Korge P, Campbell K B
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, USA.
Int J Sports Med. 1995 Apr;16(3):172-9. doi: 10.1055/s-2007-972987.
A broadly held opinion is that fatigue is not due to an insufficient supply of ATP to the energy consuming mechanisms because tissue [ATP] always remains at least one order of magnitude higher than Km for ATP of any ATPase. In general these findings also suggest that ATP consumption is well balanced with ATP regeneration even in the fatigued muscles. This balance is achieved by down-regulation of ATP consumption. Potentially this down-regulation could be accomplished by any product of the ATPase reaction and the role of Pi and H+ accumulation in this regulation has been discussed in the literature. The purpose of this paper is to describe known compartmentalization of ATP regeneration systems in muscle cell, their importance in the regulation of [adenine nucleotide] in the vicinity of ATPases and how such local ATP regeneration maybe important in the etiology of muscle fatigue. Available experimental evidence suggests that the binding of creatine kinase and glycolytic enzymes in the vicinity of sites where ATP is hydrolyzed and functional coupling between these ATP regenerating mechanisms and ATPase can generate ATPase microenvironments that have an important role in the regulation of ATPase function. Main function of this ATP regeneration is to keep the local ADP/ATP ratios favorable for ATPase function, which seems to be especially important when ATPase turnover is high. Unfortunately, the maximum rate of local ATP regeneration relative to that of ATP hydrolysis in vivo is not known, mainly because in vitro determinations underestimate this value due to a decrease in the fractional of loosely abound enzyme to the preparation during isolation procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
一种广泛持有的观点是，疲劳并非由于能量消耗机制的ATP供应不足，因为组织中的[ATP]总是比任何ATP酶的ATP Km值至少高一个数量级。一般来说，这些发现还表明，即使在疲劳的肌肉中，ATP消耗与ATP再生也保持着良好的平衡。这种平衡是通过下调ATP消耗来实现的。潜在地，这种下调可以由ATP酶反应的任何产物来完成，并且文献中已经讨论了Pi和H+积累在这种调节中的作用。本文的目的是描述肌肉细胞中已知的ATP再生系统的区室化、它们在ATP酶附近调节[腺嘌呤核苷酸]的重要性，以及这种局部ATP再生在肌肉疲劳病因学中可能如何重要。现有实验证据表明，肌酸激酶和糖酵解酶在ATP水解位点附近的结合以及这些ATP再生机制与ATP酶之间的功能偶联可以产生对ATP酶功能调节具有重要作用的ATP酶微环境。这种ATP再生的主要功能是保持局部ADP/ATP比值有利于ATP酶功能，当ATP酶周转率高时，这一点似乎尤为重要。不幸的是，体内局部ATP再生相对于ATP水解的最大速率尚不清楚，主要是因为体外测定由于在分离过程中制备物中松散结合酶的分数降低而低估了该值。（摘要截于250字）
