running speed toward the end of a race. However, even in the subjects with the
lowest initial .... Lore of Running. Champaign, IL: Human Kinetics. 5. Åstrand P-O
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Nutrition Performance By Anssi H. Manninen, MHS Low-Carb Diets and Exercise Performance A Story Beyond Carbo-Loading “When first thrown wholly upon a diet of reindeer meat, it seem inadequate to properly nourish the system, and there is apparent weakness and inability to perform severe exertive fatiguing journeys. But this soon passes away in the course of two or three weeks.” Lt. Frederick Schwatka Quoted in Nutrition & Metabolism, 2004;1:2 Basic Facts About Carb Metabolism Commonly known as blood sugar, glucose serves as an energy source for the body’s activities. Glycogen is a storage form of glucose in the human body. The liver stores one-third of the body’s total glycogen and releases glucose as needed. Muscle cells also store glucose as glycogen (the other two-thirds), but they hoard most of their own supply, using it just for themselves during activity. If you follow a carbohydrate-containing diet (i.e., non-ketogenic diet), the cells of your brain and the rest of your nervous system depend primarily on glucose for their energy. To maintain the supply, a steady stream of blood moves past these cells bringing more glucose from either the intestine (carbcontaining foods) or the liver (via glycogen breakdown or glucose synthesis). “Healthy” High-Carb/Low-Fat Diet: A Miserable Myth Certainly, living organisms thrive best in the milieu in which, and on the diet to which, they were evolutionarily adapted. From all indications, Homo sapiens sapiens (anatomically modern humans) has remained biologically unchanged during at least the last 50,000 years. It was not until some 10,000 years ago that the transition from a roaming hunter and gatherer to a stationary farmer began. Consequently, our diet has become progressively more divergent from those of our ancient ancestors. It’s biologically implausible how an animal that adapted to a high-protein diet for five million years suddenly in 10,000 years becomes such a great carbohydrate burner. Indeed, when hunter-gatherer societies transitioned to an agricultural grain-base diet, their general health deteriorated. High-carb diets, which reduce good cholesterol and raise triglycerides (harmful blood lipids), exacerbate the metabolic manifestations of the insulin resistance syndrome. Although not appreciated by the high-carb/low-fat mafia, all fats raise good cholesterol. Interestingly, the relative potency of fatty acid classes in raising good cholesterol is: saturated is greater than monounsaturated, which is greater than polyunsaturated.
Thus, it’s crystal clear that the replacement of total fat (of any fatty acid distribution) with carbs results in significant reductions in good cholesterol. Indeed, recent studies of carb intake and its relationship to the development of heart disease and type 2 diabetes have been rather revealing, showing that an increased carb intake is related to an increase in both conditions. The so-called “heart healthy” American Heart Association (AHA) diet, supported by the animal right activists and vegetarian zealots, is nothing but a miserable myth. The primary remaining justification for high-carb/low-fat diets has been weight control, but Drs. Willett and Leibel at Harvard School of Public Health concluded that fat consumption within the range of 18 to 40 percent energy appears to have little if any effect on body fatness. Thus, they felt diets high in fat do not appear to be the primary cause of obesity, and reductions in fat will not be the solution. Also, the recent Cochrane review concluded that fat-restricted diets are no better than calorie-restricted diets in achieving long-term weight loss in overweight or obese people. In fact, participants lost slightly more weight on the control diets. So, the reality is that if the low-fat weight loss diet were to be marketed according to the laws governing the pharmaceutical industry, it would not pass the scrutiny, as the low-fat weight loss diet has not been shown to be more effective than the control diet. Consequently, progressive scientists and health care professionals are beginning to question the wisdom of recommending low-fat/highcarbohydrate diets. For example, Dr. Sylvan Weinberg, a former president of the American College of Cardiology, argued that high-carbohydrate/low-fat diets could no longer be defended by appealing to the authority of prestigious medical organizations. According to Dr. Weinberg, the high-carbohydrate/lowfat diet may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type 2 diabetes and metabolic syndromes. In contrast, recent clinical investigations support the efficacy of highprotein/low-carb diets for weight loss/fat loss, as well as for improved insulin sensitivity, glycemic control and blood lipid profiles. High-protein/low-carb diets indeed provide a “metabolic advantage,” a greater weight loss per calorie consumed compared to an isocaloric, high-carb diet. (See the recent paper by Drs. Feinman and Fein published in the Nutrition Journal; free fulltext paper is available at http://www.nutritionj.com/content/3/1/9). In the opinion of most exercise scientists, however, the high-carb diet is a must for optimal exercise performance. So, I decided to write a story beyond carbo-loading. History of Carbo-Loading The Scandinavian scientist group led by a dude named Jonas Bergström performed the classic studies of the effects of exercise and carb manipulation on muscle glycogen levels in 1967. The key findings of their studies were the following: • Exercising to exhaustion made muscle glycogen levels fall to very low levels.
