Thursday, April 12, 2012
Fructose to the rescue
Many claim fructose should be avoided especially for people with the so-called metabolic syndrome. Yudkins started most of the hysteria with his book "Pure, White and Deadly", during the time "the cholesterol hypothesis" was very popular and he argued that it was fructose and not fat that raised the so-called "bad lipids". Uffe Ravnskov member of the editorial board of cholesterol has reviewed the literature and he see's no connection between blood lipids and disease(0).
In 1864 Dr. William Budd in England used large amounts of sucrose to treat diabetes, P.A. Priorry did the same in France in 1867.
Free fatty acids block glucose metabolism.(1) One of the points where free fatty acids block glucose is at the point where it is converted to fructose. When fructose is available it can bypass this barrier to the use of glucose and continue to provide pyruvic acid for oxidative metabolism. If mitochondria are damaged and not producing energy pyruvate can leave the cell as lactate allowing continued glycolitic energy. This can provide enough energy to the brain to sustain life in an emergency.
Liver has the highest capacity for metabolizing fructose but other organs and skeletal muscles can metabolize it via the Glut5 expression.(2, 3)
The ability of mitochondria to oxidize pyruvic acid and glucose is lost to some degree in cancer.(4) This disturbed redox balance of the cell will usually lead to the cell's death but if the cell can survive, the disturbed redox balance favors growth and cell division, rather than the normal differentiated function. Fructose prevents oxidative damage by maintaining and restoring the cell's redox balance(5).
Fructose lowers serum phosphate and fruit is protective against prostate cancer by lowering serum phosphate(6). Age suppressing gene Klotho suppresses the re-absorption of phosphate by the kidneys and inhibits the formation of activated vitamin D opposing the effect of the parathyroid hormone. In the absence of the gene animals serum phosphate is high; these animals age and die prematurely(7). Serum phosphate is increased in osteoporosis(8), treatments that lower serum phosphates improve bone remineralization with retention of calcium phosphate(9). Close association between high serum phosphate in normal range in humans and increased risk of cardiovascular disease has been found(10). Increase in respiratory quotient and co2 production by fructose/glucose is probably a factor for lowering serum phosphates because high altitude and carbonic anhydrase inhibitor increase blood co2 and decrease serum phosphate(11,12,13).
Sucrose is less fattening than glucose because more calories can be consumed without gaining weight. In one study rats ate 50% more calories in the form of coca cola or sucrose compared to a normal diet without gaining additional weight(14)
Fructose protects against Vitamin D deficiency in rats(15).
Sucrose is used to decrease pain in many settings including infants and adults.(16)
0. http://www.ravnskov.nu/cholesterol.htm#a
1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC507380/
2. http://www.ncbi.nlm.nih.gov/pubmed/9781312
3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652499/?tool=pmcentrez
4. http://www.nutritionandmetabolism.com/content/7/1/7
5. http://www.ncbi.nlm.nih.gov/pubmed/8783811
6. http://www.ncbi.nlm.nih.gov/pubmed/11036473
7. http://www.nature.com/ki/journal/v79/n121s/full/ki201126a.html
8. http://www.ncbi.nlm.nih.gov/pubmed/7354241
9. http://www.ncbi.nlm.nih.gov/pubmed/20428857
10. http://circ.ahajournals.org/content/112/17/2627.full
11. http://informahealthcare.com/doi/abs/10.3109/00365517209080248
12. http://www.ncbi.nlm.nih.gov/pubmed/19188744
13. http://www.ijem.org.ir/browse.php?a_id=193&sid=1&slc_lang=en
14. http://ajpregu.physiology.org/content/244/4/R500.a
15. http://www.ncbi.nlm.nih.gov/pubmed/1221903
16. www.sciencedirect.com/science/article/pii/S0091305796002274
Sunday, April 8, 2012
The Battle of Theories in Cell Physiology
Ken Muldrew from University of Calgary gives an unbiased view of cell physiology-
Evolution of the membrane and bulk phase theories
Two opposing concepts developed within the context of studies on osmosis, permeability, and electrical properties of cells. The first held that these properties all belonged to the plasma membrane whereas the other predominant view was that the protoplasm was responsible for these properties.
