Landesberg A, Sideman S
Department of Biomedical Engineering, Julius Silver Institute, Heart System Research Center, Haifa 32000, Israel.
Am J Physiol. 1999 Mar;276(3):H998-H1011. doi: 10.1152/ajpheart.1999.276.3.H998.
The well-known linear relationship between oxygen consumption and force-length area or the force-time integral is analyzed here for isometric contractions. The analysis, which is based on a biochemical model that couples calcium kinetics with cross-bridge cycling, indicates that the change in the number of force-generating cross bridges with the change in the sarcomere length depends on the force generated by the cross bridges. This positive-feedback phenomenon is consistent with our reported cooperativity mechanism, whereby the affinity of the troponin for calcium and, hence, cross-bridge recruitment depends on the number of force-generating cross bridges. Moreover, it is demonstrated that a model that does not include a feedback mechanism cannot describe the dependence of energy consumption on the loading conditions. The cooperativity mechanism, which has been shown to determine the force-length relationship and the related Frank-Starling law, is shown here to provide the basis for the regulation of energy consumption in the cardiac muscle.
本文分析了等长收缩时耗氧量与力-长度面积或力-时间积分之间著名的线性关系。该分析基于一个将钙动力学与横桥循环相结合的生化模型，结果表明，随着肌节长度变化，产生力的横桥数量的变化取决于横桥产生的力。这种正反馈现象与我们报道的协同机制一致，即肌钙蛋白对钙的亲和力以及横桥募集取决于产生力的横桥数量。此外，研究表明，一个不包含反馈机制的模型无法描述能量消耗对负荷条件的依赖性。协同机制已被证明可决定力-长度关系及相关的弗兰克-斯塔林定律，本文表明其为心肌能量消耗的调节提供了基础。
