Increasing sarcomere length significantly decreased myofilament lattice spacing in both skinned and intact isolated rat myocardium, supporting its role in length-dependent activation.
The study provides structural evidence supporting the hypothesis that decreased myofilament lattice spacing at longer sarcomere lengths underlies length-dependent activation (the Frank-Starling mechanism) in the myocardium.
The Frank-Starling relationship of the heart has, as its molecular basis, an increase in the activation of myofibrils by calcium as the sarcomere length increases. It has been suggested that this phenomenon may be due to myofilaments moving closer together at longer lengths, thereby enhancing the probability of favorable acto-myosin interaction, resulting in increased calcium sensitivity. Accordingly, we have developed an apparatus so as to obtain accurate measurements of myocardial interfilament spacing (by synchrotron X-ray diffraction) as a function of sarcomere length (by video microscopy) over the working range of the heart, using skinned as well as intact rat trabeculas as model systems. In both these systems, lattice spacing decreased significantly as sarcomere length was increased. Furthermore, lattice spacing in the intact muscle was significantly smaller than that in the skinned muscle at all sarcomere lengths studied. These observations are consistent with the hypothesis that lattice spacing underlies length-dependent activation in the myocardium.
Irving et al. (Wed,) reported a other. Sarcomere length increase vs. Shorter sarcomere lengths was evaluated on Myocardial interfilament (lattice) spacing. Increasing sarcomere length significantly decreased myofilament lattice spacing in both skinned and intact isolated rat myocardium, supporting its role in length-dependent activation.