Leonard T R, Herzog W
Human Performance Laboratory, University of Calgary, 2500 University Drive N.W., Calgary, Canada AB T2N 1N4.
J Biomech. 2005 Nov;38(11):2190-7. doi: 10.1016/j.jbiomech.2004.09.028.
It has been stated repeatedly for the past 50 years that the steady-state force depression following shortening of an activated muscle depends on the speed of shortening. However, these statements were based on results from experiments in which muscles were shortened at different speeds but identical activation levels. Therefore, the force during shortening was changed in accordance with the force-velocity relationship of muscles: that is, increasing speeds of shortening were associated with decreasing forces, and vice versa. Consequently, it is not possible at present to distinguish whether force depression is caused by the changes in speed, as frequently stated, or the associated changes in force, or both. The purpose of this study was to test if force depression depends on the speed of shortening. We hypothesized that force depression was dependent on the force but not the speed of contraction. Our prediction is that the amount of force depression after shortening contractions at different speeds could be similar if the force during contraction was controlled at a similar level. Cat soleus muscles (n=7) were shortened by 9 or 12 mm at speeds of 3, 9, and 27 mm/s, first with a constant activation during shortening (30Hz), then with activation levels that were reduced (<30Hz) for the slow speeds (3 and 9 mm/s) to approximate the shortening forces of the fast speed contractions (27 mm/s). If done properly, force depression could be precisely matched at the three different speeds, indicating that force depression was related to the force during the shortening contraction but not to the speed. However, in order to match force depression, the forces during shortening had to be systematically greater for the slow compared to the fast speeds of shortening, suggesting that force depression also depends on the level of activation, as force depression at constant activation levels can only be matched if the force during shortening, evaluated by the mechanical work, is identical. Therefore, we conclude that force depression depends on the force and activation level during shortening, but does not depend on the speed of shortening as has been assumed for half a century. These results support, but do not prove, the current hypothesis that force depression is caused by a stress-related cross-bridge inhibition in the actin-myosin overlap zone that is newly formed during muscle shortening.
在过去的50年里，人们反复指出，激活的肌肉在缩短后出现的稳态力下降取决于缩短速度。然而，这些说法是基于这样的实验结果：肌肉以不同速度缩短，但激活水平相同。因此，缩短过程中的力根据肌肉的力-速度关系而变化：也就是说，缩短速度增加与力减小相关，反之亦然。因此，目前无法区分力下降是如经常所说的由速度变化引起，还是由相关的力变化引起，或者两者皆有。本研究的目的是测试力下降是否取决于缩短速度。我们假设力下降取决于力而不是收缩速度。我们的预测是，如果收缩过程中的力控制在相似水平，那么以不同速度进行缩短收缩后力下降的量可能相似。猫的比目鱼肌（n = 7）以3、9和27毫米/秒的速度缩短9或12毫米，首先在缩短过程中保持恒定激活（30Hz），然后对于低速（3和9毫米/秒）降低激活水平（<30Hz），以接近高速收缩（27毫米/秒）的缩短力。如果操作得当，在三种不同速度下力下降可以精确匹配，这表明力下降与缩短收缩过程中的力有关，而与速度无关。然而，为了匹配力下降，与高速缩短相比，低速缩短过程中的力必须系统性地更大，这表明力下降也取决于激活水平，因为只有当通过机械功评估的缩短过程中的力相同时，在恒定激活水平下的力下降才能匹配。因此，我们得出结论，力下降取决于缩短过程中的力和激活水平，但不像半个世纪以来所假设的那样取决于缩短速度。这些结果支持但未证明当前的假设，即力下降是由肌肉缩短过程中新形成的肌动蛋白-肌球蛋白重叠区域中与应力相关的横桥抑制引起 的。
