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Conversation with the Nutritional Wizard Part Two
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Conversation with the Nutritional Wizard Part Two
(conversation between Lyle McDonald and Jamie Hale)
Click here to read part one http://www.maxcondition.com/page.php?73
JH: Erasmus talks about fatty acid synthase gene In what manner does
this occur?
LM; Fatty acid synthazse would be a key enzyme in synthesizing fatty acids.
For the most part, outside of rather extreme dietary interventions(including dietary fat intake <10% and massive sustained carb intakes),fatty acid synthesis doesn't seem to play a major role in human fat gain.
Very chronic high carb intakes probably up regulates the activity of thegene.
JH: Couple of interesting notes to share. I trained a Brazilian jiu-jitsu guy that consumed only meats greens and Atkins bars for almost one year. His performance did not suffer. I also work with a strongman who has consumed only meats and greens the past two weeks. He seems to only be getting
stronger. I have numerous case studies such as these that indicated an individual on a low carb diet can function at high intensity levels. While it might be possible that the strongman such as Paul still has a large ins release due to the consumption of 6000 calories per day. Another
interesting note my MMa champ Ryan Farhat consumed meats, nuts and greens preparing for his last fight. Prior to the night before he had a big carb load.
Next day he performed awesome. What are the implications?
LM: A few random thoughts that we can discuss on Sunday.
1. With sufficient protein, you actually get quite a bit of glucose
produced. In the keto book, I mention a conversion rate of just overhalf. So a guy eating 300-400 grams of protein may actually be making150-200 grams of glucose via gluconeogenesis. Clearly that is goingtowards keeping muscle glycogen sustained, insulin up, etc. I know that Poliquin advocates that sort of diet, 2 g/lb of protein or so which may be
making just over 1 g/lb of carbs.
2. I think some sports are more likely to sustain performance on that typeof regimen. The types of low-rep, ATP/CP training I imagine you're usingwith your BJJ/strongman guy is probably one of them. Not a whole lot ofglycogen depletion going on (compared to someone doing a lot of glycolytic or high rep work).
3. As to your last observation, there are at least 3 studies out thereright now (admittedly in endurance weenies) that did a 5 day fatadaptation period followed by a 1 day carb load. Although performancegains were inconsistent, if you look at the individual data, some folks clearly performed better with fat adaptation + CL (they were typically the guys who performed slightly worse on the carb-based diet). It looks
like the body was able to adapt to using fat for fuel but still have sufficient glycogen after the CL to sustain high intensity performance. That might explain what you saw with a short carb-load prior to your guys competition.
Anyhow, looking forwards to talking with you on Sunday.
Lyle
Proc Nutr Soc. 2005 May;64(2):213-6. Related Articles, Books, LinkOutPeptide YY, appetite and food intake.le Roux CW, Bloom SR. Department of Metabolic Medicine, Imperial College London, W12 0NN, UK.
Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.
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Lyle
JH: another question often oligosaccharrides are not mentioned in classification systems. Also a disaccharide is a oligo saccharine correct (in some classification systems) Could you differentiate?
LM: Oligo technically means many and there are scant few oligosaccharides that occur under normal dietary conditions. About the only one you ever hear about are the fructoligosaccharides (like inulin) which is a fiber that
affects gut health. IN practice, with normal food choices, you get saccharides, disaccharides and anything larger ends up being starch.
Thanks for sending the book, I'm looking forwards to it, I'll get to your other emails tomorrow, been one of those weeks.
Lyle
JH: I understand what the glycemic index is, but if protein can cause a blood glucose conversion of over 50% it would seem like it could have an affect on insulin release to a moderate degree. Maybe not also. Just thoughts.
LM: Yeah, it's a weird ass thing.
They've done a few studies recently looking at this and find that the expected blood glucose conversion doesn't seem to be showing up. a few possibilities
1. The theoretical conversion isn't really occurring
2. The protein is being converted to glucose but stored as liver glycogen
3. The protein is being converted to glucose but released into the bloodstream at the same rate that the body is using it so there's no net increase in blood glucose levels
I had a link to an article on the topic but can't find it now.
JH: Thanks for the book Bromocriptine. This has lead to my massive research in regards to hypothalamus and hunger hormones.
LM: Trust me, it just gets more complicated the more you look into it. I've got a couple of recent review PDF"s, I'll send 'em your way.
JH: Could be of interest I used to work with prader willi syndrome patients. They had insatiable appetites would literally eat themselves to death. we had to lock up food and cook their meals. Had a propensity to get obese easily as well. Any research on this disorder. Leptin disorder maybe?
