Triathlon on LCHF
Can you exercise without a lot of carbohydrates? You certainly can.
But can you also handle tough exercise for a triathlon on LCHF? Staffan Leandersson decided to try:
My name is Staffan Leandersson and I’m 45 years old. I’ve eaten LCHF for three years and feel fantastic.
I’ve been training for triathlon regularly for a few years, and this past year with many more tough workouts per week with the goal of doing half an Ironman race, 1.2 miles (1900 m) of swimming, 56 miles (90 km) biking and 13 miles (21 km) running. I successfully completed the race in glorious weather this summer (Tjörn Triathlon, Sweden).
I had decided to do this without carb loading and with a minimal intake during the actual race. I went stricter in the final three weeks before the race, but I increased my protein intake, in the form of mackerel in tomato sauce, avocados and a few more eggs than usual. Triathlon actually consists of four parts, and the last one is food & drink.
I’ve talked to athletes, who didn’t eat or drink enough and lost 9 lbs (4 kg). I don’t have those margins as I’m 5′ 11″ (180 cm) tall and weigh 163 lbs (74 kg). I had scrambled eggs with heavy cream for breakfast. During the biking I drank water with High 5 Zero (electrolytes and magnesium, to prevent cramps), and I ate Björn Ferry’s egg muffins (egg, cheese and cream) and cheese sticks. During the last half of the biking I also had 4 figs. During the race I only had water and half a banana at 10 miles (17 km).
It went great, no cramping and I was able to sustain the same speed throughout the entire distance. I’m not among the super fast, but I made it in 5 hrs and 57 minutes. (Swimming 40 min, Biking 2hrs 56 min and running 2 hrs 11 min).
Please feel free to write about my race and that it is perfectly possible to do endurance sports at a fairly high pace for 6 hours. It may even motivate somebody to try!
Before the competition I tried to drink my own sport drink with pineapple juice, water and Alpha Plus sport drink powder during my biking, but the only thing that happened was that my digestive system protests…
I’ve followed your blog closely for a long time and thanks to your blog my wife and I changed our eating habits. She was diagnosed with fibromyalgia 3 years ago and has almost recovered! Her IBS is gone and all of our allergies and asthma are gone as well!
Please keep doing what you do – you do it so well!
I’m enclosing a picture to use if you think it will add to the story!
Congratulations on your accomplishments and health improvements!
Very Low-Carb Performance with Peter Attia
Legendary Exercise Professor Embraces LCHF!
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Here is his blog.
In the case of low-carb nuts like hazelnuts, macadamia, pecans and walnuts, is it purely because they're easy to overeat? So, if you control your portions strictly and count the carbs they'd be okay?
I have a hypothesis that there is a significant difference between unprocessed nuts and nut butters. Nut butters affect my blood sugar and ketones the next day but whole nuts don't unless I have a large amount. I expect the absorption and fermentation pattern differs in the gut when the oil and sugars in the nuts are not extruded from the cells. Also, a good portion of whole nuts just chewed simply passes through, whereas this may not be the case with nut butters.
Nutrients. 2014 Jun 27;6(7):2493-2508.
The Effects of a Ketogenic Diet on Exercise Metabolism and Physical Performance in Off-Road Cyclists.
Zajac A1, Poprzecki S2, Maszczyk A3, Czuba M4, Michalczyk M5, Zydek G6.