The membrane theory developed as a succession of ad hoc additions and changes to the theory to overcome experimental hurdles. Overton (a distant cousin of Charles Darwin) first proposed the concept of a lipid (oil) plasma membrane in 1899. The major weakness of the lipid membrane was the lack of an explanation of the high permeability to water, so Nathansohn (1904) proposed the mosaic theory. In this view, the membrane is not a pure lipid layer, but a mosaic of areas with lipid and areas with semipermeable gel. Ruhland refined the mosaic theory to include pores to allow additional passage of small molecules. Since membranes are generally less permeable to anions, Michaelis concluded that ions are adsorbed to the walls of the pores, changing the permeability of the pores to ions by electrostatic repulsion. Michaelis demonstrated the membrane potential (1926) and proposed that it was related to the distribution of ions across the membrane. Harvey and Danielli (1939) proposed a lipid bilayer membrane covered on each side with a layer of protein to account for measurements of surface tension. In 1941 Boyle & Conway showed that the membrane of frog muscle was permeable to both K+ and Cl-, but apparently not to Na+, so the idea of electrical charges in the pores was unnecessary since a single critical pore size would explain the permeability to K+ , H+, and Cl- as well as the impermeability to Na+, Ca+, and Mg++.
Over the same time period, it was shown (Procter & Wilson, 1916) that gels, which do not have a semipermeable membrane, would swell in dilute solutions. Loeb (1920) also studied gelatin extensively, with and without a membrane, showing that more of the properties attributed to the plasma membrane could be duplicted in gels without a membrane. In particular, he found that an electrical potential difference between the gelatin and the outside medium could be developed, based on the H+ concentration. Some criticisms of the membrane theory developed in the 1930's, based on observations such as the ability of some cells to swell and increase their surface area by a factor of 1000. A lipid layer cannot stretch to that extent without becoming a patchwork (thereby losing its barrier properties. Such criticisms stimulated continued studies on protoplasm as the principle agent determining cell permeability properties. In 1938, Fischer proposed that water in the protoplasm is not free but in a chemically combined form—the protoplasm represents a combination of protein, salt and water—and demonstrated the basic similarity between swelling in living tissues and the swelling of gelatin and fibrin gels. Nasonov (1944) viewed proteins as the central components responsible for many properties of the cell, including electrical properties.
By the 1940’s, the bulk phase theories were not as well developed as the membrane theories. In 1941, Brooks & Brooks published a monograph The Permeability of Living Cells, which rejects the bulk phase theories.
The emergence of the steady-state membrane pump concept
With the development of radioactive tracers, it was shown that cells are not impermeable to Na+. This was difficult to explain with the membrane barrier theory, so the sodium pump was proposed to continually remove Na+ as it permeates cells. This drove the concept that cells are in a state of dynamic equilibrium, constantly using energy to maintain ion gradients. In 1935, Lohmann discovered ATP and its role as a source of energy for cells, so the concept of a metabolically-driven sodium pump was proposed.
The tremendous success of Hodgkin, Huxley, and Katz in the development of the membrane theory of cellular potentials, with differential equations that modeled the phenomena correctly, provided even more support for the membrane pump hypothesis.
The modern view of the plasma membrane is of a fluid lipid bilayer that has protein components embedded within it. The structure of the membrane is now known in great detail, including 3D models of many of the hundreds of different proteins that are bound to the membrane.
These major developments in cell physiology placed the membrane theory in a position of dominance and stimulated the imagination of most physiologists, who now apparently accept the theory as fact—there are, however, a few dissenters.