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There was minimal glycogen re-synthesis when a high-fat/high-protein diet (carb depletion) was followed. • A very-high-carb diet (90 percent) caused muscle glycogen levels to be re-synthesized rapidly so that pre-exercise muscle glycogen levels were exceeded within 24 hours. Dr. Bergström and colleagues also showed that if athletes were placed on a very-high-fat (90 percent), low-carb diet, their exercise performance was markedly impaired compared to their performance when they had eaten a high-carb diet before exercise. Further, it was observed that the lower the initial glycogen content, the lower the subjects´ ability to maintain a high running speed toward the end of a race. However, even in the subjects with the lowest initial muscle glycogen content, the speed was maintained during the first hour of the race. In other words, a high muscle glycogen content didn’t enable the subjects to attain a higher speed at the beginning of the race any more than did low initial glycogen levels. Nevertheless, the corollary was that all athletes, especially those involved in endurance events, must be advised to eat high-carb diets. In fact, this recommendation forms the central pillar onto which the “traditional sports nutrition” advice is cemented: “Eat a truckload of pasta before exercise, 18 liters of Gatorade during exercise and 245 potatoes after exercise.” However, as pointed out by Dr. Timothy Noakes, a prominent exercise physiologist and sports physician from South Africa, only two carbo-loading studies have included adequate placebo controls, and both failed to show any added benefit over placebo. Furthermore, the classical carbo-loading studies showing a close relationship between pre-exercise muscle glycogen concentrations and subsequent exercise performance applied specifically to an acute effect— that is, one lasting a few days. However, there is a growing body evidence showing that athletes can adapt to a low-carb diet without sacrificing their endurance performance. Importantly, it has been demonstrated that full adaptation of carb, protein and fat metabolism requires a number of weeks. The idea that exercise terminates only when a specific (critically low) muscle glycogen concentration is reached does not apply in subjects who have adapted to a low-carb diet. Dr. J.W. Helge and colleagues concluded that factors other than carbohydrate availability are responsible for the differences in endurance time between groups eating high- and low-carb diets. Their results also indicate that fatigue during prolonged moderately intense exercise does not always seem to be closely related to glycogen depletion. Nevertheless, the latest edition of the classic work/exercise physiology textbook by the prominent Scandinavian physiologists states, “The available evidence suggests that at work rates exceeding about 75 percent of the individual’s maximal oxygen uptake, the initial glycogen content in the skeletal muscle determines the individual’s ability to sustain such exercise more than an hour.”
Ketogenic Diets, Exercise Performance and Body Comp When the rate of mobilization of fatty acids from fat tissue is accelerated, as during very low carbohydrate intake (ketogenic diet), the liver produces ketone bodies. However, the liver cannot utilize ketone bodies and thus, they flow from the liver to extra-hepatic tissues (e.g., brain, muscle) for use as a fuel. This spares glucose metabolism via a mechanism similar to the sparing of glucose by burning of fatty acids as an alternative fuel. Indeed, the use of ketone bodies replaces most of the glucose required by the brain. Don’t confuse diabetic ketoacidosis with dietary ketosis! Diabetic patients know the detection in their urine of the ketone bodies is a danger signal that their diabetes is poorly controlled. However, during very low carbohydrate intake, the regulated and controlled production of ketone bodies causes a harmless physiological state known as dietary ketosis. In ketosis, the blood pH remains buffered within normal limits. Recently, Dr. Stephen Phinney published a state-of-the-art review on ketogenic diets and exercise performance in a new scientific journal called Nutrition & Metabolism (www.nutritionandmetabolism.com). As pointed out by Dr. Phinney, lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium intake, and constraint of protein to 15-25 percent of daily energy intake allow unimpaired endurance performance despite dietary ketosis. In 1980, Dr. Phinney and co-workers undertook a study of subjects given a very-low-calorie ketogenic diet for six weeks in a metabolic research ward. The protein for this diet, along with a modicum of inherent fat, was provided by lean meat, fish and poultry yielding 1.2 grams of protein per kilogram of reference (“ideal”) bodyweight daily. Importantly, the subjects were also prescribed three grams of sodium and one gram of potassium (the excessive loss of sodium in the urine could reduce blood volume and cause secondary potassium wasting). Interestingly, subjects´ peak aerobic power didn’t decline despite six weeks of a carb-free, very-low-calorie diet. This implies that protein and mineral contents of the diet were adequate to preserve functional tissue. It should be noted, however, that the subjects experienced delayed adaptation to the ketogenic diet, having reduced endurance after one week followed by a recovery to, or above, baseline in the period between one and six weeks. In 2001, the AHA Nutrition Committee incorrectly suggested that the low-carb intake led to progressive loss of muscle mass. This urban legend apparently comes from the poorly controlled “Turkey Study” published in the New England Journal of Medicine in 1980. The authors of this study reported that the protein-only diet subjects were losing nitrogen (muscle mass) but gaining potassium. As pointed out by Dr. Phinney, however, potassium and nitrogen losses are closely related, as they are both contained in lean tissue. This anomaly occurred because the authors assumed the potassium intake of their subjects was based upon handbook values for raw turkey, but half of this potassium was being discarded in the unconsumed broth. Deprived of potassium, these subjects were unable to benefit from dietary protein and thus lost muscle mass.