The main objective of this research was to determine the effects of a long-term ketogenic diet, rich in polyunsaturated fatty acids, on aerobic performance and exercise metabolism in off-road cyclists. Additionally, the effects of this diet on body mass and body composition were evaluated, as well as those that occurred in the lipid and lipoprotein profiles due to the dietary intervention. The research material included eight male subjects, aged 28.3 ± 3.9 years, with at least five years of training experience that competed in off-road cycling. Each cyclist performed a continuous exercise protocol on a cycloergometer with varied intensity, after a mixed and ketogenic diet in a crossover design. The ketogenic diet stimulated favorable changes in body mass and body composition, as well as in the lipid and lipoprotein profiles. Important findings of the present study include a significant increase in the relative values of maximal oxygen uptake (VO2max) and oxygen uptake at lactate threshold (VO2 LT) after the ketogenic diet, which can be explained by reductions in body mass and fat mass and/or the greater oxygen uptake necessary to obtain the same energy yield as on a mixed diet, due to increased fat oxidation or by enhanced sympathetic activation. The max work load and the work load at lactate threshold were significantly higher after the mixed diet. The values of the respiratory exchange ratio (RER) were significantly lower at rest and during particular stages of the exercise protocol following the ketogenic diet. The heart rate (HR) and oxygen uptake were significantly higher at rest and during the first three stages of exercise after the ketogenic diet, while the reverse was true during the last stage of the exercise protocol conducted with maximal intensity. Creatine kinase (CK) and lactate dehydrogenase (LDH) activity were significantly lower at rest and during particular stages of the 105-min exercise protocol following the low carbohydrate ketogenic diet. The alterations in insulin and cortisol concentrations due to the dietary intervention confirm the concept that the glucostatic mechanism controls the hormonal and metabolic responses to exercise.
Retrospective study on the efficacy of a low-carbohydrate diet for impaired glucose tolerance.
Maekawa S1, Kawahara T2, Nomura R1, Murase T1, Ann Y1, Oeholm M1, Harada M3.
In recent years, the number of people with impaired glucose tolerance (IGT) has increased steadily worldwide. It is clear that the prevention of diabetes is important from the perspective of public health, medical care, and economics. It was recently reported that a low-carbohydrate diet (LCD) is useful for achieving weight loss and glycemic control, but there is no information about the effects of the LCD on IGT. We designed a 7-day in-hospital educational program focused on the LCD for IGT.
The subjects were 72 patients with IGT (36 in the LCD group and 36 in the control group) who were enrolled from April 2007-March 2012 and followed for 12 months. We retrospectively compared the LCD group with the control group.
In 69.4% of the LCD group, blood glucose was normalized at 12 months and the 2-hour plasma glucose level in the oral glucose tolerance test (OGTT) was reduced by 33 mg/dL. In addition, the incidence of diabetes was significantly lower in the LCD group than in the control group at 12 months (0% versus 13.9%, P=0.02). The LCD group showed a significant decrease in fasting plasma glucose, hemoglobin A1c, the homeostasis model of assessment of insulin resistance value, body weight and serum triglycerides (TGs) at 12 months, while there was a significant increase of the serum high-density lipoprotein (HDL) cholesterol level.
The LCD is effective for normalizing blood glucose and preventing progression to type 2 diabetes in patients with IGT.
Wow. It's what we would expect but--wow.
I agree, it is - wow, even more so as these studies were done on healthy high carbohydrate diet loving, 'long living' Japanese
(and LCD diet was kind of 'lowerish' carb)
J Child Neurol. 2013 Aug;28(8):1009-14. doi: 10.1177/0883073813487596. Epub 2013 May 16.
Treatment of diabetes and diabetic complications with a ketogenic diet.
Mobbs CV1, Mastaitis J, Isoda F, Poplawski M.
Accumulating evidence suggests that low-carbohydrate, high-fat diets are safe and effective to reduce glycemia in diabetic patients without producing significant cardiovascular risks. Most of these studies have been carried out specifically restricting carbohydrates, which tends to lead to increased protein intake, thus reducing the ketosis. However, diets that limit protein as well as carbohydrates, entailing a composition very high in fat, appear even more effective to reduce glucose and whole-body glucose metabolism in humans. In animal models, low-carbohydrate, high-protein diets do not produce ketosis or reduce glycemia but rather cause obesity. However, limiting both protein and carbohydrates as in a classic ketogenic diet remarkably reduces blood glucose in animal models of type 1 and type 2 diabetes and reverses diabetic nephropathy. Future studies should assess if ketogenic diets would be effective to reverse diabetic complications in humans.
A couple of observations. First, they attribute much of the benefit to polyunsaturated fats, but table 2 shows the polyunsaturated fats went from 28 to 35 grams per day, whereas saturated and monounsaturated went from 30 to 68 and 33 to 130, respectively. So saturated fats doubled and monounsaturated quadrupled. Perhaps the discussion referred to polyunsaturated when they meant monounsaturated.
