De Haan A, Bien M, Verdijk P W
Institute for Fundamental and Clinical Human Movement Sciences, Faculty of Human Movement Sciences, Vrije University, Amsterdam, The Netherlands.
Acta Physiol Scand. 1999 Jul;166(3):217-22. doi: 10.1046/j.1365-201X.1999.00560.x.
Force and speed parameters were obtained from isometric contractions at different stimulation frequencies of creatine kinase-deficient and wildtype in situ mouse medial gastrocnemius muscles. The absence of creatine kinase did not affect force production at higher stimulation frequencies. However, at frequencies below 140 Hz, forces were lower than the controls (P < 0.05); at the lowest frequency applied (80 Hz) the force was reduced to approximately 60% compared with the wildtype muscles. In contrast, twitch force was not affected. When the contractions were preceded by a brief tetanus (50 ms), the effects of lacking creatine kinase on force production were more pronounced; at 80 Hz stimulation isometric force was further reduced to 66.5 +/- 6.2% (mean +/- SD; n=5) of the single contractions of the deficient muscles and to approximately 42% of the wildtype muscles. Twitch force was now also reduced (by approximately 50%) after the tetanus. The speed of the muscles was not affected in the single contractions. However, after a preceding tetanus, the rate of force rise was reduced by approximately 14% at high frequencies of stimulation. With decreasing frequencies (below 250 Hz), the reduction in speed became more pronounced; at 80 Hz the rate in the creatine kinase-deficient muscles was only 55.2 +/- 3.9% (mean +/- SD; n=5) of the wildtype muscles. No effects of the deficiency were found for the half relaxation times. The data suggest that an impaired creatine kinase system leads to lower activation levels at submaximal stimulation frequencies, possibly by a reduction in Ca2+-release during repetitive stimulation. Similar effects may be expected in normal fatigued muscle when phosphocreatine is depleted.
在不同刺激频率下，对肌酸激酶缺陷型和野生型原位小鼠内侧腓肠肌进行等长收缩，从而获得力和速度参数。肌酸激酶的缺失并不影响较高刺激频率下的力产生。然而，在低于140Hz的频率下，力低于对照组（P<0.05）；在施加的最低频率（80Hz）时，与野生型肌肉相比，力降低至约60%。相比之下，单收缩力不受影响。当收缩前有短暂强直收缩（50ms）时，缺乏肌酸激酶对力产生的影响更为明显；在80Hz刺激下，等长力进一步降低至缺陷型肌肉单收缩力的66.5±6.2%（平均值±标准差；n=5），约为野生型肌肉的42%。强直收缩后，单收缩力现在也降低了（约50%）。单收缩时肌肉的速度不受影响。然而，在强直收缩后，高频刺激下力上升速率降低了约14%。随着频率降低（低于250Hz），速度降低变得更加明显；在80Hz时，肌酸激酶缺陷型肌肉的速率仅为野生型肌肉的55.2±3.9%（平均值±标准差；n=5）。未发现缺陷对等长半松弛时间有影响。数据表明，肌酸激酶系统受损会导致次最大刺激频率下的激活水平降低，可能是由于重复刺激期间Ca2+释放减少所致。当磷酸肌酸耗尽时，正常疲劳肌肉中可能会出现类似的影响。
