Titlebook: Skeletal Muscle Metabolism in Exercise and Diabetes; Erik A. Richter,Bente Kiens,Bengt Saltin Book 1998 The Editor(s) (if applicable) and

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Hepatic Glucose Production during Exercise, exercise, the latter contributes substantially with prolonged exercise and the concomitant decline in liver glycogen stores and with increased gluconeogenic precursor supply. Afferent neural feedback signals from contracting muscle and feedback signals mediated via the blood stream, can stimulate g

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hypertension

Fat Metabolism in Exercise,blood to active muscle. During higher intensity exercise, triglyceride within the muscle can also be hydrolyzed to release fatty acids for subsequent direct oxidation. Control of fatty acid oxidation in exercise can potentially occur via changes in availability, or via changes in the ability of the

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Mechanisms Regulating Adipocyte Lipolysis, primary regulators of adipose tissue lipolysis, the catecholamines, bind to the α2, β1, β2, and β3 adrenergic receptors. The α2 receptor couples with Gi-proteins to inhibit cyclic AMP formation and lipolysis, while the β receptors couple with Gs-proteins to stimulate cyclic AMP formation and lipoly

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沉積物

Transport of Long-Chain Fatty Acids across the Muscular Endothelium,k. Under normal conditions fatty acids are continuously supplied from the microvascular compartment to the contracting myocytes. Exogenous fatty acids are transported to muscle tissue via the blood either complexed to albumin or covalently bound in triacylglycerols forming the neutral lipid core of

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Intracellular Transport of Fatty Acids in Muscle,enzymatic capacity. Following their uptake from the extracellular compartment the fatty acids have to translocate through the aqueous cytoplasm of the myocytes to reach the mitochondria where they undergo oxidative degradation. This intracellular transport is assisted by cytoplasmic fatty acid-bindi

intuition

Insulin Sensitivity, Muscle Fibre Types, and Membrane Lipids,re; and for the interrelationships between these variables. Taken with results provided in other chapters in this volume, the literature described gives insights into the role that certain dietary fats and physical inactivity may play in the development of insulin resistance and hence the disease cluster of the Metabolic Syndrome.