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ATP regeneration in skeletal muscle is a collective term for the metabolic systems and enzymatic pathways responsible for rapidly and repeatedly resynthesizing adenosine triphosphate (ATP), the major energy currency of the cell, during and after periods of muscle contraction. This process primarily involves three energy systems: the phosphagen (creatine phosphate) system, glycolysis (anaerobic), and mitochondrial oxidative phosphorylation (aerobic metabolism)[1][2][3][4][5]. Since ATP stores in muscle are limited, these pathways are essential for sustaining muscle force and work output, especially during exercise. Dysfunction of ATP regeneration mechanisms contributes to muscle fatigue, decreased exercise capacity, insulin resistance, and muscle degeneration in various diseases[3][4][5]. There is no single molecular drug target named "ATP regeneration in skeletal muscle"; instead, multiple enzymes and transporters are involved in the process, such as creatine kinase, adenylate kinase, glycolytic enzymes (phosphofructokinase), fatty acid transporters (CD36), mitochondrial respiratory chain complexes, and TCA cycle enzymes[1][3][5]. Drugs typically modulate these individual components, not the overall process of ATP regeneration as a discrete target.
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