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The major source of carbon for gluconeogenesis during exercise is effective 30gm acticin, of course buy 30 gm acticin visa, lac- tate cheap 30 gm acticin visa, produced by the exercising muscle cheap acticin 30 gm otc, but amino acids and glycerol are also used (Fig discount 30 gm acticin visa. Epinephrine released during exercise stimulates liver glycogenolysis and gluconeogenesis by causing cAMP levels to increase. During long periods of exercise, blood glucose levels are maintained by the liver through hepatic glycogenolysis and gluconeogenesis. The amount of glucose that the liver must export is greatest at higher work loads, in which case the muscle is using a greater proportion of the glucose for anaerobic metabolism. With increasing duration of exercise, an increasing proportion of blood glucose is supplied by gluconeogene- sis. However, for up to 40 minutes of mild exercise, glycogenolysis is mainly respon- sible for the glucose output of the liver. However, after 40 to 240 minutes of exercise, the total glucose output of the liver decreases. This is caused by the increased utiliza- tion of fatty acids, which are being released from adipose tissue triacylglycerols (stim- ulated by epinephrine release). Glucose uptake by the muscle is stimulated by the increase in AMP levels and the activation of the AMP-activated protein kinase, which stimulates the translocation of GLUT4 transporters to the muscle membrane. The hormonal changes that direct the increased hepatic glycogenolysis, hepatic glu- coneogenesis, and adipose tissue include a decrease in insulin and an increase in glucagon, epinephrine, and norepinephrine. Plasma levels of growth hormone, cortisol, and thyroid-stimulating hormone (TSH) also increase and may make a contribution to 876 SECTION EIGHT / TISSUE METABOLISM Remember from Chapter 1 that a 2. One gram of glucose Glycogen can give rise to 4 kcal of energy, so at a rate of consumption of 500 Calories per hour we 1. In the fasting state, blood glucose levels are approximately 90 mg/dL, or 900 mg/L. Glycerol If not replenished, that amount of glucose Pyruvate Amino acids would only support 2. Amino acids Lactate 25% Lactate 23% 45% 40 min 240 min Basal Exercise Fig. Production of blood glucose by the liver from various precursors during rest and during prolonged exercise. The shaded area represents the contribution of liver glycogen to blood glucose, and the open area represents the contribution of gluconeogenesis. Metabolic Adaptation to Prolonged Phys- ical Exercise. The activation of hepatic glycogenolysis occurs through glucagon and epinephrine release. Hepatic gluconeogenesis is activated by the increased supply of precursors (lactate, glycerol, amino acids, and pyruvate), the induction of gluconeogenic enzymes by glucagon and cortisol (this only occurs in pro- longed exercise), and the increased supply of fatty acids to provide the ATP and NADH needed for gluconeogenesis and the regulation of gluconeogenic enzymes. Free Fatty Acids as a Source of ATP The longer the duration of the exercise, the greater the reliance of the muscle on free fatty acids for the generation of ATP (Fig. Because ATP generation from 100 Muscle glycogen 75 Blood–borne fatty acids 50 Blood–borne glucose 25 Exhaustion 0 1 2 3 4 Hours Fig. The pattern of fuel utilization changes with the dura- tion of the exercise. CHAPTER 47 / METABOLISM OF MUSCLE AT REST AND DURING EXERCISE 877 free fatty acids depends on mitochondria and oxidative phosphorylation, long-dis- tance running uses muscles that are principally slow-twitch oxidative fibers, such as the gastrocnemius. It is also important to realize that resting skeletal muscle uses free fatty acids as a principle fuel. At almost anytime except the postprandial state (right after eating), free fatty acids are the preferred fuel for skeletal muscle. The preferential utilization of fatty acids over glucose as a fuel in skeletal mus- cle depends on the following factors: 1. The availability of free fatty acids in the blood, which depends on their release from adipose tissue triacylglycerols by hormone-sensitive lipase. During pro- longed exercise, the small decrease of insulin, and increases of glucagon, epi- nephrine and norepinephrine, cortisol, and possibly growth hormone all activate adipocyte tissue lipolysis.