The reemergence of the bulk phase theories
In 1956, Troshin published a book, The Problems of Cell Permeability, in Russian (1958 in German, 1961 in Chinese, 1966 in English) in which he found that permeability was of secondary importance in determination of the patterns of equilibrium between the cell and its environment. Troshin showed that cell water decreased in solutions of galactose or urea although these compounds did slowly permeate cells. Since the membrane theory requires an impermeant solute to sustain cell shrinkage, these experiments cast doubt on the theory. Others questioned whether the cell has enough energy to sustain the sodium/potassium pump. Such questions became even more urgent as dozens of new metabolic pumps were added as new chemical gradients were discovered.
In 1952, Gilbert Ling became the champion of the bulk phase theories (almost completely isolated from the rest of biology for his cheek) and proposed his association-induction hypothesis of living cells.
The Association-Induction Hypothesis
The association-induction (AI) hypothesis is based on the concept that water in cells is in a unique state and that the living state does not exist without such water. This state is called polarized multilayers and relies on the spacing of polarized groups on the protein backbone to increase the effective distance over which they affect water molecules. Water in polarized multilayers is in a higher energy state than in bulk water and can differentially exclude solutes. The AI hypothesis holds that the majority of intracellular ions are adsorbed onto charged sites on macromolecules; the preferential adsorption of K+ being due to the inductive effect of the neighboring molecular groups affecting the electron densities of carboxyl groups on proteins. Surprisingly, this apparently radical theory yields almost identical experimental predictions as the membrane pump theory for most questions. Ling and others have doggedly pursued the areas where there seem to be differences in the predictions, and have claimed success in showing that the AI hypothesis is the better.
Biologists, unlike physicists, seems to show very little inclination to question the fundamental building blocks of the modern conceptual model. Thus Ling and his followers have been largely ignored or dismissed as crackpots. Interestingly, Raymond Damadian, the inventor of MRI based the idea on the AI hypothesis. At worst, they have exposed many weaknesses involved with treating cells as bags of salty water.
The outside of a cell is a complicated structure.
http://people.ucalgary.ca/~kmuldrew/cryo_course/cryo_chap3_2.html
Saturday, April 7, 2012
The big fat difference between HFCS and Sucrose.
Many claim high fructose corn syrup(HFCS) and table sugar(sucrose) are exactly the same. HFCS intake has increased drastically in the past 40 years at the expense of other sweeteners.
High-fructose corn syrup is produced by milling corn to produce corn starch, then processing that starch to yield corn syrup, which is almost entirely glucose, and then adding enzymes that change some of the glucose into fructose.
Whajudi analyzed samples of HFCS in 10 commercial beverages before and after hydrolyzing it in acid to break down the other carbohydrates present in it; they found that the carbohydrate content was 4-5 times higher than the listed values.(1)
Many of the extra calories are in the form of maltodextrin, an oligosaccharide, which is digested into glucose. It is easy to think sugar causes obesity when your soda contains 4-5x the listed calories.
1. http://www.fasebj.org/cgi/content/meeting_abstract/24/1_MeetingAbstracts/562.1
Practical ways to lose fat
Much attention is put on weight loss at the sacrifice to all other health markers. Most weight loss protocols lower metabolism and leave the dieter with long term health problems. Weight loss protocols often focus on the number on the scale and not how much actual fat mass is lost. Weight loss on these diets often occurs mostly from the loss of lean tissue, water and glycogen in the short term which gives the impression that these diets are beneficial. This breakdown of tissue and glycogen lowers metabolism and releases stress hormones. The stress hormones such as ACTH, PTH, cortisol, adrenalin etc. are protective in the short term but when they are relied on too heavily which is common in dieting they often lead to degenerative diseases.
