Spriet L L
School of Human Biology, University of Guelph, Ontario, Canada.
Pflugers Arch. 1990 Nov;417(3):278-84. doi: 10.1007/BF00370993.
Rat soleus muscles were tetanically stimulated in situ with an occluded circulation to examine anaerobic adenosine triphosphate (ATP) provision and the regulation of glycolytic ATP production. Soleus muscles were stimulated for 30-60 s at 1 Hz with 100-200 ms trains (40-80 Hz). Muscles were sampled pre- and post-stimulation for measurements of pH, high energy phosphates and glycolytic intermediates. Total ATP provision by the slow oxidative fibres was 65-121 mumol/g dry muscle and 27-35% of the amount produced by fast glycolytic fibres. Contributions to total ATP provision in the initial 30 contractions were: phosphocreatine, 71%; glycolysis, 28%; and endogenous ATP, 1%. Following 60 contractions the contributions were 45-54%, 44-51% and 2-4%, respectively. During the initial 30 contractions, glycogenolysis (phosphorylase activity) and glycolysis [phosphofructokinase (PFK) activity] were similar as glucose-6-phosphate (G-6-P) and fructose-6-phosphate (F-6-P) did not accumulate. Small accumulations of PFK deinhibitors inorganic phosphate, adenosine diphosphate, adenosine monophosphate and fructose-1,6-diphosphate appeared to account for the PFK activity. In the final 30 contractions, phosphorylase activity increased above PFK as G-6-P and F-6-P accumulated. PFK activity and glycolytic ATP production also increased despite increasing hydrogen ion concentration [H+]. During intense tetanic stimulation of soleus muscle, glycolytic ATP production is initially limited by a low glycogen phosphorylase activity. The activity of PFK increases during in situ contraction through the accumulation of deinhibitors, despite increasing [H+].
对大鼠比目鱼肌在原位进行强直刺激,同时阻断血液循环,以研究无氧三磷酸腺苷(ATP)的供应及糖酵解ATP生成的调节。比目鱼肌以1Hz的频率、100 - 200ms的串刺激(40 - 80Hz),持续30 - 60秒。在刺激前后对肌肉进行采样,以测量pH值、高能磷酸盐和糖酵解中间产物。慢氧化纤维提供的总ATP为65 - 121μmol/g干肌肉,是快糖酵解纤维产生量的27 - 35%。在最初30次收缩中,对总ATP供应的贡献分别为:磷酸肌酸,71%;糖酵解,28%;内源性ATP,1%。60次收缩后,贡献分别为45 - 54%、44 - 51%和2 - 4%。在最初30次收缩期间,糖原分解(磷酸化酶活性)和糖酵解[磷酸果糖激酶(PFK)活性]相似,因为6 - 磷酸葡萄糖(G - 6 - P)和6 - 磷酸果糖(F - 6 - P)没有积累。PFK去抑制剂无机磷酸盐、二磷酸腺苷、一磷酸腺苷和1,6 - 二磷酸果糖的少量积累似乎是PFK活性的原因。在最后的30次收缩中,随着G - 6 - P和F - 6 - P的积累,磷酸化酶活性高于PFK。尽管氢离子浓度[H⁺]增加,但PFK活性和糖酵解ATP生成也增加。在比目鱼肌的强烈强直刺激期间,糖酵解ATP生成最初受到糖原磷酸化酶低活性的限制。尽管[H⁺]增加,但在原位收缩过程中,PFK活性通过去抑制剂的积累而增加。