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Philadelphia: Lippincott leukocytes themselves may be de- Williams & Wilkins cheap 30 gm acticin free shipping, 2000 discount acticin 30gm on-line. A mixture of dead and living THE BLOOD 269 Bacterium Leukocyte Lysosome Bacterium Vesicle Lysosome Blood Digestive products Erythrocyte Capillary wall Epithelial cell Residue A B Figure 13-6 Phagocytosis purchase acticin 30 gm otc. ZOOMING IN What type of epithelium makes up the capillary wall? A collection of pus localized in one area is known as lining of the blood vessels generic acticin 30 gm with amex, as in the case of injury generic acticin 30 gm free shipping, the an abscess. The platelets then release chemicals that partici- ture into macrophages (MAK-ro-faj-ez), which are highly pate in the formation of a clot to stop blood loss. More de- active in disposing of invaders and foreign material. Some lymphocytes become plasma cells, active in the production of circulating antibodies needed for immu- ◗ Hemostasis nity. The activities of the various white cells are further discussed in Chapter 17. Hemostasis (he-mo-STA-sis) is the process that prevents blood loss from the circulation when a blood vessel is Checkpoint 13-8 What are the types of granular leukocytes? Events in hemostasis include the following: Checkpoint 13-9 What is the most important function of leuko- cytes? Contraction of the smooth muscles in the blood vessel wall. This reduces the flow of blood and loss from the defect in the vessel wall. The term for this reduction in Platelets The blood platelets (thrombocytes) are the the diameter of a vessel is vasoconstriction. Activated platelets be- tiny structures are not cells in them- selves but rather fragments constantly Platelets released from giant bone marrow cells called megakaryocytes (meg-ah-KAR- Erythrocytes e-o-sites) (Fig. Platelets do not have nuclei or DNA, but they do con- Platelets tain active enzymes and mitochondria. The number of platelets in the circulat- ing blood has been estimated to range from 150,000 to 450,000 per L A Platelets B Megakaryocyte (mm3). Philadelphia: Lippincott Williams & Wilkins, agulation (clotting). Blood Clotting The fluid that remains after clotting has occurred is called serum (plural, sera). Serum contains all the com- The many substances necessary for blood clotting, or co- ponents of blood plasma except the clotting factors, as ex- agulation, are normally inactive in the bloodstream. A pressed in the formula: balance is maintained between compounds that promote clotting, known as procoagulants, and those that prevent Plasma serum clotting factors clotting, known as anticoagulants. In addition, there are Several methods used to measure the body’s ability to chemicals in the circulation that act to dissolve any un- coagulate blood are described later in this chapter. Under normal conditions, the substances that prevent clot- Checkpoint 13-11 What happens when fibrinogen converts to ting prevail. The clotting process is a well-controlled series of sep- arate events involving 12 different factors, each desig- nated by a Roman numeral. The final step in these reac- ◗ Blood Types tions is the conversion of a plasma protein called If for some reason the amount of blood in the body is se- fibrinogen (fi-BRIN-o-jen) into solid threads of fibrin, verely reduced, through hemorrhage (HEM-eh-rij) (ex- which form the clot. One possible measure to tion are described below and diagrammed in Figure 13-8: take in such an emergency is to administer blood from ◗ Substances released from damaged tissues result in the another person into the veins of the patient, a procedure formation of prothrombinase (pro-THROM-bih-nase), called transfusion. Care must be taken in transferring a substance that triggers the final clotting mechanism. Fibrin forms a network of threads that are said to be hemolyzed (HE-mo-lized), and the result- entraps plasma and blood cells to form a clot. Certain proteins, called antigens (AN-ti-jens) or ag- Blood clotting occurs in response to injury. Blood also glutinogens, on the surface of the red cells cause these in- clots when it comes into contact with some surface other compatibility reactions.

