Upon a sudden rise in work rate, ATP turnover increases immediately, whereas the adjustment of ATP resynthesis from oxidative phosphorylation is substantially slower. An “O₂ deficit” (energy borrowed from substrate level phosphorylation) is therefore generated. A greater O₂ deficit represents an epiphenomenon of a lower “metabolic stability” during the transition, a circumstance directly related to impaired exercise tolerance. In the search for factors responsible for the delayed adjustment of oxidative phosphorylation, we performed studies in the surgically isolated canine gastrocnemius muscle in situ. Enhancement of convective and diffusive microvascular O₂ delivery, with respect to a “normal” condition, did not affect skeletal muscle V̇O₂ kinetics during transitions to submaximal metabolic rates. V̇O₂ kinetics, however, was slowed after experimentally impairing convective O₂ delivery, a condition frequently encountered in pathological conditions. Among potential metabolic factors (pyruvate dehydrogenase activation, nitric oxide inhibition of cytochrome oxidase) a limiting role in V̇O₂ kinetics was observed only for creatine kinase (CK) mediated phosphocreatine (PCr) breakdown. Following CK inhibition, faster muscle V̇O₂ kinetics was observed. Thus, in skeletal muscle CK-catalysed PCr breakdown at contractions onset slows the increase of oxidative phosphorylation. By acting as a high-capacitance energy buffer, PCr breakdown delays or attenuates the increased concentrations of metabolites (such as ADP, Pi, Cr) mediating the V̇O₂ increase. Upon sudden increases in ATP turnover, skeletal muscle fibers rely first on the bioenergetic pathway (PCr breakdown), which is fast to adjust to increased metabolic needs. Metabolites related to PCr breakdown regulate, but inevitably slow down, the adjustment of oxidative phosphorylation.

当工作率突然上升时，ATP转换立即增加，而氧化磷酸化对ATP重新合成的调节则要慢得多。因此产生“ O ₂缺乏”（从底物水平的磷酸化中借来的能量）。O ₂缺乏症越大，表示过渡过程中“代谢稳定性”越低的现象，这种情况直接与运动耐力受损有关。在寻找导致氧化磷酸化延迟调节的因素时，我们在外科手术隔离的犬腓肠肌原位进行了研究。对流和扩散微血管O _2的增强就“正常”状况而言，分娩过程并不影响骨骼肌V transitionO ₂动力学，其转变为次最大代谢速率。然而，在实验上削弱了对流O _2的传递后，V afterO ₂动力学减慢了，这是病理条件下经常遇到的条件。间潜在的代谢因素（丙酮酸脱氢酶活化，细胞色素氧化酶的一氧化氮抑制）在VO限流的作用₂代观察到对肌酸激酶（CK）介导的磷酸肌酸（PCR）击穿动力学。继CK抑制，快肌VO ₂观察到动力学。因此，在骨骼肌中，CK催化的PCr在收缩开始时的分解会减慢氧化磷酸化的增加。通过作为高电容能量缓冲器的PCR击穿延迟或衰减代谢物的浓度增加（如ADP，PI，Cr）的介导VO ₂增加。ATP转换量突然增加时，骨骼肌纤维首先依赖于生物能途径（PCr分解），该途径可以快速适应新陈代谢的需求。与PCr分解相关的代谢产物可调节，但不可避免地会减慢氧化磷酸化的调节。