Sahlin K, Edström L, Sjöholm H
Am J Physiol. 1983 Jul;245(1):C15-20. doi: 10.1152/ajpcell.1983.245.1.C15.
Isolated extensor digitorum longus muscles from rat were exposed to atmospheres of 30% CO2 (high-CO2 muscles) or 6.5% CO2 (control muscles) in O2 for 95 min. Muscle contraction characteristics were studied before and after the incubation. Tetanic tension decreased in high-CO2 muscles to 55% of initial value but remained unchanged in control muscles. Relaxation time was prolonged in high-CO2 muscles but not in control muscles. Intracellular pH was 6.67 +/- 0.04 (SD) in high-CO2 muscles and 7.01 +/- 0.04 in control muscles. CO2-induced acidosis had a marked influence on the intermediary energy metabolism as shown by a fourfold increase of glucose 6-phosphate, a 14% increase of ADP, and a decrease of phosphocreatine to 44% of the control value. Lactate and pyruvate contents were unchanged. The observed metabolic changes can be explained by an effect of H+ on the activity of phosphofructokinase and on the creatine kinase equilibrium. It can be concluded that H+ concentration causes muscular fatigue. It is, however, uncertain whether this is an effect of increased H+ per se or by high-energy phosphate depletion induced by acidosis.
将大鼠的离体趾长伸肌置于含30%二氧化碳的环境（高二氧化碳肌肉组）或含6.5%二氧化碳的氧气环境（对照组肌肉）中95分钟。在孵育前后研究肌肉收缩特性。高二氧化碳肌肉组的强直张力降至初始值的55%，而对照组肌肉则保持不变。高二氧化碳肌肉组的舒张时间延长，而对照组肌肉则未延长。高二氧化碳肌肉组的细胞内pH值为6.67±0.04（标准差），对照组肌肉为7.01±0.04。二氧化碳诱导的酸中毒对中间能量代谢有显著影响，表现为6-磷酸葡萄糖增加四倍、ADP增加14%以及磷酸肌酸降至对照值的44%。乳酸和丙酮酸含量未变。观察到的代谢变化可以通过H⁺对磷酸果糖激酶活性和肌酸激酶平衡的影响来解释。可以得出结论，H⁺浓度会导致肌肉疲劳。然而，尚不确定这是H⁺本身增加的作用，还是酸中毒诱导的高能磷酸盐耗竭的作用。
