Chesky J A, Rockstein M, Lopez T
Mech Ageing Dev. 1980 Mar;12(3):237-43. doi: 10.1016/0047-6374(80)90046-9.
Myocardial creatine phosphokinase (CPK) was extracted from crushed tissue in 0.01 M Tris buffer at pH 9.0 and purified by successive ammonium chloride and ethanol precipitations. The CPK activity was estimated by measuring the rate of phosphocreatine formation by the transphosphorylation of creatine by ATP. There was a slight rise in CPK activity from 1 to 2 months of age. Thereafter, there was a progressive fall in the CPK activity of 14% by 7-9 months of age, 20% by about one year of age, and 25% by 16-24 months of age. These data indicate that, with advancing age, there is an inability to rapidly restore adequate cellular levels of the high-energy substrate ATP during muscular contraction. Since the loss with age of myocardial CPK parallels a strong biochemical correlate for known declining cardiac function in aging mammals, including man.
心肌肌酸磷酸激酶（CPK）从pH 9.0的0.01 M Tris缓冲液中的破碎组织中提取，并通过连续的氯化铵和乙醇沉淀进行纯化。通过测量ATP将肌酸转磷酸化形成磷酸肌酸的速率来估计CPK活性。CPK活性在1至2个月大时略有上升。此后，CPK活性逐渐下降，7至9个月大时下降14%，约1岁时下降20%，16至24个月大时下降25%。这些数据表明，随着年龄的增长，在肌肉收缩过程中无法迅速恢复高能底物ATP的足够细胞水平。因为随着年龄增长心肌CPK的损失与衰老哺乳动物（包括人类）已知的心脏功能下降的强烈生化关联平行。
