Triathlon and the Missing Link of Nutrition

Stephen Phinney and Jeff Volek have done a tremendous work on nutrition for athletes.  Their seminal work published in 2016, Metabolic Characteristic of Keto-Adapted Ultra-Endurance Runners.  Metabolism, needed a subject to proof that great athletes can follow this adaptation to perform at the highest level.  This athlete was study by Edward Coyle few years earlier.  Maximal blood lactate concentration was remarkably low in the trained state. It appears that an 8% improvement in muscular efficiency and thus power production when cycling at a given oxygen uptake (V̇o₂) is the characteristic that improved most as this athlete matured from ages 21 to 28 yr.

This case describes the physiological maturation from ages 21 to 28 yr of the bicyclist who has now become the six-time consecutive Grand Champion of the Tour de France, at ages 27–32 yr. Maximal oxygen uptake (V̇o_{2 max}) in the trained state remained at ∼6 l/min, lean body weight remained at ∼70 kg, and maximal heart rate declined from 207 to 200 beats/min. Blood lactate threshold was typical of competitive cyclists in that it occurred at 76–85% V̇o_{2 max}, yet maximal blood lactate concentration was remarkably low in the trained state. It appears that an 8% improvement in muscular efficiency and thus power production when cycling at a given oxygen uptake (V̇o₂) is the characteristic that improved most as this athlete matured from ages 21 to 28 yr. It is noteworthy that at age 25 yr, this champion developed advanced cancer, requiring surgeries and chemotherapy. During the months leading up to each of his Tour de France victories, he reduced body weight and body fat by 4–7 kg (i.e., ∼7%). Therefore, over the 7-yr period, an improvement in muscular efficiency and reduced body fat contributed equally to a remarkable 18% improvement in his steady-state power per kilogram body weight when cycling at a given V̇o₂ (e.g., 5 l/min). It is hypothesized that the improved muscular efficiency probably reflects changes in muscle myosin type stimulated from years of training intensely for 3–6 h on most days.

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00216.2005

This subject studied by Coyle developed keto-adaptation even when his nutrition was out of whack.  How do I know this?  I checked his hemoglobin and hematocrit in his biological passport and it appeared he was anemic at one point.  This being anemic can give us a clue regarding caloric intake and fasting states.   When caloric intake is low, anemia could be a side effect but it promotes keto adaptation as well as fasting in this case.  This is an advantage taken by anorexic athletes until the body breaks down due to malnutrition.  Michael Phelps used to have lactates around 20 right after one of his competition; this cyclist can hardly reach 7:

Furthermore, at this time of reduced training, maximal blood lactate concentration measured 4 min after exhaustion was 9.2 mM compared with previously recorded values in the range of 6.3–7.5 mM. Maximal heart rate declined from 207 to 200 beats/min from 1992 through 1999. The V̇o₂ corresponding to the blood lactate threshold was 4.5–4.7 l/min when measured in 1992–1993 and, as expected, it was reduced to 4.02 l/min during the period of reduced training in August 1997.

Phinney tested athletes where the peak of fat oxidation was closed to their Vo2 max (see graph below), but what can we learn following the athlete tested by Coyle?:

1)   Keto-adaptation is a state that last a long time even when we do not pay attention to our nutrition as long as we continue training at the same level with same conditions.  It involves activation of genes and it is difficult to deactivate them.

2)   Keto-adaptation is obtained with five hours rides, fasting and low caloric intake for a long time.  Simulating an anorexic.  No wonder Eufemiano Fuentes said that he was helping cyclists to overcome illness when doping them; he used to give transfusions.

3)   The lactate curves should be interpreted differently depending on the diet the athlete is eating.  The lactate curves are designed for athletes eating a high carbohydrate diet without the training of the champion described by Coyle and/or without the anorexic twist.

4)   Training is directly related to the development of keto-adaptation.  The better we adapt the better engine we have; leaving technique as the other physical aspect of performing at high level.

5)   The used of glucose or fatty acid depending on the diet it is shown by Volek in the two graph below when testing two different groups, high carbohydrate diet vs low carb diet.

6)   Muscle glycogen was the same after exercise for the two groups.  This helps to understand that the keto-adapted athletes were burning fat instead of glycogen.  See the graph taken from Phinney and Volek.

Triathlon and Sports Science (part 2)

 The second part of Sports Science was written before but it was called Triathlon Nutrition.  It was written before Blummenfelt’s ironman, where he ran a new world mark for the distance.  I needed to make the connection with Sports Science because Christian could do much better by changing nutrition.  I am pasting below what was written then, and will give you information on how I started inducing the use of fats in myself.  You should read the beautiful paper lead by Jeff Volek before joining this venture: https://www.sciencedirect.com/science/article/pii/S0026049515003340

People have changed the entire soccer team nutrition with a great success as it happened with the Columbus Crew in Ohio, USA. https://www.virtahealth.com/blog/steve-tashjian-carbohydrate-restriction-soccer

3 mai 2021

Triathlon and Nutrition

A long time ago, when I went to medical school, the concept of glucose production from ketones was considered very small and very rare.  It was like a myth, because glucose level in blood was controlling hormones related to metabolism minute to minute in normal people, and nobody wanted to investigate ketones which were present in patients with diabetes. It was considered irrelevant to study ketone bodies to win a Nobel prize.  Severo Ochoa worked on glycolysis (breakdown of glucose for fuel) and fermentation since 1936 and won the Nobel Prize in 1959 (https://en.wikipedia.org/wiki/Severo_Ochoa). The Krebs cycle was studied from the point of view of glycolysis, I was told that glucose was needed in order to burn fat.  George Cahill lost the political battle in science and his research on ketone bodies was not the one to follow.  Marketing carbohydrates changed our lives and put us in this obesity crisis worldwide, as one of Cahill’s students put it:

