Munkvik Morten, Lunde Per Kristian, Sejersted Ole M
Institute for Experimental Medical Research, Oslo Univ. Hospital, Ullevål, Kirkeveien 166, N-0407 Oslo, Norway.
Am J Physiol Regul Integr Comp Physiol. 2009 Sep;297(3):R900-10. doi: 10.1152/ajpregu.91043.2008. Epub 2009 Jul 22.
Skeletal muscle fatigue is most often studied in vitro at room temperature and is classically defined as a decline in maximum force production or power output, exclusively linked to repeated isometric contractions. However, most muscles shorten during normal use, and we propose that both the functional correlate of fatigue, as well as the fatigue mechanism, will be different during dynamic contractions compared with static contractions. Under isoflurane anesthesia, fatigue was induced in rat soleus muscles in situ by isotonic shortening contractions at 37 degrees C. Muscles were stimulated repeatedly for 1 s at 30 Hz every 2 s for a total of 15 min. The muscles were allowed to shorten isotonically against a load corresponding to one-third of maximal isometric force. Maximal unloaded shortening velocity (V(0)), maximum force production (F(max)), and isometric relaxation rate (-dF/dt) was reduced after 100 s but returned to almost initial values at the end of the stimulation protocol. Likewise, ATP and creatine phosphate (CrP) were reduced after 100 s, but the level of CrP was partially restored to initial values after 15 min. The rate of isometric force development, the velocity of shortening, and isotonic shortening were also reduced at 100 s, but in striking contrast, did not recover during the remainder of the stimulation protocol. The regulatory myosin light chain (MLC2s) was dephosphorylated after 100 s and did not recover. Although metabolic changes may account for the changes of F(max), -dF/dt, and V(0), dephosphorylation of MLC2s may be involved in the fatigue seen as sustained slower contraction velocities and decreased muscle shortening.
骨骼肌疲劳通常是在室温下进行体外研究，传统上被定义为最大力量产生或功率输出的下降，这完全与重复的等长收缩有关。然而，大多数肌肉在正常使用时会缩短，我们认为与静态收缩相比，动态收缩过程中疲劳的功能关联以及疲劳机制都会有所不同。在异氟烷麻醉下，通过在37℃下的等张缩短收缩在大鼠比目鱼肌原位诱导疲劳。每隔2秒以30Hz重复刺激肌肉1秒，共刺激15分钟。使肌肉靠着相当于最大等长力三分之一的负荷进行等张缩短。最大无负荷缩短速度（V(0)）、最大力量产生（F(max)）和等长舒张速率（-dF/dt）在100秒后降低，但在刺激方案结束时恢复到几乎初始值。同样，ATP和磷酸肌酸（CrP）在100秒后减少，但15分钟后CrP水平部分恢复到初始值。等长力量发展速率、缩短速度和等张缩短在100秒时也降低，但与之形成鲜明对比的是，在刺激方案的剩余时间内没有恢复。调节性肌球蛋白轻链（MLC2s）在100秒后去磷酸化且未恢复。虽然代谢变化可能解释F(max)、-dF/dt和V(0)的变化，但MLC2s的去磷酸化可能与持续较慢的收缩速度和肌肉缩短减少所导致的疲劳有关。