LM: I haven't paid much attention to the prader-willi stuff but there is something weird going on, I see a lot of papers on it in the leptin research.
J Clin Nutr. 2005 Jul;82(1):41-8. Related Articles, Links
A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations.
Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, Purnell JQ.
University of Washington School of Medicine, Seattle, WA, and the Oregon Health and Science University, Portland, OR.
BACKGROUND: Ad libitum, low-carbohydrate diets decrease caloric intake and cause weight loss. It is unclear whether these effects are due to the reduced carbohydrate content of such diets or to their associated increase in protein intake. OBJECTIVE: We tested the hypothesis that increasing the protein content while maintaining the carbohydrate content of the diet lowers body weight by decreasing appetite and spontaneous caloric intake. DESIGN: Appetite, caloric intake, body weight, and fat mass were measured in 19 subjects placed sequentially on the following diets: a weight-maintaining diet (15% protein, 35% fat, and 50% carbohydrate) for 2 wk, an isocaloric diet (30% protein, 20% fat, and 50% carbohydrate) for 2 wk, and an ad libitum diet (30% protein, 20% fat, and 50% carbohydrate) for 12 wk. Blood was sampled frequently at the end of each diet phase to measure the area under the plasma concentration versus time curve (AUC) for insulin, leptin, and ghrelin. RESULTS: Satiety was markedly increased with the isocaloric high-protein diet despite an unchanged leptin AUC. Mean (+/-SE) spontaneous energy intake decreased by 441 +/- 63 kcal/d, body weight decreased by 4.9 +/- 0.5 kg, and fat mass decreased by 3.7 +/- 0.4 kg with the ad libitum, high-protein diet, despite a significantly decreased leptin AUC and increased ghrelin AUC. CONCLUSIONS: An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.
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Lyle
Sports Med. 2002;32(11):667-73. Related Articles, Links
Influence of racial origin and skeletal muscle properties on disease prevalence and physical performance.
Suminski RR, Mattern CO, Devor ST.
Section of Sport and Exercise Sciences, The Ohio State University, Columbus, Ohio 43210-1284, USA. -email-
Skeletal muscle properties are related to disease (e.g. obesity) and physical performance. For example, a predominance of type I muscle fibres is associated with better performance in endurance sports and a lower risk of obesity. Disease and physical performance also differ among certain racial groups. African Americans are more likely than Caucasians to develop obesity, diabetes mellitus and hypertension. Empirical studies indicate that aerobic capacity is lower in African Americans than Caucasians. Because genetics is a partial determinant of skeletal muscle properties, it is reasonable to assume that skeletal muscle properties vary as a function of race. As such, genetically determined and race-specific skeletal muscle properties may partially explain racial disparities in disease and physical performance. However, additional research is needed in this area to enable the development of more definitive conclusions.
Effects of glycogen loading
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1) glut 4 transporter- uptake enzyme
2) phosrphorylase- binding enzyme
3) glycogen synthase- storage enzyme
4) pyruvate dehydrogenase- fuel utilization , acts to store , partioning
And not used for energy production
JH: question
does glycogen resynthesis become enhanced after a pre workout carb intake due to raised insulin levels which begin to prime body for carb load? Is there conclusive evidence suggesting the pre carb is superior to only taken post or during? Does this apply to tkd as well?
LM: I can't recall anything looking at pre vs. post workout in terms of glycogen synthesis. If glycogen synthesis was higher with pre-workout carbs, I would suspect it's simply as a consequence of having carb available immediately. The reason we split TKD into pre and post workout carbs had more to do with limiting the insulin spike (exercise inhibits insulin response) and to raise/maintain blood glucose during the workout. Basically pre-workout was more to support the workout itself, post-workout carbs were to resynthesize some glycogen.
JH: another question in regards to other macronutrients while carbing up. pg 135 keto book it is suggested as long as carb intake is sufficient the level of prot and fat really does not effect carb up. Does this apply only in regards to multiple carb feedings 24-36hr? Can this apply post workout in short-tern as well?
LM: Good question and I"d have to look to be sure. You usually do see differences in short vs. long-term (say 4-6 hours vs. 24-36). Quality and the rest of it makes a much bigger difference in the short-term and almost none in the long-term. So if you have an athlete doing extensive/intensive workouts 2X/day who has to reload glycogen in-between it makes a huge difference. Beyond that, I"d have to look at the data to be sure. I think, in general, keeping fat and fiber low and doing carbs/protein (protein has been shown in some studies to enhance glycogen resynthesis with carbs) immediately after is the best strategy.
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