The second study by Dr. Phinney and colleagues reported that subjects lost 0.7 kilograms in the first week of the eucaloric ketogenic diet, after which their weight remained stable. So, they observed a reduction in glycogen stores, but otherwise excellent preservation of lean body mass during the eucaloric ketogenic diet. However, they also reported that subjects´ sprint capability remained constrained during the period of carb restriction. More recently, Dr. Jeff Volek and co-workers examined the effects of a six-week very-low-carb diet on total and regional body composition. Twelve healthy normal-weight men switched from their habitual diet (48 percent carbohydrate) to a carbohydrate-restricted diet (eight percent carbohydrate) for six weeks and eight men served as controls, consuming their normal diet. Subjects were encouraged to consume adequate dietary energy to maintain body mass during intervention. Fat mass was significantly decreased (-3.4 kg) and lean body mass significantly increased (+1.1 kg) at week six. However, there were no significant changes in composition in the control group. According to Dr. Phinney, “Both observational and prospectively designed studies support the conclusion that submaximal endurance performance can be sustained despite the virtual exclusion of carbohydrate from the human diet… Therapeutic use of ketogenic diet [e.g., fat loss] should not require constraint of most forms of physical labor or recreational activity, with the one caveat that anaerobic (i.e., weightlifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics.” Closing Remarks It’s my view that the very-low-carb diet works well for guys who want to maximize fat loss and are only moderately active. If you want to give it a try, you may need to modify your resistance training program. For example, it’s good idea to focus on heavier weights for fewer reps (three to eight), because the energy is primarily derived from phosphocreatine stores. Phosphocreatine serves as the cell’s energy reservoir to provide rapid phosphate-bond energy to resynthesize ATP, a high-energy molecule serving as the ubiquitous energy currency of cells. This is a more rapid pathway than ATP regeneration in glycogen breakdown (glycogenolysis). Therefore, phosphocreatine becomes important in maximum efforts lasting up to 10 seconds. Ingesting creatine monohydrate at the dosage of 20 to 30 grams per day for two weeks increases intramuscular concentrations of free creatine and phosphocreatine by up to 30 percent. Consequently, creatine is a very useful supplement in the very-low-carb diet. Also, make sure you take in adequate amounts of potassium and sodium. However, serious gym rats who want to maximize muscle growth should eat enough carbs to maintain optimal exercise performance. Although the jury has not yet returned to deliver its final verdict, there is evidence showing that carb supplementation before, during and after resistance
exercise can attenuate the rate of muscle glycogen depletion during exercise and speed the rate of glycogen re-synthesis after exercise There are examples in the animal kingdom of superior “athletes” that eat a mixed grain diet (e.g., Arabian race horses), a predominantly protein-fat diet (e.g., the African hunting dog), or a high-fat/moderate-protein/absent carb diet (e.g., Alaskan huskies). It is of some interest that the athletic performances of Alaskan huskies fall immediately when they are placed on a high-carb diet, whereas thoroughbred racehorses placed on a high-carb diet risk developing the muscle breakdown syndrome. Certainly, it’s time to emphasize the metabolic individuality of humans, too. Also, it’s important to keep an open mind; the fact that current nutrition recommendations are so narrow-minded means we have a model for what not to do. References 1. O´Keefe JH, Cordain L (2004). Cardiovascular disease resulting from a diet and lifestyle at odds with our Paleolithic genome: How to become a 21st-century hunter-gatherer. Mayo Clin Proc, 79:101-108. 2. Ginsberg HN, Karmally W (2000). Nutrition, lipids, and cardiovascular disease. In: Stipanuk MH, ed. Biochemical and Physiological Aspects of Human Nutrition. Philadelphia, PA: W.B. Saunders Company, pp. 917-944. 3. Aljada A, Mohanty P, Dandona P (2003). Lipids, carbohydrates, and heart disease. Metab Synd Relat Disord,1:185-188. 4. Noakes T (2003). Lore of Running. Champaign, IL: Human Kinetics. 5. Åstrand P-O, Rodahl K, Dahl HA, Stromme SB (2004). Textbook of Work Physiology. Champaign, IL: Human Kinetics. 6. Phinney SD (2004). Ketogenic diets and physical performance. Nutr Metab,1:2. 7. Phinney SD, Horton ES, Sims EAH et al. (1980). Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric ketogeni diet. J Clin Invest, 66:1152-1161. 8. Phinney SD, Bistrian BR, Evans WJ et al. (1983). The human metabolic response to chronic ketosis without calorix restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism, 32:769-776. 9. Volek JS, Sharman MJ, Love DM et al. (2002). Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism, 51:864-870 10. Volek JS (2004). Influence of nutrition on responses to resistance training. Med Sci Sports Exerc, 36:689-696.
