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Free fatty acids during exercise

Inherited aldolase A deficiency and pyruvate kinase deficiency in erythrocytes cause hemolytic anemia. The exercise capacity of patients with muscle phos-phofiaictokinase deficiency is low, particularly on high-carbohydrate diets. By providing an alternative lipid fuel, eg, during starvation, when blood free fatty acids and ketone bodies are increased, work capacity is improved. [Pg.143]

McNaughton, L., Two levels of caffeine ingestion on blood lactate and free fatty acid responses during incremental exercise, Research Quarterly, 58, 255, 1987. [Pg.254]

Figure 5 - Interaction of carbohydrate snd lipid metabolistn during exercise. G6P, glucose--6-phosphate F6P, fructose-6-phosphate FDP, fructose-1,6-diphosphate Pyr, Pyruvate FFA, free fatty acid TG, triglyceride HK, hexokinase PL, phosphorylase PFK, phosphofructokinase and PDH, pyruvate dehydrogenase. Figure 5 - Interaction of carbohydrate snd lipid metabolistn during exercise. G6P, glucose--6-phosphate F6P, fructose-6-phosphate FDP, fructose-1,6-diphosphate Pyr, Pyruvate FFA, free fatty acid TG, triglyceride HK, hexokinase PL, phosphorylase PFK, phosphofructokinase and PDH, pyruvate dehydrogenase.
As noted previously, like skeletal muscle, glycogen depletion in liver during endurance exercise is much less in trained animals and in animals who have had free fatty acids artificially elevated. No evidence exists that the mechanism proposed by Randle to account for the inhibition of carbohydrate metabolism in muscle by oxidation of fatty acids is operative in the liver. Thus other factors must be responsible for the slower rate of liver glycogen depletion in these situations. Such factors may include a smaller increase in catecholamine levels, a smaller reduction in insulin levels, and a smaller reduction in blood flow to the liver during exercise (19,20). [Pg.40]

During the early minutes of exercise, carbohydrate (plasma glucose and muscle glycogen) is the predominant fuel for the working muscles. When the exercise is prolonged and intensive, carbohydrate remains a predominant fuel with lipids (plasma free fatty acids and muscle triglycerides) being of lesser importance. When the exercise is of moderate intensity, lipids eventually become the primary fuel as carbohydrate stores are reduced. [Pg.40]

The level of plasma albumin-bound fatty acids increases when lipolysis rates are high. The tissue uptake of fatty acids is proportional to their concentration in plasma and is therefore largely dependent on blood flow. During intense exercise, the flow of blood through the splanchnic bed is reduced and more fatty acids are available to skeletal muscle. With the exception of nerve tissue and blood cells, tissues can use fatty acids by /3-oxidation and by the TCA cycle. Fatty acid uptake is not regulated by hormones or intracellular effectors. Free fatty acids readily diffuse across the plasma membrane of cells where they are used strictly in response to supply and demand. This is illustrated for cardiac muscle in Figure 22-20. [Pg.506]

The availability of free fatty acids in the blood, which depends on their release from adipose tissue triacylglycerols by hormone-sensitive lipase. During prolonged exercise, the small decrease of insulin, and increases of glucagon, epinephrine and norepinephrine, cortisol, and possibly growth hormone all activate adipocyte tissue lipolysis. [Pg.877]

Ketone body oxidation also increases during exercise. Their utilization as a fuel is dependent on their rate of production by the liver. Ketone bodies are, however, never a major fuel for skeletal muscle (muscles prefer free fatty acids). [Pg.877]

At rest, skeletal muscle burns free fatty acids almost exclusively (85-90 % of total energy) [25]. During exercise, muscle glycogen stores... [Pg.262]

Qolizadeh MR, Ebrahim K, Rahbar B, Karami E, Rostamkhany H, Musavi SH (2011) The effect of choline supplementation on the level of plasma free fatty acids and beta-hydroxybutyrate during a session of prolonged exercise. Annals Bio Res 2(6) 253-260... [Pg.147]

Another goal of the USDA study was to determine whether CLA enhanced energy expenditure, lipolysis, or fat oxidation in humans, similar to the effects observed in animals. Accordingly, measurements of metabolic rate and respiratory quotient were made by indirect calorimetry, and stable isotope tracers of palmitate and glycerol were used to measure the rate of appearance of free fatty acids and glycerol as well as whole body lipolysis and apparent reesterification. CLA supplementation had no effect on metabolic rate or whole-body fat oxidation rate during rest or exercise. Similarly, CLA did not change lipolytic rate, fatty acid release from adipose tissue, or apparent FFA reesterification rates under conditions of rest or exercise (33). [Pg.327]

Ahlborg G, Felig P, Hagenfeldt L, Hendler R, Wahren J. Substrate turnover during prolonged exercise in man. Splanchnic and leg metabolism of glucose, free fatty acids, and amino acids. J Clin Invest 1974 53 1080-1090. [Pg.350]


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During exercise

Free fatty acids

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