Minimizing the stress induced breakdown of tissue that accompanies weight loss can help to prevent these problems. Calcium inhibits bone loss accompanied by weight loss(1), dairy has an even greater effect due to the protein.(2) Increasing 1,25-dihydroxyvitamin D in response to low-calcium diets stimulates adipocyte Ca2+ influx and, as a consequence, stimulates lipogenesis, suppresses lipolysis, and increases lipid accumulation, whereas increasing dietary calcium inhibits these effects and markedly accelerates fat loss in mice subjected to caloric restriction.(3) Calcium lowers PTH, high PTH is associated with insulin resistance, diabetes and weight gain.(4) Sucrose lowers ACTH the main pituatry stress hormone but glucose has no effect.(5) Low sodium diet raises plasma and tissue catecholamine levels.(6)
Factors that raise metabolism and thermogenesis can help preserve metabolism during calorie deficits and can promote fat loss in calorie stable diets. Substitution of calcium-rich foods(dairy) in isocaloric diets reduced adiposity and improved metabolic profiles in obese African Americans without energy restriction or weight loss.(7) Increasing dietary calcium significantly augmented weight and fat loss secondary to caloric restriction and increased the percentage of fat lost from the trunk region, whereas dairy products exerted a substantially greater effect.(8) 800 calorie Sucrose diet prevented the fall in both resting metabolic rate and triiodothyronine(T3) concentrations as compared with values during an isocaloric carbohydrate-free diet.(9) Rats given a sucrose solution ad libitum increase energy consumption by 15% compared to water.(10) Salt increases thermogenesis by increasing active brown adipose tissue.(11) Animals on low salt diet have higher weight gain and lower thyroid hormone levels than animals on high salt diet.(12)
Many low carbohydrate proponents claim it is the carbohydrates that stimulate fat storage but numerous studies have shown this to be false.
A review of the literature by Eric Jequier(13) found normal glycogen stores are between 250 - 500g, on the order of magnitude of "normal" carb consumption of 250-300g/day and Chronic overeating of carbs results in an increase of glycogen stores by about 500g before DNL becomes significant. Only with chronic overfeeding and saturated glycogen stores does conversion of carbs to fat become significant. Excessive carbohydrate ingestion is accommodated for by increasing carbohydrate oxidation and glycogen synthesis. Minor lipids formed by DNL are subsequently oxidized. So even during overfeeding conditions it is nearly impossible to induce fat gain from pure carbohydrate diets due to carbohydrates ability to promote its own oxidation through increased metabolism and thermogenesis.
Fat on the other hand suffers a much different fate, Most dietary fat transported in chylomicrons is taken up by fat tissue. Dietary fat does not induce marked increases in lipid oxidation rates in an acute manner. So if you overfeed on fat you just get fat, no increase in metabolism. Insulin does suppress non-esterfied fatty acid release, but never entirely. Running on fatty acids as is recommended by low carb proponents is correlated with reductions in insulin-mediated glucose oxidation and elevated free fatty acids(which accompanies low carb/low calorie diets) plays a role in the development of insulin resistance.
Based on all these factors a moderate plan for weight loss would be a diet of mostly low fat milk/dairy products free of allergens(such as vitamins, enzymes, cultures, vegetable/microbial rennet and gums), ripe fruits such as fresh squeezed strained OJ, grapes, cherries, melons, tropical fruits and nutrient dense foods such as liver, shellfish, eggs, cocoa. If you have no sources of clean dairy or do not tolerate it you could use bony cuts or muscle meat+gelatin from ruminant animals and potatoes. Egg shell or oyster shell can be used as a supplement to get the needed calcium. Sodium can also replace calcium to a certain degree and a high sodium diet will help keep stress hormones low and metabolism high. Unripe fruits such as bananas, apples, peaches etc. can be cooked to be made more tolerable, other wise they should be avoided.
Eating frequent small meals that always contain some sugar and protein will keep stress hormones low and metabolism high. Using temperature is a useful tool, it should rise after breakfast and if it falls through out the day you know you need to eat more sugar/protein. Measuring every couple hours to monitor temp changes can be of benefit at first and using bodily cues such as cold feet and cold hands can help signal when to eat more. You can use temperature stats to determine how much you can safely restrict without lowering metabolism and associated health declines. During the first week or 2 temperature may go lower after a meal which means stress hormones were high, once your body adapts to the increase in sugar and protein temperature should normalize.
