Metabolic bases of excess post-exercise oxygen consumption: a review.
Metabolic bases of excess post-exercise oxygen consumption: a review.
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DOI：
10.1249/00005768-198401000-00008
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发表时间：
1984
影响因子：
4.1
通讯作者：
G. Gaesser;G. Gaesser;G. Brooks;G. Brooks
中科院分区：
文献类型：
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作者：
G. Gaesser;G. Gaesser;G. Brooks;G. Brooks
Hill及其同事在20世纪20年代提出的经典“氧债”假说试图将乳酸代谢与运动后休息时过量的O2消耗联系起来。假设O2债代表运动期间形成的乳酸的一小部分（1/5）的氧化，以提供能量在恢复期间将乳酸的剩余部分（4/5）再转化为糖原。在1933年，Margaria等人通过区分初始的、快速的（“半乳糖”）和第二个、缓慢的（“乳酸”）O2-债务曲线分量来修改这一假设。他们假设运动后O2消耗曲线的快速阶段是由于磷酸酶原（ATP + CP）的恢复。现在看来，最初的乳酸对O2债务的解释可能过于简单化。对几个物种的大量研究提供了证据，证明乳酸清除动力学与运动后VO 2的缓慢成分之间存在分离。运动后乳酸（一种易氧化底物）的代谢似乎主要指向线粒体中的能量产生。运动结束时乳酸盐浓度升高可被视为“碳库”，其可作为氧化ATP产生的来源或作为合成葡萄糖、糖原、氨基酸和TCA循环中间体的碳骨架的来源。运动后VO 2升高的代谢基础可以根据直接或间接影响线粒体O2消耗的因素来理解。这些因素包括儿茶酚胺、甲状腺素、糖皮质激素、脂肪酸、钙离子和温度。其中，高温可能是最重要的。由于运动后代谢没有完整的解释，建议使用术语“O2债”来描述运动恢复期间的一系列现象。“乳酸债务”和“乳酸债务”这两个术语暗示了一种机制，是不恰当的。使用替代术语，例如，“运动后过量耗氧量”（EPOC）和“恢复O2”将避免在描述运动后代谢率高于静息水平时暗示因果关系。
The classical "oxygen debt" hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2 consumption in excess of resting that occurs after exercise. The O2 debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between initial, fast ("alactacid"), and second, slow ("lactacid"), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2 consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2 debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2. The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a "reservoir of carbon," which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2 may be understood in terms of those factors which directly or indirectly influence mitochondrial O2 consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise. The terms "alactacid debt" and "lactacid debt," which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., "excess post-exercise oxygen consumption" (EPOC) and "recovery O2," will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.