The lipid component of the typical Western diet consists of triglycerides, phospholipids, and cholesterol. Triglycerides constitute the majority of dietary lipid intake, reaching approximately 150 g/day. Digestion of triglycerides is initiated by lingual lipase, which is secreted by glands in the mouth, contributing to limited digestion in the stomach. In order for lingual lipase to exert its effect on triglycerides, emul-sification must take place by a combination of stomach contraction and acid milieu. The partially digested lipid emulsion exits the stomach and is introduced to bile, composed mostly of bile acids and salts, in the proximal small intestine. In the fasting state, bile acids are concentrated in the gallbladder.
After food consumption, bile enters the duodenum in response to cholecystoki-nin-pancreozynim.6 Bicarbonate from the pancreas creates a favorable pH for emul-sification and hydrolysis of triglycerides and, in conjunction with bile, creates an optimal environment for pancreatic lipase. Hydrolysis of triglycerides by pancreatic lipase results in a mixture of monoglycerides, diglycerides, and free fatty acids. Only a small portion of triglycerides are completely hydrolyzed to glycerol and free fatty acids. Bile acids and salts, along with phospholipids, aid in lipid absorption by forming micelles. This aggregation of molecules in a colloidal system allows for the solubility of the hydrophobic molecules by positioning the polar portions of bile salts, bile acids, and phospholipids outward. This outward polarity allows the micelle to penetrate the unstirred water layer, allowing for absorption into the intestinal mucosal cells, or enterocytes. The lipid contents of the micelles then enter the enterocytes by several mechanisms, i.e., simple diffusion, facilitated diffusion, and active transport involving membrane transporters. For fatty acids longer than 10 to 12 carbons in length, an intracellular re-formation of triglycerides then occurs. Shorter-chained fatty acids (up to 10 to 12 carbons in length) are directly shuttled into the portal blood and transported to the liver.
After absorption and reassembly of the long-chain fatty acids into triglycerides in the intestine, the triglycerides are packaged into chylomicrons. Chylomicrons are lipoprotein particles containing approximately 90% triglyceride, with the remaining 10% consisting of cholesterol, phospholipids, and protein.7 Several apolipoproteins, protein components in lipoprotein particles, are present in chylomicrons, including apoB-48, apoAs of intestinal origin, apoCs, and apoE. After dietary intake of lipids, chylomicrons are generated in intestinal mucosal cells and play a role in the postprandial transport of exogenous (dietary) cholesterol and triglycerides to other tissues. Triglyceride hydrolysis occurs in the circulation by the action of lipoprotein lipase, an extracellular enzyme that resides on the capillary walls, predominantly in adipose tissue and cardiac and skeletal muscle, releasing free fatty acids and dig-lycerides to be absorbed into the tissues for energy. The remaining lipoprotein particle, termed a chylomicron remnant, travels through the bloodstream to be taken into the liver by endocytosis mediated by a specific receptor for apoE.8
Fatty acids introduced to the tissues are either utilized for energy or stored for later use, depending on the energy state of the body. In a fed state, fatty acids are primarily used for the synthesis of triglycerides in subcutaneous and deep visceral adipose tissue. While only approximately 450 g of glycogen can be stored in the body at one time, a nearly unlimited capacity for fat storage exists. Fat storage depends on the individual. For nonobese males, average triglyceride storage ranges between 9 and 15 kg, translating into a total energy storage of 80,000 to 140,000 kcal.9 While trained athletes have less fat reserves, ample amounts remain to provide energy in times of prolonged periods of insufficient energy intake. Not only in caloric deprivation, but in states of high energy expenditure, carbohydrate availability may be limited and utilization of fat stores may be warranted.
In addition to the fat storage in adipose tissue, a small amount of fat is present as lipid droplets in muscle tissues, or in circulation as free fatty acids associated with albumin or as part of a lipoprotein particle. The amount of fat both in the plasma and stored in muscle varies according to several factors, including energy state, fitness level, and dietary fat intake. Within the muscle cells, free fatty acids are primarily oxidized for energy.
Triglycerides in the body are continuously being hydrolyzed and esterified, depending on the body's energy status, i.e., a fed or fasting state. When the body is in an energy-deficient state, as occurs with exercise, increased hydrolysis of triglyceride stores and resultant liberation of fatty acids from adipose and muscle tissue occur. During exercise, fat and carbohydrate metabolism are tightly coupled, both controlled by nervous and hormonal mechanisms. At rest, total energy provision is greatly supplemented by fat oxidation, whereas a majority of the energy is obtained from glycogen stores during intense, short-term exercise. As exercise continues, the use of carbohydrate as a fuel source decreases while the utilization of fat via oxidation of muscle and adipose triglyceride stores increases. The proportion of each substrate utilized depends on factors such as the duration and intensity of exercise, the fitness level of the individual, and the meal prior to exercise.
Specific hormones increase during exercise, stimulating fat mobilization, transport, and oxidation. Lipolysis is initiated in the adipocytes, stimulated by epinephrine and norepinephrine, which can activate hormone-sensitive lipase (HSL). The release of epinephrine and norepinephrine also inhibits pancreatic insulin secretion, decreasing its inhibition of HSL. The free fatty acids produced by lipolysis are transported across the adipocyte plasma membrane either passively or via transport proteins such as fatty acid binding protein and fatty acid translocase.10 Once the free fatty acids reach circulation, they are bound to albumin and transported to muscle tissue. Since exercise-induced energy deficiency is occurring, reesterification of fatty acids to triglycerides is suppressed and lipolysis is accelerated, increasing blood levels of free fatty acid bound to albumin during exercise.11
Once the fatty acids are in the cytoplasm of the muscle cells, they are transported across the mitochondrial membrane by carnitine palmityol transferases I and II for P-oxidation and energy production. During exercise, total fat oxidation rates can increase more than ten-fold during the transition from rest to moderate-intensity exercise.9 The availability of glucose, rather than that of fatty acids, controls the rate of fatty acid oxidation because glucose can decrease the oxidation of long-chain fatty acids by inhibiting their transport into the mitochondria.12
In addition to the use of fatty acids liberated from adipocytes, or obtained from the plasma as albumin-bound long-chained fatty acids or in very low-density lipoproteins (VLDLs), research indicates that the intramuscular triglyceride (IMTG) pool can serve as a dynamic fuel source during physical activity. Because no blood transport is required, intramuscular fatty acids can be readily used for energy in exercising muscle. A detailed discussion on IMTG can be found in Section 2.4.1.
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