Strength training a couple times a week can help build lean mass which will increase metabolism and rate of fat burning. Supplements such as a daily aspirin with minimal ingredients and baking soda can be used along with diet to get your metabolism working in the right direction.
1. http://onlinelibrary.wiley.com/doi/10.1359/jbmr.2001.16.1.141/full
2. http://jn.nutrition.org/content/134/3/568.short
3. http://www.nature.com/oby/journal/v12/n4/abs/oby200467a.html
4. http://www.ncbi.nlm.nih.gov/pubmed/14592784
5. http://www.ncbi.nlm.nih.gov/pubmed/19709691
6. http://www.ncbi.nlm.nih.gov/pubmed/6509785
7. http://www.nature.com/oby/journal/v13/n7/abs/oby2005144a.html
8. http://www.nature.com/oby/journal/v12/n4/abs/oby200467a.html
9. http://www.ncbi.nlm.nih.gov/pubmed/3740086
10. http://www.sciencedirect.com/science/article/pii/S1262363607701842
11. http://www.ncbi.nlm.nih.gov/pubmed/6086543
12. http://www.ncbi.nlm.nih.gov/pubmed/6086543
13. journals.cambridge.org/action/displayFulltext?type=1&fid=789552&jid=PNS&volumeId=54&issueId=01&aid=789544
Friday, April 6, 2012
Benefits of fructose
-Fructose is the main sugar involved in reproduction, developing fetus, seminal and intrauterine fluid. It has been suggested that the predominance of fructose rather than glucose in the embryo's environment helps to maintain ATP and oxidative state during development in a low oxygen environment.(1)
-Fructose protects the liver from hypoxic cell death.(2)
-Fructose can protect against the stress of increased hydrogen peroxide and it's metabolite fructose1,6-bisphosphate is an even more effective antioxidant.(3)
-Fructose decreases capillary leakage; after 4 weeks and 8 weeks on a 60% fructose diet it produced a 51% and a 56% decrease in capillary leakage, respectively.(4)
-During exercise addition of fructose to glucose increases carbohydrate metabolism.(5,6)
-Glucose causes smaller increases in metabolic rate in overweight people versus healthy people but fructose increases there metabolic rate to the same levels.(7, 8)
-Fructose increases CO2 more, blood temperature more, and causes a greater oxygen consumption compared to glucose.(9)
-Fructose reduces hypoglycemia associated with glucose even when insulin secretion is compromised.(10)
-Fructose decreases the glycemic response to an oral glucose test.(11)
-Glucose causes an increase in ROS formation and nf-kappab binding; these changes are absent when fed fructose or orange juice.(12)
-Fructose affects the body's ability to retain nutrients including magnesium, copper, calcium and other minerals. Comparing a diet with 20% calories as fructose or from cornstarch researchers conclude dietary fructose enhances mineral balance.(13)
-Glucose rather than fructose exerts a more deleterious effects on mineral balance and bone.(14)
-Rats on high sucrose diet deficient in vitamin D maintain calcium homoestasis unlike rats fed glucose, they have normal uptake by bone and development but they have lighter bones than vitamin D fed rats.(15)
-The extracellular phosphorylated fructose metabolite, diphosphoglycerate, has an essential regulatory effect in the blood.(16)
-Another fructose metabolite fructose diphosphate can reduce mast cell histamine release(17) and protect against hypoxic injury.(18)
- Fructose-1,6-bisphosphate (FBP) inhibits cytokine/chemokine-induced sensitivity to pain.(19)
1. http://jcem.endojournals.org/content/90/2/1171.short
2. http://ajpgi.physiology.org/content/253/3/G390.abstract
3. http://www.sciencedirect.com/science/article/pii/S0008621509002456
4. http://www.nature.com/ajh/journal/v11/n5/full/ajh199884a.html
5. http://www.ncbi.nlm.nih.gov/pubmed/15946410
6. http://jap.physiology.org/content/76/3/1014.short
7. http://www.ncbi.nlm.nih.gov/pubmed/2099997
