運動後過量氧耗

運動後過量氧耗（英語：Excess post-exercise oxygen consumption，簡稱為EPOC，非正式稱為後燃燒）是身體在劇烈運動後產生的氧氣攝入速率顯著增加。在運動生理學發展歷程中，以往曾用「氧債」（英語：oxygen debt）一詞來解釋無氧供能的消耗，或是嘗試量化無氧供能，特別是有關乳酸代謝的部份。不過，直接及間接熱量計的實驗都認為乳酸代謝和氧氣攝入速率增加沒有關係^[1]。

在運動後，身體會用過量氧耗讓身體恢復到平衡狀態，並使身體適應所進行的鍛煉。其中會進行的有：激素平衡、補充燃料儲備、細胞修復、神經支配及合成代謝。運動後過量氧耗會補充磷酸原系統（英語：Bioenergetic_systems）。會生成新的ATP，其中也有一些ATP的磷酸根會提供給肌酸，直到ATP和肌酸恢復到平衡狀態為止。運動後過量氧耗也透過在運動時的體溫升高來加速身體的代謝^[2]。

運動後過量氧耗會伴隨著體內燃料消耗率的上昇。為了應對運動所需的能量，身體會分解脂肪儲備，釋放游離脂肪酸（FFA）到血流之中。在運動後，一方面會將游離脂肪酸直接氧化，作為能量來源，有些FFA消耗後轉換的能量也會再將FFA恢復成脂肪儲備^[3]^[4]^[5]

效應的維持時間

EPOC的效果在剛運動完後最強，並隨著時間逐漸減弱。一項實驗特別設計要確認在運動後16小時之後，是否還有EPOC的效果，進行了48小時的實驗，發現在運動後38小時後，仍可以量測到EPOC的效果^[6]。

另見

參考文獻

^ 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.

深入閱讀

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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