Stretch of Contracting Muscle Fibres: Evidence for Regularly Spaced Active Sites along the Filaments and Enhanced Mechanical Performance

Author(s):  
K. A. P. Edman ◽  
G. Elzinga ◽  
M. I. M. Noble
Nature ◽  
1982 ◽  
Vol 300 (5894) ◽  
pp. 776-778 ◽  
Author(s):  
Roger Cooke ◽  
Mark S. Crowder ◽  
David D. Thomas

Studies of the interaction between actin and myosin subfragment 1 (S1) in solution have shown that the association reaction takes place in at least two steps. Initially the association is relatively weak to form a complex called the A state which can then isomerize to the R state. The rate and equilibrium constants for the isomerization have been measured and are shown to depend upon the nucleotide bound to the SI ATPase site; with ATP bound the A state is preferred but as ATP is hydrolysed and the products are sequentially released then the complex gradually shifts to the A state. An extensive series of experiments have characterized the A-to-R isomerization both in solution and in contracting muscle fibres and have shown it to be closely associated with the key events in the ATP-driven contraction cycle: the conformational change from the A to the R state can be monitored by fluorescent probes on either actin or the nucleotide; the isomerization can be perturbed by increases in hydrostatic pressure; the actin-induced acceleration of the rate of product release from myosin is coupled to the A-to-R isomerization; tropomyosin may control actin and myosin interaction by controlling the ismoerization step and finally pressure perturbations of contracting muscle fibres shows there to be a close coupling between the isomerization of acto.S1 and the force generating event of muscle contraction.


Author(s):  
Fyodor A. Syomin ◽  
Andrey K. Tsaturyan

AbstractAn axisymmetric model is suggested to simulate mechanical performance of the left ventricle of the heart. Cardiac muscle is treated as incompressible anisotropic material with active tension directed along muscle fibres. This tension depends on kinetic variables that characterize interaction of contractile proteins and regulation of muscle contraction by calcium ions. For numerical simulation of heartbeats the finite element method was implemented. The model reproduces well changes in ventricle geometry between systole and diastole, ejection fraction, pulse wave of ventricular and arterial pressure typical for normal human heart. The model also reproduces well the dependence of the stroke volume on end-diastolic and arterial pressures (the Frank–Starling law of the heart and Anrep effect). The results demonstrate that our model of cardiac muscle can be successfully applied to multiscale 3D simulation of the heart.


1979 ◽  
Vol 56 (3) ◽  
pp. 7P-7P
Author(s):  
M. I. M. Noble ◽  
G. Elzinga ◽  
K. A. P. Edman

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