8. http://www.ajcn.org/content/58/5/766S.short
9. http://ajpendo.physiology.org/content/264/4/E504.abstract
10. http://diabetes.diabetesjournals.org/content/51/2/469.short
11. http://care.diabetesjournals.org/content/24/11/1882.full
12. http://care.diabetesjournals.org/content/30/6/1406.short
13. http://www.ajcn.org/content/49/6/1290.abstract
14. http://www.sciencedirect.com/science/article/pii/S8756328208000823
15. http://www.ncbi.nlm.nih.gov/pubmed/1221903
16. http://www.ncbi.nlm.nih.gov/pubmed/2383774
17. http://www.ncbi.nlm.nih.gov/pubmed/6193798
18. http://www.ncbi.nlm.nih.gov/pubmed/6238213
19. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757696
-Fructose protects the liver from hypoxic cell death.(2)
-Fructose can protect against the stress of increased hydrogen peroxide and it's metabolite fructose1,6-bisphosphate is an even more effective antioxidant.(3)
-Fructose decreases capillary leakage; after 4 weeks and 8 weeks on a 60% fructose diet it produced a 51% and a 56% decrease in capillary leakage, respectively.(4)
-During exercise addition of fructose to glucose increases carbohydrate metabolism.(5,6)
-Glucose causes smaller increases in metabolic rate in overweight people versus healthy people but fructose increases there metabolic rate to the same levels.(7, 8)
-Fructose increases CO2 more, blood temperature more, and causes a greater oxygen consumption compared to glucose.(9)
-Fructose reduces hypoglycemia associated with glucose even when insulin secretion is compromised.(10)
-Fructose decreases the glycemic response to an oral glucose test.(11)
-Glucose causes an increase in ROS formation and nf-kappab binding; these changes are absent when fed fructose or orange juice.(12)
-Fructose affects the body's ability to retain nutrients including magnesium, copper, calcium and other minerals. Comparing a diet with 20% calories as fructose or from cornstarch researchers conclude dietary fructose enhances mineral balance.(13)
-Glucose rather than fructose exerts a more deleterious effects on mineral balance and bone.(14)
-Rats on high sucrose diet deficient in vitamin D maintain calcium homoestasis unlike rats fed glucose, they have normal uptake by bone and development but they have lighter bones than vitamin D fed rats.(15)
-The extracellular phosphorylated fructose metabolite, diphosphoglycerate, has an essential regulatory effect in the blood.(16)
-Another fructose metabolite fructose diphosphate can reduce mast cell histamine release(17) and protect against hypoxic injury.(18)
- Fructose-1,6-bisphosphate (FBP) inhibits cytokine/chemokine-induced sensitivity to pain.(19)
1. http://jcem.endojournals.org/content/90/2/1171.short
2. http://ajpgi.physiology.org/content/253/3/G390.abstract
3. http://www.sciencedirect.com/science/article/pii/S0008621509002456
4. http://www.nature.com/ajh/journal/v11/n5/full/ajh199884a.html
5. http://www.ncbi.nlm.nih.gov/pubmed/15946410
6. http://jap.physiology.org/content/76/3/1014.short
7. http://www.ncbi.nlm.nih.gov/pubmed/2099997
8. http://www.ajcn.org/content/58/5/766S.short
9. http://ajpendo.physiology.org/content/264/4/E504.abstract
10. http://diabetes.diabetesjournals.org/content/51/2/469.short
11. http://care.diabetesjournals.org/content/24/11/1882.full
12. http://care.diabetesjournals.org/content/30/6/1406.short
13. http://www.ajcn.org/content/49/6/1290.abstract
14. http://www.sciencedirect.com/science/article/pii/S8756328208000823
15. http://www.ncbi.nlm.nih.gov/pubmed/1221903
16. http://www.ncbi.nlm.nih.gov/pubmed/2383774
17. http://www.ncbi.nlm.nih.gov/pubmed/6193798
18. http://www.ncbi.nlm.nih.gov/pubmed/6238213
19. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757696
Saturated fat versus Unsaturated fat
Saturated fats(butter, coconut oil, hard fats) are very beneficial.
