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碱中毒对运动期间骨骼肌代谢及运动能力的影响。

Effects of alkalosis on skeletal muscle metabolism and performance during exercise.

作者信息

Spriet L L, Lindinger M I, Heigenhauser G J, Jones N L

出版信息

Am J Physiol. 1986 Nov;251(5 Pt 2):R833-9. doi: 10.1152/ajpregu.1986.251.5.R833.

DOI:10.1152/ajpregu.1986.251.5.R833
PMID:3777210
Abstract

This study examined the effects of extracellular alkalosis on the metabolism and performance of perfused rat hindlimb muscles during electrical stimulation. Three acid-base conditions were used: control (C, normal acid-base state), metabolic alkalosis (MALK, increased bicarbonate concentration), and respiratory alkalosis (RALK, decreased PCO2). A one-pass system was used to perfuse the hindlimb via the femoral artery for 20 min at rest and during 5 min of tetanic stimulation via the sciatic nerve. The isometric tension generated by the gastrocnemius-plantaris-soleus muscle group was recorded. Arterial and venous perfusates were periodically sampled for substrate and metabolite measurements, and muscle samples were taken pre- and postperfusion. Peak isometric tensions in C, MALK, and RALK were similar: 3,367 +/- 107, 3,317 +/- 110, and 3,404 +/- 69 g, respectively. The rate of tension decay was also unaffected by alkalosis and represented 78 and 55% of the peak tension following 2 and 5 min of stimulation, respectively. Muscle O2 uptake, glycogen utilization, and total lactate (La-) production were similar following 5 min of stimulation in all conditions. However, alkalosis resulted in an enhanced La- release from working muscle (peak La- release: C, 15.5 +/- 1.1; MALK, 19.7 +/- 1.6; RALK, 18.3 +/- 2.2 mumol/min), and a 15-20% reduction in intramuscular La- accumulation. Alkalosis had no effect on muscle creatine phosphate and ATP concentrations. Thus, in the perfused rat hindlimb, alkalosis was not associated with changes in tetanic force or glycolysis, but La- release from the working muscle was enhanced by increased extracellular pH and bicarbonate.

摘要

本研究检测了细胞外碱中毒对电刺激期间灌注大鼠后肢肌肉代谢及功能的影响。采用了三种酸碱状态:对照组(C,正常酸碱状态)、代谢性碱中毒(MALK,碳酸氢盐浓度升高)和呼吸性碱中毒(RALK,PCO2降低)。采用单通道系统经股动脉灌注后肢20分钟,休息时灌注,经坐骨神经进行5分钟强直刺激时也进行灌注。记录腓肠肌-比目鱼肌-跖肌肌群产生的等长张力。定期采集动脉和静脉灌注液样本用于底物和代谢物测量,并在灌注前后采集肌肉样本。C组、MALK组和RALK组的峰值等长张力相似,分别为3367±107、3317±110和3404±69克。张力衰减速率也不受碱中毒影响,分别在刺激2分钟和5分钟后占峰值张力的78%和55%。在所有状态下,刺激5分钟后肌肉的氧气摄取、糖原利用和总乳酸(La-)生成相似。然而,碱中毒导致工作肌肉的La-释放增加(峰值La-释放:C组,15.5±1.1;MALK组,19.7±1.6;RALK组,18.3±2.2 μmol/min),肌肉内La-积累减少15%-20%。碱中毒对肌肉磷酸肌酸和ATP浓度无影响。因此,在灌注的大鼠后肢中,碱中毒与强直力或糖酵解的变化无关,但细胞外pH值和碳酸氢盐升高会增强工作肌肉的La-释放。

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