race to the South Pole comes to mind).

The answers can be classified as stranger than fiction, however, by going down to the fundamentals of nutrition, if you can call it that, and the human body and ultimately high performance is an absolutely fascinating story.

Staying alive or using the full medical term – survival – is the goal behind every species on the planet earth. To survive we require energy and as such we posses a fascinating system in place to take care of that. In addition storing energy for the times when food is/will not available is an integral part of the way humans are programmed. What to eat for optimal body function has evolved over roughly 2 million years (with its final version more or less settled around 200,000 years ago) and unlike most of the creatures in nature that eat predominantly food of animal or plant origin (carnivores and herbivores respectively), we have a curse of being omnivores (all eating).

Furthermore at the time of this post the last 30 or so years marked an increase or I should even going as  far as saying explosion of metabolic related diseases such as obesity, Type 2 diabetes, hypertension, cardiovascular diseases. The cynics might say is that we have gotten lazier and eating junk food, and you would be half correct, however, obesity and type 2 diabetes are increasing in children younger than 6 years as well as in newborns. Therefore the heart of the problem lies somewhere else…

In 1977 the infamous McGovern report announcing saturated fat as the end all-be all cause of the cardiovascular disease epidemic ravaging through the United States and hence announcing the first dietary guidelines stating that carbohydrates, rice and grains should form the basis of the food pyramid. Rewinding the clock a bit further we get to a man named Ancel Keys who has gotten himself on the good side of some people in high places. Mr. Keys had been put by the government in charge of determining the minimum amount of calories a soldier can survive on while still being combat worthy. Granted he performed a lot of experiments which would be extremely unethical today such as starvation and testing on mentally challenged patients, the result of his studies were the so called K-rations that are still a staple  (albeit highly modified) in the US army. Following his early successes, while on sabbatical in England in 1952, he noticed that there were enormous increases of cardiovascular disease on the typical English high fat and high cholesterol diet as well as that the richer people both in the UK and US who could afford meats had higher incidence of heart problems.

Throughout the 1960s and 1970s Ancel Keys published a plethora of studies showing higher cholesterol in heart disease patients as well as that diets high in fat raise blood cholesterol. Keys’s ‘masterpiece’ though was the published in 1980 500-page 6-countries study demonstrating that Japan, Italy, England, Australia, Canada and the United States in that order showed a correlation between dietary fat and heart disease (i.e Japan the lowest fat and disease, the United States highest). The first huge gaping hole among the many (excellently detailed by Gary Taubes) in the study’s methodology is that Ancel Keys had data on 22, yes almost 4 times as many countries, and if he had plotted that data he would have gotten a scatter, ie absolutely no correlation even for the most creatively minded statistician. Yet he chose the 6 that nicely fit his hypothesis. In addition and it is something equally important that will come many times in content of this site – association does not equal causation, I repeat association IS NOT causation. A very general and simple example to illustrate: I am Bulgarian and 2m (6’7″) tall, so that leads to the conclusion that Bulgarians are a tall folk. I can tell you that is not the case, and judging by the fact that I get asked almost daily “All Bulgarians must be tall as you, no?” association is very often mistaken for causation.

However, to get back to Mr. Keys, he chose to leave out indigenous tribes such as the Inuit (North America) and Tokelau (Oceania), Maasai and Rendille (Afirca) who predominantly animal fat and have the lowest prevalence of heart disease on the planet. Vihjalmur Stefansson a Canadian Arctic explore and ethnologist (pictured dragging a seal) spent 10 years living with the inuit and learned to eat their food, composed mostly of seal blubber, karibou meat, fish and eggs, and had never felt healthier. Interestingly the inuit viewed plant food as not being “proper human food” and only ate some roots when in dire need. He documented his experiences in a number of publications which I highly recommend, particularly The Fat of the Land. After his return back to New York, he couldn’t stand the food and had to import Inuit food. His observations were immediately labeled controversial in the light the conventional wisdom that ‘balanced diet’ is the healthy diet.  In 1928 himself and Karsten Anderson, 38 year old Danish Explorer, became the subjects of a yearlong experiment to put an end to the meat-diet controversy. The whole experiment was strictly supervised by a committee of a dozen respected nutritionists, anthropologists, and physicians. For the initial three weeks Stefansson and  Anderson were fed a mixed diet (fruits, grains, vegetables, meat) while being subject to a LOT of tests. Afterwards they were moved to Bellevue hospital where under 24hour surveillance they were fed only meat. After 3 weeks (Stefansson) and thirteen weeks (Anderson) both men were released and ate only meat for one year. The constant urine tests showed that the “acetone [ketone] bodies were present in amounts so constant that fluctuations in the carbohydrate intake was practically ruled out.” The conclusions were dramatic due to the fact the expected severe vitamin deficiencies and health decline in both men did not occur, quite the opposite. Albert Scheiwzer, who later went on to win the Nobel Peace in 1952 for his missionary work,  and Samuel Hutton were among some of the colonial and missionary physicians who provided historical observations of the changes that occurred to the indigenous populations that were exposed to the “Western diet.” In the early 1900s carbohydrate foods such as sugar, molasses, white flour and white rice were the staples that the colonists could bring by ship without spoiling or becoming rodent feed. Soon after exposure or the now popular term ‘nutrition transition,’ Western or diseases of civilisation such as obesity, diabetes mellitus, cardiovascular disease, hypertension and stroke, various forms of cancer, peptic ulcers, diverticulitis, gal stones, haemorrhoids, varicose veins and constipation. When any of those condition appeared, the other would follow eventually. Investigators proposed a hypothesis that the disorders had one common cause – easily digestible, refined carbohydrates. In the light of Ancel Keys’ (bold and unsubstantiated) claims that it was fat was the problem with carbohydrates being the solution, the carbohydrate hypothesis was rejected without any further examination.

