As cardiac end-diastolic volume (preload) rises, the cardiac stroke volume rises too.
This happens because the contractile fibres work more efficiently as they are stretched more. There are many factors involved:
- The calcium sensitivity of troponin rises, and consequently, the number of actin-myosin bridges increases.
- There is more calcium release from the sarcoplasmic reticulum.
- There is reduced spacing between the thin and thick fibres, allowing more actin-myosin bridges to form.
This can only continue up to a point, because the cardiac muscle has physical limitations. Maximal contractile force is generated at an initial sarcomere length of 2.2 micrometers. Beyond this limit, the increases in stroke volume become exponentially smaller. Eventually heart failure will occur.
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