去负荷比目鱼肌高频强直收缩疲劳性的动态变化

Time course of changes in fatigability of high-frequency tetanic contraction in rat unloaded soleus

目的 :探讨肌纤维膜离子通道变化对骨骼肌强直收缩疲劳性产生的可能影响 .方法 :采用离体骨骼肌条灌流技术 ,观测模拟失重 1,2和 4wk大鼠比目鱼肌 (SOL)等长收缩的阈刺激电压与高频强直收缩功能的动态变化 .结果 :与同步对照组相比 ,模拟失重 1wk组引起SOL等长收缩的阈刺激电压呈非常显著性增高 (P <0 .0 1) ;2wk组无差别 (P >0 .0 5 ) ;4wk组又出现明显增高 (P <0 .0 5 ) .与对照组比较 ,悬吊 1wk大鼠SOL高频强直收缩的最大张力 (Po)降低 32 .8% ,但统计学无差异 (P >0 .0 5 ) ;悬吊 2wk组降低 6 0 .1% (P <0 .0 1) ;4wk进一步降低至 77.6 % (P <0 .0 1) .对照组大鼠SOL的强直收缩张力在第 33s处衰退 18.0 %～ 2 6 .0 % ,而悬吊 1wk组衰退 4 0 .9% (P <0 .0 5 ) ;2wk组衰退 5 1.1% (P <0 .0 1) ;4wk组则衰退 73.1% (P <0 .0 1) .结论 :短期模拟失重即可引起比目鱼肌肌纤维的兴奋性降低 ,同时导致高频强直收缩疲劳性增加 .而去负荷SOL膜离子通道的变化可能是其高频强直收缩疲劳性增加的内在机制之一 .

AIM: To explore the effects of unloaded hindlimb on tetanic contraction fatigability of soleus. METHODS: Isometric twitch and high-frequency tetanic contraction were examined by perfusion technique of isolated skeletal muscle strip. The contractile functions of soleus were observed in 1-week, 2-week, or 4-week tail-suspended rats. RESULTS: The threshold voltage induced isometric twitch contraction significantly increased in 1 week of unloaded soleus (P<0.01) as compared with that of control. There was no difference in the threshold voltage between control and 2-week unloaded soleus (P>0.05). But the threshold voltage increased again in 4-week unloaded soleus (P< 0.05). In high-frequency tetanic contraction, the maximal tension (Po) of soleus was reduced respectively by 32.8%, 60.1% and 77.6 % after one (P<0.05), two and four weeks of (P<0.01) tail-suspension (SUS). The tension at the thirty-third second of tetanic contraction (P33) in control decreased 18.0%-26.0%, while the P33/Po in the SUS group decreased 40.9% after one week of unloading (P<0.05), 51.1% after two weeks and 73.1% after four weeks of SUS, respectively. CONCLUSION: These results suggest that the excitability of unloaded soleus is decreased and the fatigability of unloaded soleus is increased. The changes in sarcolemma ion channels in unloaded soleus may be one of the underlying mechanisms of increasing the fatigability.