运动后过量氧耗

运动后过量氧耗（英语：Excess post-exercise oxygen consumption，简称为EPOC，非正式称为后燃烧）是身体在剧烈运动后产生的氧气摄入速率显著增加。在运动生理学发展历程中，以往曾用“氧债”（英语：oxygen debt）一词来解释无氧供能的消耗，或是尝试量化无氧供能，特别是有关乳酸代谢的部分。不过，直接及间接热量计的实验都认为乳酸代谢和氧气摄入速率增加没有关系^[1]。

在运动后，身体会用过量氧耗让身体恢复到平衡状态，并使身体适应所进行的锻炼。其中会进行的有：激素平衡、补充燃料储备、细胞修复、神经支配及合成代谢。运动后过量氧耗会补充磷酸原系统（英语：Bioenergetic_systems）。会生成新的ATP，其中也有一些ATP的磷酸根会提供给肌酸，直到ATP和肌酸恢复到平衡状态为止。运动后过量氧耗也透过在运动时的体温升高来加速身体的代谢^[2]。

运动后过量氧耗会伴随着体内燃料消耗率的上升。为了应对运动所需的能量，身体会分解脂肪储备，释放游离脂肪酸（FFA）到血流之中。在运动后，一方面会将游离脂肪酸直接氧化，作为能量来源，有些FFA消耗后转换的能量也会再将FFA恢复成脂肪储备^[3]^[4]^[5]

效应的维持时间

EPOC的效果在刚运动完后最强，并随着时间逐渐减弱。一项实验特别设计要确认在运动后16小时之后，是否还有EPOC的效果，进行了48小时的实验，发现在运动后38小时后，仍可以量测到EPOC的效果^[6]。

另见

参考文献

^ Scott CB, Kemp RB. Direct and indirect calorimetry of lactate oxidation: implications for whole-body energy expenditure. Journal of Sports Sciences. January 2005, 23 (1): 15–9. PMID 15841591. doi:10.1080/02640410410001716760.
^ Saladin, Kenneth. Anatomy & Physiology: The Unity of Form and Function. New York: McGraw Hill. 2012: 425. ISBN 978-0-07-337825-1.
^ Bahr R. Excess postexercise oxygen consumption--magnitude, mechanisms and practical implications. Acta Physiologica Scandinavica. Supplementum. 1992, 605: 1–70. PMID 1605041.
^ Bahr R, Høstmark AT, Newsholme EA, Grønnerød O, Sejersted OM. Effect of exercise on recovery changes in plasma levels of FFA, glycerol, glucose and catecholamines. Acta Physiologica Scandinavica. September 1991, 143 (1): 105–15. PMID 1957696. doi:10.1111/j.1748-1716.1991.tb09205.x.
^ Bielinski R, Schutz Y, Jéquier E. Energy metabolism during the postexercise recovery in man. The American Journal of Clinical Nutrition. July 1985, 42 (1): 69–82. PMID 3893093.
^ Schuenke MD, Mikat RP, McBride JM. Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: implications for body mass management. European Journal of Applied Physiology. March 2002, 86 (5): 411–7. PMID 11882927. doi:10.1007/s00421-001-0568-y.

深入阅读

Hill, A. V.; Long, C. N. H.; Lupton, H. Muscular Exercise, Lactic Acid, and the Supply and Utilisation of Oxygen. Proceedings of the Royal Society B: Biological Sciences. 1924, 96 (679): 438–75. JSTOR 81203. doi:10.1098/rspb.1924.0037.

[1] Scott CB, Kemp RB. Direct and indirect calorimetry of lactate oxidation: implications for whole-body energy expenditure. Journal of Sports Sciences. January 2005, 23 (1): 15–9. PMID 15841591. doi:10.1080/02640410410001716760.

[2] Saladin, Kenneth. Anatomy & Physiology: The Unity of Form and Function. New York: McGraw Hill. 2012: 425. ISBN 978-0-07-337825-1.

[3] Bahr R. Excess postexercise oxygen consumption--magnitude, mechanisms and practical implications. Acta Physiologica Scandinavica. Supplementum. 1992, 605: 1–70. PMID 1605041.

[4] Bahr R, Høstmark AT, Newsholme EA, Grønnerød O, Sejersted OM. Effect of exercise on recovery changes in plasma levels of FFA, glycerol, glucose and catecholamines. Acta Physiologica Scandinavica. September 1991, 143 (1): 105–15. PMID 1957696. doi:10.1111/j.1748-1716.1991.tb09205.x.

[5] Bielinski R, Schutz Y, Jéquier E. Energy metabolism during the postexercise recovery in man. The American Journal of Clinical Nutrition. July 1985, 42 (1): 69–82. PMID 3893093.

[6] Schuenke MD, Mikat RP, McBride JM. Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: implications for body mass management. European Journal of Applied Physiology. March 2002, 86 (5): 411–7. PMID 11882927. doi:10.1007/s00421-001-0568-y.

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