Haugen P
Division of Physiological Sciences, John Curtin School of Medical Research, Australian National University, Canberra.
J Muscle Res Cell Motil. 1991 Dec;12(6):566-78. doi: 10.1007/BF01738445.
The transient change in the sarcoplasmic concentration of Ca2+ was measured in intact fibres isolated from the anterior tibial muscle of the frog Litoria moorei. The fibres had been injected with the calcium-sensitive dye arsenazo III and the change of the calcium concentration was calculated from the changes in light absorbance at 570, 600 and 720 nm wavelengths. Absorbance and force were measured under three different conditions: (1) during a normal isometric twitch, (2) when a quick ramp-and-hold stretch had been applied to the fibre during onset of the contraction, and (3) when the fibre was allowed to contract isometrically at a length corresponding to the final length of the stretch. A method was devised to neutralize most of the movement artefacts encountered in such measurements. While the quick stretch caused substantial increase in the level and the duration of the contractile force such as originally described in whole muscle by A. V. Hill, the calcium transients appeared basically unaffected. It thus seems that the mechanism behind the phenomenon of the force enhancement lies at a step in the excitation-contraction coupling subsequent to the calcium release. From the present results, however, it is not clear whether the phenomenon is caused by an increase in the level of activation of the calcium-dependent regulatory system, or whether it is to be found in the acto-myosin interaction itself. The latter alternative would be consistent with the stiffness measurements published earlier.
在从莫氏雨滨蛙(Litoria moorei)胫前肌分离出的完整肌纤维中,测量了肌浆中Ca2+浓度的瞬时变化。这些肌纤维已注射了钙敏染料偶氮胂III,并根据570、600和720nm波长处吸光度的变化计算钙浓度的变化。在三种不同条件下测量吸光度和力:(1)在正常等长收缩时,(2)在收缩开始时对肌纤维施加快速斜坡-保持拉伸时,以及(3)当肌纤维在对应于拉伸最终长度的长度下进行等长收缩时。设计了一种方法来消除此类测量中遇到的大多数运动伪影。虽然快速拉伸导致收缩力的水平和持续时间大幅增加,如A.V.希尔最初在整块肌肉中所描述的那样,但钙瞬变基本不受影响。因此,似乎力增强现象背后的机制位于钙释放后的兴奋-收缩偶联步骤中。然而,从目前的结果来看,尚不清楚该现象是由钙依赖性调节系统激活水平的增加引起的,还是存在于肌动蛋白-肌球蛋白相互作用本身中。后一种可能性与早期发表的刚度测量结果一致。