Then there is a brief review of keto complications in the literature, which I have quoted below. Is this based on experience with epileptics? Do you see these in your experience Paul? The keto people I know don't, but they stay on it because it seems to go well for them, so there may be a filtering effect where only those for whom it goes well tend to stick with keto.
"Despite some therapeutic benefits, ketogenic diets create several physiological consequences of which the most significant for physical exercise includes ketosis. Other side effects of ketogenic diets for sport performance include dehydration, hypoglycemia and increased risk of kidney stones [25–27]. Additionally, high fat, low carbohydrate ketogenic diets may induce metabolic disturbances, causing acidosis, weight loss, inadequate growth, hyperlipidemia, vitamin and trace elements deficiency (zinc, selenium and copper), hypoglycemia, hyperuricemia, anemia and leukopenia "
Presumably the experience with epileptics is not self-selective regarding suitability to keto and so metabolic deficiencies are exposed. Plus what I have seen from the keto diets prescribed for epileptics they are gruesome. Many of the epileptics using keto are children as a treatment when drugs have failed and I expect these kids hardly gravitate to liver and greens.
So it seems to me that keto should come with a warning that it is nutrient demanding and perhaps not suitable for casual, unstructured diets based on what foods are made easily available. I try to follow Dr. Terry Wahl's general structure for a keto diet and it seems to work fine for me. I don't mean to sound unduly negative, but of course I am ever on the lookout for downside risks, to assess possible angles to falsify the keto hypothesis. Paul Jaminet is a good source for that.
Might one say that the brain "prefers" ketones? I'd have to do some genealogical analysis to figure that out. One might say the presence of ketones generally implies less available sugar and switching to ketones conserves sugar for cells lacking mitochondria. On the other hand, Kruse makes arguments why ketones are better fuel in terms of heat and other constraints on brain metabolism.
This talk is on the science of nutrition while undergoing treatment for cancer. Dr. Colin Champ is in Physicians and Ancestral Health.
Considering the seemingly toxic effect of glucose on the Alzheimer brain, down-regulation of glucose uptake when ketones exceed 1 mmol/L is a fantastic mechanism.
Among other things, it suggests that elevating ketones with either coconut oil/MCT oil or through very low carb diet, would at some point result in an abrupt non-linear downshift shift in the ongoing rate of blood glucose consumption, since the brain uses some 25% of energy.
Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1607-15. Epub 2007 Feb 6.
Diet-induced ketosis increases capillary density without altered blood flow in rat brain.
Puchowicz MA1, Xu K, Sun X, Ivy A, Emancipator D, LaManna JC.
It is recognized that ketone bodies, such as R-beta-hydroxybutyrate (beta-HB) and acetoacetate, are energy sources for the brain. As with glucose metabolism, monocarboxylate uptake by the brain is dependent on the function and regulation of its own transporter system. We concurrently investigated ketone body influx, blood flow, and regulation of monocarboxylate transporter (MCT-1) and glucose transporter (GLUT-1) in diet-induced ketotic (KG) rat brain. Regional blood-to-brain beta-HB influx (micromol.g(-1).min(-1)) increased 40-fold with ketosis (4.8 +/- 1.8 plasmabeta-HB; mM) in all regions compared with the nonketotic groups (standard and no-fat diets); there were no changes in regional blood flow. Immunohistochemical staining revealed that GLUT-1 density (number/mm2) in the cortex was significantly elevated (40%) in the ketotic group compared with the standard and no-fat diet groups. MCT-1 was also markedly (3-fold) upregulated in the ketotic group compared with the standard diet group. In the standard diet group, 40% of the brain capillaries stained positive for MCT-1; this amount doubled with the ketotic diet. Western blot analysis of isolated microvessels from ketotic rat brain showed an eightfold increase in GLUT-1 and a threefold increase in MCT-1 compared with the standard diet group. These data suggest that diet-induced ketosis results in increased vascular density at the blood-brain barrier without changes in blood flow. The increase in extraction fraction and capillary density with increased plasma ketone bodies indicates a significant flux of substrates available for brain energy metabolism.