The above examples are merely one aspect of a greater concept and I am quoting Gary Taubes directly:

You should not let preconceived notions about a ‘healthy diet’ bias the science and the interpretation of the evidence itself.

Which brings me to the next point…

vihjalmur_stefansson_seal

Vihjalmur Stefansson dragging a seal. Photo courtesy of the Dartmouth Library

As far as humans are concerned we have no essential need for carbohydrates, which means to say our metabolism is perfectly capable of making all the stuff it needs, be it carbohydrates (glucose) from non-carbohydrate food. There is NOT A SINGLE clinical condition (disease) of carbohydrate deficiency. If it is essential and we are missing it, we will get sick. Not the case with carbohydrates, not even close. To get an idea why here is a short description of how to body responds to food and calories as well as bring in some hormones into play – enter Insulin and Leptin.

Not surprisingly, like all things human it starts with the brain. Driven by brain signals (hunger, reward, stress) we ingest various foods – ie a combination of fat, protein, carbohydrates, fiber and some micronutrients. It enters the stomach where hydrochloric acid starts the digestion and afterwards the food passes to the small intestine where enzymes break it down to its building blocks – fats gets turned to fatty acids, proteins are broken down to their individual amino acids and carbohydrates are cleaved to simple sugars – mostly glucose with varying amounts of fructose. I underline fructose because it is quite interesting and will be the focus of the next part of the series. We cannot digest fiber so it speeds up the transit of food through the small intestine as well as causing the other nutrients to be absorbed slower. From the small intestine the simple sugars and amino acids travel via the circulation to the liver, while the fatty acids travel via the lymphatic system. The important point it that all nutrients go to the liver first for processing and whatever can’t be taken up there ends up in the general circulation (bloodstream). The rising blood levels of fatty acids, amino acids and glucose reach the pancreas which starts the release of insulin.

Insulin signalling causes several events – glucose gets converted to glycogen to top up the liver energy reserves, amino acids gets shunted to muscle cells, excess fatty acids (blood lipids) get cleared and put in storage inside the fat cells as triglycerides as reserves for a “rainy day.” The take home message from the process is that insulin causes energy storage (fat), no insulin no energy storage, lots of insulin = lots of fat and NO fat burning. Once the insulin levels drop, the whole process goes in reverse – the triglycerides from the fat cells get broken down to fatty acids and mobilized in the bloodstream where they to go to the liver and other organs where they are used to energy. These two processes happen in the human body all the time 24/7/365 – burn what you need, store the rest.

The next logical question is how does the body know how much energy it needs? As mentioned above it starts with the brain and no two opinions about it – energy balance is absolutely vital for survival and as such it is extremely regulated with multiple redundant systems to make sure we don’t die. If there is enough energy in storage the brain signalling is to go out and spend energy. When not enough energy is in storage the brain goes into energy preservation/acquisition mode – and minimizes energy expenditure and in short you feel like crap. That by the way is what happens in calorie restricted diets – you are hungry all the time and have low energy and want to sleep the whole day and you might even gain weight since the brain wants to store energy at all costs to ensure survival. But I digress…. How does the brain know how much stored energy (fat) is there? It receives information from the fat cells that release a hormone called – leptin. Low or no leptin equals brain starvation and energy preservation and increased appetite, high leptin translates into normal energy balance and utilising the stored fat. In addition high leptin levels send a signal back that no energy storage is needed so less (of the energy storage hormone) insulin (see above) is released. Mice that are genetically engineered to lack the leptin gene get humongous and don’t move unless you put their food at the other end of their cage. Then they move there eat the food and sit again – lazy, hungry and overweight. All in all we are perfectly capable of regulating how much energy we need to consume according to what we have to do – cycling or otherwise. The famous example goes that if you eat 20kcal more per day (a bite of food) you will be 10kg (20lb) overweight in 10 years. Nobody can count calories that precisely no matter the willpower, period.

