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An abnormal accumulation of glycogen in the liver and kidneys was described by von Gierke in 1929; shortly thereafter, Pompe (1932) reported a similar disorder involving cardiac and skeletal muscle Major contributions to our understanding of glycogen metabolism were made by McArdle, by Cori and Cori, and by Hers, who discovered the de ciency of acid maltase in Pompe disease and enunciated the concept of inborn lysosomal diseases (see Chap 37) Since then, many nonlysosomal enzyme de ciencies have been identi ed and have become the basis of the classi cation presented in Table 51-1 These enzymatic de ciencies alter the metabolism of many cells but most strikingly those of the liver, heart, and skeletal muscle In about half of the affected individuals, a chronically progressive or intermittent myopathic syndrome is the major manifestation of the disease It is a curious fact, that with the exception of the rare phosphoglycerate kinase de ciency (X-linked recessive inheritance), all the glycogenoses are inherited as autosomal recessive traits The most impressive and common of these glycogen storage diseases from the standpoint of the clinical neurologist are 1,4-glucosidase (acid maltase) and myophosphorylase de ciencies Acid Maltase De ciency (Glycogenosis Type II; Pompe Disease and Related Disorders) A de ciency of this enzyme takes three clinical forms, of which the rst (Pompe disease) is the most malignant Pompe disease develops in infancy, between 2 and 6 months; dyspnea and cyanosis call attention to enlargement of the heart, and the liver may be enlarged as well The skeletal muscles are found to be weak and hypotonic, though their bulk may be increased The tongue may be enlarged, giving the infant a cretinoid appearance Hepatomegaly, while often present, is not pronounced Exceptionally, the heart is relatively normal in size, and the central nervous system and muscles bear the brunt of the disorder The clinical picture then resembles infantile spinal muscular atrophy (Werdnig-Hoffmann disease) and, to add to dif culty in differential diagnosis, there may be fasciculations The disease is rapidly progressive and ends fatally in a few months The electromyogram (EMG) shows myopathic changes, but there are, in addition, brillation potentials, heightened insertional activity, and pseudomyotonia Large amounts of glycogen accumulate in muscle, heart, liver, and neurons of the spinal cord and brain All tissues lack alpha glucosidase (acid maltase) The gene encoding acid maltase
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PRIMARY METABOLIC DISORDERS OF MUSCLE
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The chemical energy for muscle contraction is provided by the hydrolysis of adenosine triphosphate (ATP) to adenosine diphosphate (ADP); ATP is restored by phosphocreatine and ADP acting in combination These reactions are particularly important during brief, high-intensity exercise During periods of prolonged muscle activity, rephosphorylation requires the availability of carbohydrates, fatty acids, and ketones, which are catabolized in mitochondria Glycogen is the main sarcoplasmic source of carbohydrate, but blood glucose also moves freely in and out of muscle cells as needed during sustained exercise The fatty acids in the blood, derived mainly from adipose tissue and intracellular lipid stores, constitute the other major source of energy Carbohydrate is metabolized during aerobic and anaerobic phases of metabolism, the fatty acids, only aerobically Resting muscle derives approximately 70 percent of its energy from the oxidation of long-chain fatty acids As stated earlier, the circumstances during exercise are somewhat different During a short period of intense exercise, the muscle utilizes carbohydrate derived from glycogen stores; myophosphorylase is the enzyme that initiates the metabolism of glycogen With longer aerobic exercise, blood ow to muscle and the availability of glucose and fatty acids is increased At rst, glucose is the main source of energy during exercise; later, with exhaustion of the glycogen stores, energy is provided by oxidation of fatty acids Thus, muscle failure at a certain phase of exercise is predictive of the type of energy failure A rising blood concentration of -hydroxybutyrate re ects the increasing oxidation of fatty acids, and an increase in blood lactate re ects the anaerobic metabolism of glucose The cytochrome oxidative mechanisms are essential in both aerobic and 1230
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