1) As the sarcomere is progressively stretched to its optimal length, and the diastolic fibre lengthens proportionately the force of contraction progressively increases. This is partly due to the fact that over the normal operating range the opposing actin filament over lap, interfering with actin-myosin cross bridge formation. With stretch the degree of overlap decreases and hence force generation increases.
2) Recent evidence suggests that calcium sensitivity of the contractile proteins increases with increase in length, providing a greater degree of activation for a calcium concentartion.
EXCITATION-CONTRACTION COUPLING: During systole there is a 50-fold increase in intracellular calcium concentration. The cardiac action potential is responsible for the increase in intracellular calcium in two ways:
1) Calcium ions enter the cell from the extracellular space during the plateau phase of action potential
2) The spike of the action potential triggers the release of calcium from the intracellular stores within the sarcoplasmic reticulum.
THE ENERGY SUPPLY: Energy is produced in the heart by the process of Oxidative phosphorylation. This results from the conversion of the energy produced by the oxidation of substrates such as glucose, lactate and fatty acid into the energy of Adenosine tri-phosphate (ATP) and creatine phosphate(CP). These substances provide the energy source for muscular contraction. Normally, free fatty acid are the main substrates, but in ischemia the glycolytic pathway is stimulated. This however cannot substitute for oxidative phosphorylation and inevitably ischemia leads to a fall in ATP levels and a consequent impairment of myocardial function.
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