The real twist comes that although different hormones insulin and leptin with their own unique mechanism of action, they both share a similar signalling cascade in the brain – insulin inhibits (blocks) the leptin signal and forces weight gain. Why? That is how we get from the small baby to the adult, and why you can eat everything ALL the time in puberty and ‘get away with it.’ Puberty and pregnancy are both characterised as hyperinsulinic states and why some women develop diabetes when pregnant. If the mechanisms didn’t work like this, we would be all stuck in pre puberty with lots of energy to use and inability to gain weight/grow/develop – not a good state for survival of the species.

Therefore high insulin state causes the feeling of starvation of sorts which in turn causes the need for more energy storage (high appetite and lack of desire to be active). The culmination of the vicious circle is obesity and all that comes with it, however, this is not the focus here. The food that drives insulin high is carbohydrates or the in their digested form glucose and when it comes to endurance performance in the 1930s several studies showed that low carbohydrate levels occurred in athletes (some of the studies can be found here, here and here). To briefly summarize – the model showed that giving athletes glucose was a way to reverse fatigue  as well as that glycogen (glucose) levels in the muscles decrease in response to exercise. In addition muscle glycogen and endurance was lower in athletes fed low carbohydrate diet as compared to their high carbohydrate peers. The grand conclusion formulated in 1973 by Costill et al. was that “depletion of endogenous carbohydrate stores has been shown to be the limiting factor in the ability to perform long-term exercise.” First the fact that two events occur at the same time does not imply causation – as stated many times on the blog – association is NOT causation.

Findings like this one coupled with the running boom in the 1970s led to the birth of the sports drinks industry which to this day continues to sponsor similar ‘research’ while the elephant in the room makes its presence more and more known. Which elephant? Even the leanest of us have 40.000+kcal worth of fat in our muscles while only ~2000kcal of glycogen as well as that the human body can burn 750+kcal per hour during exercise, however, can only absorb  ~350kcal/hour.  No matter what type of magic wonder simple or complex sugar the manufacturers shove in their products, it cannot overcome the physiological specificities of us as humans. The carbohydrate model further stated that fat simply cannot be oxidized (burned) fast enough to support high intensity endurance exercise, which of course is supported by the fact that insulin (released in response to carbohydrates) inhibits fat burning. The absolutely fascinating work by Dr.Stephen Phinney and Prof. Jeff Volekshowed among many studies that after a ~4 week adaptation to a very low carbohydrate diet (<50g) endurance in highly trained  athletes (cyclists included), did not suffer and quite the opposite. The science and what is just starting to slowly gain ground brings me back to where this post started.  The african hunters chasing the antelopes for hours without fatiguing and not having the wonder sugar drinks we see advertised and to as pointed out by Vihjalmur Stefansson and his life with the inuit, not by bread alone is how we will endure.

Conclusion

The human body is perfectly capable of regulating it’s energy balance thought the hormones insulin and leptin, that no calorie counting methodology can better. In addition there is no essential need for carbohydrates in the human metabolism. Ingestion of carbohydrates, particularly ones that are very rapidly absorbed (refined carbohydrates present in any processed food such as flour, sugar, starch) leads to elevation of blood glucose and subsequent release of insulin that causes the storage of excess energy as fat and inhibition of using fat as fuel. Persistently elevated levels of insulin block the action of the starvation hormone leptin, effectively tricking the body that it’s in a state of malnutrition with all of the common symptoms such as increased appetite, low energy, etc.  Furthermore the insulin induced starvation increases the body’s need for preserving energy (into fat) hence causing further release of the energy stowaway hormone insulin into a vicious circle, with obesity and metabolic syndrome as the final stages.

Incorrect conclusions about the role of dietary fat in the cause of heart disease culminating in the 1977 dietary guidelines stating that carbohydrates, specifically grains and bread should form the basis of the human diet as well as misguided understanding of the role of carbohydrate need during exercise further reinforced by the sports drink/supplement industry has created the popular model that endurance exercise and carbohydrates go hand in hand. However, by looking at examples that still exist today such as the african antelope hunters as well as historical evidence by travellers like Vihjalmur Stefansson together with recent research by Dr. Stephen Phinney and Prof. Jeff Volek, carbohydrates are not essential for endurance athletes as well as the main cause behind the now pandemic levels of metabolic diseases such as obesity, type II diabetes and cardiovascular diseases in the general population.

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Cycling Nutrition Series

Continuing Education

Good Calories, Bad Calories – Gary Taubes

Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health

Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease – Dr. Robert Lustig

Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease

The Art and Science of Low Carbohydrate Performance – Dr. Stephen Phinney and Prof. Jeff Volek.

The Art and Science of Low Carbohydrate Performance

 

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This article is for my personal use and educational purposes only, please always consult a licensed health professional. I cannot be held responsible for any damages caused by the information contained in this article.

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