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对“乳酸钳夹法”的代谢和心肺反应。

Metabolic and cardiorespiratory responses to "the lactate clamp".

作者信息

Miller Benjamin F, Fattor Jill A, Jacobs Kevin A, Horning Michael A, Suh Sang-Hoon, Navazio Franco, Brooks George A

机构信息

Department of Integrative Biology, University of California, Berkeley, California 94720, USA.

出版信息

Am J Physiol Endocrinol Metab. 2002 Nov;283(5):E889-98. doi: 10.1152/ajpendo.00266.2002.

DOI:10.1152/ajpendo.00266.2002
PMID:12376315
Abstract

To evaluate the hypothesis that precursor supply limits gluconeogenesis (GNG) during exercise, we examined training-induced changes in glucose kinetics [rates of appearance (R(a)) and disappearance (R(d))], oxidation (R(ox)), and recycling (R(r)) with an exogenous lactate infusion to 3.5-4.0 mM during rest and to pretraining 65% peak O(2) consumption (VO(2 peak)) levels during exercise. Control and clamped trials (LC) were performed at rest pre- (P(R)R, P(R)R-LC) and posttraining (P(O)R, P(O)R-LC) and during exercise pre- (P(R)E(X)) and posttraining at absolute (P(O)A(B), P(O)A(B)-LC) and relative (P(O)R(L), P(O)R(L)-LC) intensities. Glucose R(r) was not different in any rest or exercise condition. Glucose R(a) did not differ as a result of LC. Glucose R(ox) was significantly decreased with LC at P(O)R (0.38 +/- 0.03 vs. 0.56 +/- 0.04 mg. kg(-1). min(-1)) and P(O)A(B) (3.82 +/- 0.51 vs. 5.0 +/- 0.62 mg. kg(-1). min(-1)). Percent glucose R(d) oxidized decreased with all LC except P(O)R(L)-LC (P(R)R, 32%; P(R)R-LC, 22%; P(O)R, 27%; P(O)R-LC, 20%; P(O)A(B), 95%; P(O)A(B)-LC, 77%), which resulted in a significant increase in oxidation from alternative carbohydrate (CHO) sources at rest and P(O)A(B). We conclude that 1) increased arterial [lactate] did not increase glucose R(r) measured during rest or exercise after training, 2) glucose disposal or production did not change with increased precursor supply, and 3) infusion of exogenous CHO in the form of lactate resulted in the decrease of glucose R(ox).

摘要

为了评估运动期间前体供应限制糖异生(GNG)这一假设,我们通过在静息状态下向外源性输注乳酸使其浓度达到3.5 - 4.0 mM,并在运动期间使其达到训练前65%峰值耗氧量(VO₂peak)水平,研究了训练引起的葡萄糖动力学[出现率(R(a))和消失率(R(d))]、氧化(R(ox))及再循环(R(r))的变化。在静息状态下训练前(P(R)R、P(R)R - LC)和训练后(P(O)R、P(O)R - LC)以及运动期间训练前(P(R)E(X))和训练后绝对强度(P(O)A(B)、P(O)A(B) - LC)及相对强度(P(O)R(L)、P(O)R(L) - LC)下进行对照和钳夹试验(LC)。在任何静息或运动条件下,葡萄糖R(r)均无差异。由于LC,葡萄糖R(a)没有差异。在P(O)R(0.38 ± 0.03对0.56 ± 0.04 mg·kg⁻¹·min⁻¹)和P(O)A(B)(3.82 ± 0.51对5.0 ± 0.62 mg·kg⁻¹·min⁻¹)时,LC使葡萄糖R(ox)显著降低。除P(O)R(L) - LC外,所有LC均使氧化的葡萄糖R(d)百分比降低(P(R)R,32%;P(R)R - LC,22%;P(O)R,27%;P(O)R - LC,20%;P(O)A(B),95%;P(O)A(B) - LC,77%),这导致静息状态和P(O)A(B)时来自其他碳水化合物(CHO)来源的氧化显著增加。我们得出结论:1)训练后静息或运动期间测量的葡萄糖R(r)不会因动脉[乳酸]增加而升高;2)葡萄糖处置或生成不会随前体供应增加而改变;3)以乳酸形式输注外源性CHO导致葡萄糖R(ox)降低。

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