Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo
Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo
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DOI：
10.1111/j.1469-7793.1998.935bg.x
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发表时间：
1998-09-15
影响因子：
5.5
通讯作者：
Jubrias, SA
中科院分区：
文献类型：
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作者：
Conley, KE;Kushmerick, MJ;Jubrias, SA
1.我们检验了糖酵解的细胞质控制机制受运动过程中氧气存在的影响的假设。我们比较了人腕屈肌和踝背屈肌在缺血和完整循环下的最大抽搐刺激。P-31磁共振波谱以6-9 s的间隔跟踪磷酸肌酸（PCr）、P-1和pH动力学。从pH和组织缓冲能力以及氧化磷酸化速率等方面测定刺激过程中糖酵解PCR的合成.缺血与有氧刺激导致两种肌肉中相似的糖酵解通量。糖酵解反应在50 ~ 70次刺激后开始，糖酵解反应的PCr合成量与刺激次数成正比.在有氧刺激和缺血刺激之间，糖酵解的假定反馈调节因子[P-1]和[ADP]存在两倍的差异。面对代谢水平的这些差异，类似的糖酵解通量消除了糖酵解中作为控制机制的反馈。这些结果表明，糖酵解通量是独立的氧合状态和代谢反馈，但肌肉激活成正比。这些结果表明肌肉刺激在糖酵解的激活和维持中起关键作用。此外，这种糖酵解控制机制独立于控制氧化磷酸化的反馈控制机制。
1. We tested the hypothesis that the cytoplasmic control mechanism for glycolysis is affected by the presence of oxygen during exercise. We used a comparison of maximal twitch stimulation under ischaemic and intact circulation in human wrist flexor and ankle dorsiflexor muscles. P-31 magnetic resonance spectroscopy followed the phosphocreatine (PCr), P-1 and pH dynamics at 6-9 s intervals. Glycolytic PCr synthesis was determined during stimulation from pH and tissue buffer capacity, as well as the oxidative phosphorylation rate.2. Ischaemic vs. aerobic stimulation resulted in similar glycolytic fluxes in the two muscles. The onset of glycolysis occured after fifty to seventy stimulations and the extent of glycolytic PCr synthesis was directly proportional to the number of stimulations thereafter.3. Two-fold differences in the putative feedback regulators of glycolysis, [P-1] and [ADP], were found between aerobic and ischaemic stimulation. The similar glycolytic fluxes in the face of these differences in metabolite levels eliminates feedback as a control mechanism in glycolysis.4. These results demonstrate that glycolytic flux is independent of oxygenation state and metabolic feedback, but proportional to muscle activation. These results show a key role for muscle stimulation in the activation and maintenance of glycolysis. Further, this glycolytic control mechanism is independent of the feedback control mechanism that governs oxidative phosphorylation.