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Then at age 9 years discount acticin 30 gm on line, Stephanie graphs of both hips showed anterior dislocations (Fig- was seen with the right hip flexed and adducted buy acticin 30 gm visa, which ure C10 purchase acticin 30 gm visa. Her mother was instructed to prevent ab- was causing her pain (Figure C10 discount acticin 30 gm with amex. Hip 591 to be a posterolateral dislocation buy 30gm acticin visa, which was reduced in flexion making seating difficult (Figure C10. The the clinic, and her mother was shown how to reduce dis- mother only agreed to allow reconstruction after she also locations if they should occur. She continued to have in- developed severe scoliosis. The scoliosis was corrected first termittent anterior dislocations over the next several years, followed by the hip reconstruction (Figure C10. By and on many occasions her mother could not reduce a this time, the hip was in a fixed dislocation for 18 months posterior dislocation and brought her to the clinic for us with hip adduction and flexion (Figure 10. By age 12 years, when she was growing ever, following reconstruction, the hip was again in good rapidly, her mother could no longer position her to keep position (Figure C10. By the 3-year follow-up, the the hip reduced and she developed a fixed posterior dis- hip remodeled and she was stable and pain free (Figure location (Figure C10. For this reason, we have tried to keep these children in either in- ternally rotating orthotics or have asked parents to keep their children’s legs together to prevent them from lying with their lower extremities in the ab- ducted, externally rotated position. Complications The major complication of a type III anterior dislocation is that a recurrent dislocation will occur. If children are ambulators, it is reasonable to make a second attempt to get the hip reconstructed. Hip 593 one child in whom a second acetabular reconstruction was required; this was successful in maintaining the hip reduced and keeping the child walking until she became a young adult. We anticipate, although we have no experi- ence, that these individuals should maintain stable hip joints once they reach full adulthood. Inferior Hip Dislocation Direct inferior dislocations of the hip are very rare. We have only treated one such deformity and have had the opportunity to examine another patient (Case 10. Both these individuals had tremendous difficulty with seating because their legs were fixed in a severe, abducted hip and knee-flexed posi- tion making seating almost impossible. A hip radiograph showed inferior hip sub- had a tracheal diversion. A redirectional varus femoral because of difficulty sitting and a complaint from the osteotomy did not greatly change the hip position but al- mother that he sometimes got his knee stuck in his axilla lowed easier sitting and lying in a more normal position when lying. On physical examination he had fixed hip (Figure C10. Our single treatment experience with this type of inferior dislocation is a varus repositioning os- teotomy that allowed this individual to sit much better. The hip did not be- come painful, although this child had severe neurologic involvement that required a tracheostomy. Six years after the varus osteotomy, this child died of aspiration through his tracheal diversion. Hyperabducted and Extended Hip Deformities A small group of children develop severe, bilateral abducted hips. Some of the children have extension contractures and have more or less flexion. This deformity creates great difficulty with seating88 and is a very socially un- appealing posture for adolescents and young adults (Case 10. Etiology There are children in whom the etiology of this hyperextended and abducted position is iatrogenic, related to too much adductor and iliopsoas lengthening with obturator neurectomies. Another large group of children develop this deformity unilaterally and it be- comes a windblown hip posture. The natural history of this hyperabduction deformity is not well docu- mented; however, in our experience, it generally does not get progressively worse as children get older. The problem occurs as children get older and bigger, making it more difficult to accommodate the deformity. With some attention to seating modifications, many of these children develop good pat- terns of sitting and can often spend long periods of time lying in a side lying position. This deformity is a very cosmetically objectionable posture, espe- cially for adolescent and young adult females, to be lying in the hyperab- ducted hip-flexed position every time they are not sitting in their wheelchairs.

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