Department of Kinesiology and Physical Education, McGill University, Montreal, Quebec, Canada.
Am J Physiol Cell Physiol. 2010 Nov;299(5):C1127-35. doi: 10.1152/ajpcell.00073.2010. Epub 2010 Aug 18.
When activated muscle fibers are stretched at low speeds [≤ 2 optimal length (L(o))/s], force increases in two phases, marked by a change in slope [critical force (P(c))] that happens at a critical sarcomere length extension (L(c)). Some studies attribute P(c) to the number of attached cross bridges before stretch, while others attribute it to cross bridges in a pre-power-stroke state. In this study, we reinvestigated the mechanisms of forces produced during stretch by altering either the number of cross bridges attached to actin or the cross-bridge state before stretch. Two sets of experiments were performed: 1) activated fibers were stretched by 3% L(o) at speeds of 1.0, 2.0, and 3.0 L(o)/s in different pCa(2+) (4.5, 5.0, 5.5, 6.0), or 2) activated fibers were stretched by 3% L(o) at 2 L(o)/s in pCa(2+) 4.5 containing either 5 μM blebbistatin(+/-) or its inactive isomer (+/+). All stretches started at a sarcomere length (SL) of 2.5 μm. When fibers were activated at a pCa(2+) of 4.5, P(c) was 2.47 ± 0.11 maximal force developed before stretch (P(o)) and decreased with lower concentrations of Ca(2+). L(c) was not Ca(2+) dependent; the pooled experiments provided a L(c) of 14.34 ± 0.34 nm/half-sarcomere (HS). P(c) and L(c) did not change with velocities of stretch. Fibers activated in blebbistatin(+/-) showed a higher P(c) (2.94 ± 0.17 P(o)) and L(c) (16.30 ± 0.38 nm/HS) than control fibers (P(c) 2.31 ± 0.08 P(o); L(c) 14.05 ± 0.63 nm/HS). The results suggest that forces produced during stretch are caused by both the number of cross bridges attached to actin and the cross bridges in a pre-power-stroke state. Such cross bridges are stretched by large amplitudes before detaching from actin and contribute significantly to the force developed during stretch.
当激活的肌纤维以低速（≤2 个最优长度（L(o)）/s）拉伸时，力会分两个阶段增加，这两个阶段的斜率变化（临界力（P(c)））发生在临界肌节长度延伸（L(c)）处。一些研究将 P(c)归因于拉伸前附着在肌动蛋白上的交联桥的数量，而另一些研究则将其归因于预功状态下的交联桥。在这项研究中，我们通过改变附着在肌动蛋白上的交联桥的数量或拉伸前的交联桥状态，重新研究了拉伸过程中产生的力的机制。进行了两组实验：1）在不同的 pCa(2+)（4.5、5.0、5.5、6.0）下，以 1.0、2.0 和 3.0 L(o)/s 的速度将激活的纤维拉伸 3% L(o)；或 2）在 pCa(2+) 4.5 中以 2 L(o)/s 的速度将激活的纤维拉伸 3% L(o)，该 pCa(2+) 中含有 5 μM blebbistatin(+/-)或其非活性异构体 (+/+). 所有拉伸均从肌节长度（SL）为 2.5 μm 开始。当纤维在 pCa(2+) 为 4.5 时被激活时，P(c)为 2.47 ± 0.11 拉伸前最大力（P(o)），并且随着 Ca(2+)浓度的降低而降低。L(c)与 Ca(2+)无关；汇总实验提供了 14.34 ± 0.34nm/半肌节（HS）的 L(c)。P(c)和 L(c) 不随拉伸速度而变化。在 blebbistatin(+/-)中激活的纤维表现出更高的 P(c)（2.94 ± 0.17 P(o)）和 L(c)（16.30 ± 0.38nm/HS）比对照纤维（P(c) 2.31 ± 0.08 P(o)；L(c) 14.05 ± 0.63nm/HS）。结果表明，拉伸过程中产生的力是由附着在肌动蛋白上的交联桥的数量和预功状态下的交联桥引起的。这些交联桥在从肌动蛋白上脱离之前会被大幅度拉伸，并对拉伸过程中产生的力有重要贡献。
