Poor relationship between arterial [lactate] and leg net release during exercise at 4,300 m altitude
Poor relationship between arterial [lactate] and leg net release during exercise at 4,300 m altitude
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DOI：
10.1152/ajpregu.1998.275.4.r1192
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发表时间：
1998-10-01
影响因子：
2.8
通讯作者：
Reeves, JT
中科院分区：
文献类型：
--
作者：
Brooks, GA;Wolfel, EE;Reeves, JT
我们评估的假设，急性暴露于低压缺氧，交感神经刺激导致增加肌肉乳酸的生产和循环[乳酸]通过β-肾上腺素能机制和β-肾上腺素能适应慢性缺氧是负责钝化运动乳酸反应适应高原后。在海平面（SL）的休息和运动期间，在急性暴露于4,300米（A1），并在海拔3周逗留后（A2），研究了5名对照和6名β受体阻滞的男性。运动是在SL峰值O-2消耗量的49%（（V）超过点O-2峰值）下通过腿部骑行进行的。（海拔高度（V）的65%超过点O-2峰值或87 +/- 2.6 W）; β受体阻滞剂为普萘洛尔（80 mg，每日3次），采集股动脉和静脉血;通过热稀释法测量腿部血流量（（Q）over dot），计算腿部乳酸净释放[（L）over dot =（2）（1-腿部Q）静脉-动脉浓度（L）]，并获得股外侧肌穿刺活检。肌肉[乳酸]随着运动和急性高原暴露而增加，但随着适应而回归到SL值; β-阻滞对肌肉[乳酸]没有影响。在SL运动期间动脉[乳酸盐]升高（0.9 +/- 0.1至1.5 +/- 0.3 mM）;在A1运动产生最大的动脉[乳酸盐]（4.4 +/- 0.8 mM），并且在A2运动产生中等响应（2.1 +/- 0.6 mM）。在所有海拔条件下，β-Blockade在运动期间减少循环[乳酸]约45%。(L)在所有条件下，在运动开始时，过dot短暂增加，但随后随时间推移而下降。血液和肌肉的“乳酸悖论”发生独立的β-肾上腺素能的影响，并在海拔β-肾上腺素能机制的血液乳酸反应的假设被拒绝。在高原运动期间，除了低氧血症、循环肾上腺素和活动肌床的净乳酸释放外，动脉[乳酸]还由其他因素决定。
We evaluated the hypotheses that on acute exposure to hypobaric hypoxia, sympathetic stimulation leads to augmented muscle lactate production and circulating [lactate] through a beta-adrenergic mechanism and that beta-adrenergic adaptation to chronic hypoxia is responsible for the blunted exercise lactate response after acclimatization to altitude. Five control and 6 beta-blocked men were studied during rest and exercise at sea level(SL), on acute exposure to 4,300 m (Al), and after a 3-wk sojourn at altitude (A2). Exercise was by leg cycling at 49% of SL peak O-2 consumption ((V) over dot O-2peak) (65% of altitude (V) over dot O-2peak or 87 +/- 2.6 W); beta-blockade was by propranolol (80 mg 3x daily), femoral arterial and venous blood was sampled; leg blood flow ((Q) over dot) was measured by thermodilution, leg lactate net release [(L) over dot = (2) (1-leg Q) venous-arterial concentration(L)] was calculated, and vastus lateralis needle biopsies were obtained. Muscle [lactate] increased with exercise and acute altitude exposure but regressed to SL values with acclimatization; beta-blockade had no effect on muscle [lactate]. Arterial [lactate] rose during exercise at SL (0.9 +/- 0.1 to 1.5 +/- 0.3 mM); exercise at Al produced the greatest arterial [lactate] (4.4 +/- 0.8 mM), and exercise at A2 an intermediate response (2.1 +/- 0.6 mM). beta-Blockade reduced circulating [lactate] similar to 45% during exercise under all altitude conditions. (L) over dot increased transiently at exercise onset but then declined over time under all conditions. Blood and muscle "lactate paradoxes" occurred independent of beta-adrenergic influences, and the hypotheses relating the blood lactate response at altitude to beta-adrenergic mechanisms are rejected. During exercise at altitude, arterial [lactate] is determined by factors in addition to hypoxemia, circulating epinephrine, and net lactate release from active muscle beds.