This story begins in the early 1960s when the general level of knowledge about whole‐body metabolism during human starvation was grossly deficient. This was partly caused by a lack of accurate and specific methods for measuring hormones and fuels in biological fluids, which became available about 1965.1 Rigidly designed protocols for studying human volunteers or obese patients, who underwent semi‐ or total starvation for prolonged periods of time, were not widely employed, and much of the published data regarding metabolic events during starvation were not readily accessible. To complicate matters further, a great deal of the available data was confusing because much of the supposition regarding mechanisms used by the body to survive prolonged periods of starvation was based upon information that was obtained from nonstandardized and often erroneous procedures for studying metabolism… The pathway to knowledge on the nature and regulation of human fuel metabolism has taken a long and circuitous route. It is easy to understand how physician‐scientists initially formulated erroneous concepts regarding the requirements of the brain and other tissues for fuels such as glucose. Ironically, studies of diabetics and patients with insulin‐induced hypoglycemia complicated (rather than clarified) the understanding of the normal metabolism of the brain. The treatment for diabetes became available with the discovery of insulin at the University of Toronto in 1921–22. This scientific breakthrough was one of the most dramatic events for the management of any disease. By lowering the level of blood glucose, insulin's impact on a diabetic patient was sensational and seemingly miraculous.2 However, initial research of brain metabolism was hindered by the widespread yet erroneous hypothesis that developed as a consequence of treating diabetic patients with insulin.3

https://iubmb.onlinelibrary.wiley.com/doi/full/10.1002/bmb.2005.49403304246

Gluconeogenesis was considered small because we were already eating great quantities of sugar (glucose), and the need to produce our own glucose was not there according to doctors.  Ketones as fuel for the brain was considered just in extreme cases.

But let’s continue with Dr. Oliver Owen narrative:

Early insulin therapy was not perfect; insulin saved the lives of experimental animals and subsequently humans, but researchers initially had no way of knowing how much to administer or how to best administer it. They recognized that in the absence of insulin the concentration of blood glucose rose to high levels and death occurred. Also, injecting too much insulin lowered the blood glucose to a point where a “peculiar” behavior occurred; animals and humans began frothing at the mouth, became unconscious, developed convulsions, and died. Eating carbohydrate‐rich foods (i.e. orange juice or candy) or receiving intravenous glucose reversed these adverse effects. Glucose was clearly the key fuel metabolized by the brain; the possibility that other fuels, such as ketone bodies, were also metabolized by this organ was completely ignored. The presence of ketone bodies in the blood and urine of insulin‐deficient diabetic patients was recognized in the 1880s and was associated with severe disease states. In the 1920s, it became evident that insulin lowered the content of glucose in the blood and urine of diabetic humans, and it also removed ketone bodies. Nonetheless, the idea that insulin controlled only glucose metabolism and that too little glucose in the blood led to brain dysfunction led to the widely held concept that glucose was the only fuel used by the brain. In the 1950–60s, researchers learned that insulin lowered not only the concentration of glucose and ketone bodies in the blood and urine but also a host of other fuels, including free fatty acids and amino acids. Unfortunately, these isolated discoveries did not correct the widely held misconception that ketone bodies were unhealthy and that glucose was the only source of fuel for the brain.

¿Are we over the persecution? Tim Noakes lost his job when he mentioned what it is here (2014), and blamed the high carb diet marketed for the obesity epidemic.  He even was accused in court, in a trial that looked like the Greek trial of Socrates.   No wonder Noam Chomsky says that our civilization is “involuding:”

The trial of Socrates (399 BC)^[1] was held to determine the philosopher’s guilt of two charges: asebeia (impiety) against the pantheon of Athens, and corruption of the youth of the city-state; the accusers cited two impious acts by Socrates: "failing to acknowledge the gods that the city acknowledges" and "introducing new deities".

I started my “low carb way of living” approximately six months ago.  I decreased the amount of carbs without measuring them, I still do not measure the amount of carbs I eat.  I bought a breathalyzer to measure ketones instead, I do not use other things than the breathalyzer. I read an article which mentions that it correlated pretty well with the blood measure of ketones.  You have to learn to use it; how you blow, how frequently you use it (first measure is the highest). At the beginning, my morning ketones levels were 0.1 or so.  I decreased the amount of carbs even more in order to increase the ketones level, slowly over the course of two weeks my ketones levels increase to above 1 in the morning. I started to present “keto flu” after two weeks which I treated with hypertonic solutions (salt in my drinks). I still present mild “keto flu” off and on depending on the salt ingested. 

Increasing the amount of proteins would stop ketosis for several hours, and I noticed that if I take external ketones from coconut (a spoon in my tea) I returned rapidly and easily to ketosis.  I use the ketones from coconut to come back to ketosis if I overeat fruits or proteins.  Six months later my ketones in the morning are between 1.5 to 2.5 without fasting.  I am in my sixties and feel energetic, with a pretty good memory and reasoning (good RAM memory), I feel better than in my fifties.  I am lighter but I am interested in a better life and not to lose weight (BMI 24-25.  BMI is another “subject” to review).  I feel that adapting physiologically to this kind of life takes longer than six months for a man like me following my methodology.  I leave you Jeff Volek:

 https://www.youtube.com/watch?v=TFqjqqJTJQ4