Unsaturated fats(fish oil, seed oil, liquid oils) have many harmful effects.
-Saturated fat protects against radiation induced intestinal damage, PUFA(polyunsaturated fatty acid) does not have this effect.(1)
-Alcohol liver disease is reversed when diet is composed of saturated fats(2); fish oils and unsaturated fats exacerbate the problem.(3)
-Cancers phospholipids contain less stearic acid(saturated fat) than the less malignant tumors.(4) Adding stearic acid to food delayed development of cancer in mice. (5,6)
-Saturated fatty acids are preferentially oxidized by many cells and albumin preferentially delivers saturated fat to actively metabolizing cells such as the heart. (7)
-In good health(children) the stress hormones are only produced in the amount needed because of negative feedback from the free saturated fatty acids which inhibit production of adrenalin and adrenal steroids. When fat stores are unsaturated the free fatty acids will contain PUFA mostly AA/LA these PUFA stimulate stress hormones, ACTH, cortisol, adrenaline, glucagon, and prolactin, which increase lipolysis producing more fatty acids in a vicious cycle. (8)
-PUFA alters structure of the protein alpha-synuclein; causing it to take the form seen in parkinsons and other brain conditions. Saturated fats have opposite effect on alpha-synuclein. (9)
-When the brain is injured AA and DHA(unsaturated fats) contribute to brain edema, weakening the blood brain barrier, increasing protein break down, inflammation and peroxidation. Stearic acid in the same amount caused no harm.(10)
1. http://ajpgi.physiology.org/content/256/1/G178.short
2. http://jpet.aspetjournals.org/content/299/2/638.short
3. http://onlinelibrary.wiley.com/doi/10.1002/hep.510260622/abstract
4. http://www.springerlink.com/content/380852k748100565
5. http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910340416/abstract
6. http://www.ncbi.nlm.nih.gov/pubmed/8621270
7. http://www.ncbi.nlm.nih.gov/pubmed/564268
8. http://www.ncbi.nlm.nih.gov/pubmed/15123208
9. http://www.ncbi.nlm.nih.gov/pubmed/12597857
10. http://www.ncbi.nlm.nih.gov/pubmed/17854901
Tuesday, April 3, 2012
Athletic advantage of Co2
During exercise the muscle cannot get enough oxygen and starts inefficiently breaking down glucose into small amounts of energy and lactic acid; this is known as anaerobic glycolysis. Anaerobic glycolysis sets off many inflammatory signals and produces far less Co2/energy than the more evolved oxidative metabolism.
Training at high altitude has been used by competitive athletes as a means of improving their potential. Because of low oxygen pressure at high altitude athletes retain more Co2 which allows more efficient use of oxygen so glucose is shuttled through oxidative metabolism.(1). Increased oxidative metabolism produces less lactic acid so athletes can train longer(2, 3).
Methods that increase Co2 concentrations in the body such as baking soda improve athletic performance and recovery(4, 5, 6). Nose breathing increases Co2 compared to mouth breathing(7). High carbohydrate diet increases Co2 more compared to low carbohydrate diet(8). A high sugar diet increases Co2 more compared to a high starch diet(9).
1. http://jap.physiology.org/content/100/6/1938.long
2. http://physiologyonline.physiology.org/content/17/3/122.full
3. http://jap.physiology.org/content/70/5/1963.abstract
4. http://www.ncbi.nlm.nih.gov/pubmed/8388767
5. http://www.ncbi.nlm.nih.gov/pubmed/9296948
6. http://www.ncbi.nlm.nih.gov/pubmed/15514504
7. http://www.ncbi.nlm.nih.gov/pubmed/3141357
8. http://www.annals.org/content/103/6_Part_1/883.abstract
9. http://ajpendo.physiology.org/content/264/4/E504.abstract
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