Mast F, Elzinga G
Laboratory for Physiology, Free University, Amsterdam, The Netherlands.
Am J Physiol. 1990 Apr;258(4 Pt 2):H1144-50. doi: 10.1152/ajpheart.1990.258.4.H1144.
Contraction-related O2 consumption of rabbit papillary muscles was determined at 20 degrees C by measuring change in saline PO2 during and after trains of 120 twitches at 0.125-1 Hz in a microrespirometer. Although anoxic cores occurred at twitch frequencies greater than 0.2 Hz, no lactate was found in saline after twitch train. To measure lactate accumulation in muscle, fully oxygenated muscles were frozen at rest and during steady-state twitches at 0.2 Hz. We also measured nucleotides and creatine (Cr) compounds. There were no differences in lactate, ATP, and phosphocreatine (PCr) content between the resting and active muscles. When a P-to-O2 ratio of 6.3 is assumed, aerobic ATP formation was compared with glycolytic ATP formation during anoxia at a stimulus frequency of 0.2 Hz. The latter value was obtained by freezing muscles between 6 and 25 min after changing from O2- to N2-saturated saline. Withdrawal of O2 caused the ratio of PCr to total Cr to fall in less than 6 min from 0.77 to 0.23, while ATP remained at approximately 15 mumol/g dry wt. Force fell initially within 4 min to approximately 70% of control value, decreasing thereafter more slowly to approximately 40% at 20 min. From the relationship between amount of lactate formed and duration of anoxia, rate of anaerobic ATP formation was calculated assuming a P-to-lactate ratio of 1. We found that despite continuing contractile activity, anaerobic ATP formation was less than that required by a fully oxygenated resting muscle and was about the same magnitude as the estimated ATP hydrolysis for the contractions in N2. We conclude that in fully oxygenated rabbit papillary muscles no net lactate is produced during stimulation and that in anoxia anaerobic glycolytic capacity may not provide sufficient ATP for processes other than the uptake of Ca by the sarcoplasmic reticulum and cross-bridge cycling.
在20℃下,通过在微量呼吸计中测量120次0.125 - 1Hz的收缩串期间及之后盐溶液中氧分压(PO₂)的变化,来测定兔乳头肌与收缩相关的耗氧量。尽管在收缩频率大于0.2Hz时会出现无氧核心,但在收缩串后盐溶液中未发现乳酸。为了测量肌肉中乳酸的积累,将完全氧合的肌肉在静息状态以及0.2Hz的稳态收缩期间进行冷冻。我们还测量了核苷酸和肌酸(Cr)化合物。静息肌肉和活动肌肉之间的乳酸、三磷酸腺苷(ATP)和磷酸肌酸(PCr)含量没有差异。当假设磷氧比为6.3时,在刺激频率为0.2Hz的缺氧条件下,将有氧ATP生成与糖酵解ATP生成进行了比较。后者的值是通过在从氧饱和盐溶液转变为氮饱和盐溶液后6至25分钟之间冷冻肌肉获得的。撤去氧气后,PCr与总Cr的比值在不到6分钟内从0.77降至0.23,而ATP保持在约15μmol/g干重。力最初在4分钟内降至对照值的约70%,此后下降得更慢,在20分钟时降至约40%。根据形成的乳酸量与缺氧持续时间之间的关系,假设磷乳酸比为1来计算无氧ATP生成速率。我们发现,尽管收缩活动持续进行,但无氧ATP生成量低于完全氧合的静息肌肉所需量,并且与氮气中收缩时估计的ATP水解量大致相同。我们得出结论,在完全氧合的兔乳头肌中,刺激期间不会产生净乳酸,并且在缺氧条件下,无氧糖酵解能力可能无法为肌浆网摄取钙和横桥循环以外的过程提供足够的ATP。