The initial phase of diastole is characterized by a flat pressure-volume curve, indicating that the ventricle can accommodate large increases in volume with only minimal increases in pressure. However, as filling pressures rise, the ventricle becomes less distensible, resulting in a sharp increase in diastolic pressure at larger intraventricular volumes.

In a normal heart, peak force is typically reached at a filling pressure of around 12 mm Hg. At this diastolic pressure, which is close to the upper limit observed in a normal heart, sarcomere length is approximately 2.2 µm. However, filling pressures can peak as high as 30 mm Hg, causing sarcomere length to increase only slightly to 2.6 µm. This ability of the myocardium to resist stretch at high filling pressures is likely due to the noncontractile constituents of the heart tissue, such as connective tissue, and serves as a protective mechanism against excessive stress on the heart during diastole.

Normally, ventricular diastolic pressure ranges from 0 to 7 mm Hg, with an average diastolic sarcomere length of approximately 2.2 µm. Thus, a normal heart operates on the ascending portion of the Frank-Starling curve.

Cardiac muscle functions as a syncytium, meaning that stimulation of any part of the muscle leads to contraction of the entire muscle. Gap junctions with high conductance are present in the intercalated disks between adjacent cells, facilitating conduction of the cardiac impulse from one cell to another.

Due to the continuous need for contraction, cardiac muscle requires a constant supply of oxygen. Therefore, it is highly rich in mitochondria, which are responsible for oxidative phosphorylation, rapid substrate oxidation, ATP synthesis, and meeting the energy demands of the myocardium.

To meet its metabolic requirements, the myocardium is also well-supplied with capillaries, with approximately one capillary per fiber. This ensures short diffusion distances, allowing for rapid exchange of oxygen, carbon dioxide, substrates, and waste materials between myocardial cells and capillaries. The transverse (T) tubular system within myocardial cells facilitates this exchange and plays a crucial role in excitation-contraction coupling. However, the T tubular system is either absent or poorly developed in the atrial cells of many mammals.
The pressure-volume curve during diastole is initially quite flat (compliant), which indicates that large increases in volume can be accommodated with only small increases in pressure. In contrast, the development of systolic pressure is considerable at the lower filling pressures. However, the ventricle becomes much less distensible with greater filling, as evidenced by the sharp rise in the diastolic pressure curve at large intraventricular volumes.
In a normal intact heart, peak force may be attained at a filling pressure of approximately 12 mm Hg. At this intraventricular diastolic pressure, which is near the upper limit observed in a normal heart, sarcomere length is near its resting length of 2.2 µm. However, the force causes filling pressures to peak as high as 30 mm Hg. At even higher diastolic pressures (>50 mm Hg), sarcomere length is no greater than 2.6 µm. This ability of the myocardium to resist stretch at high filling pressures probably resides in the noncontractile constituents of the heart tissue (connective tissue), and it may serve as a safety factor against overloading of the heart in diastole. Usually, ventricular diastolic pressure is approximately 0 to 7 mm Hg, and the average diastolic sarcomere length is approximately 2.2 µm. Thus a normal heart operates on the ascending portion of the Frank-Starling curve, as depicted in
Fig. 16.36 •Fig. 16.36 Relationshipofmyocardialrestingfiberlength(sarco-merelength)orend-diastolicvolumetotheforcedevelopedorpeaksystolicventricularpressureduringventricularcontractioninanintactheart.(RedrawnfromPattersonSW,etal.J Physiol. 1914;48:465.)
Cardiac muscle functions as a syncytium; that is, a stimulus applied to any part of the cardiac muscle results in contraction of the entire muscle. Gap junctions with high conductance are present in the intercalated disks between adjacent cells and facilitate conduction of the cardiac impulse from one cell to the next.
Cardiac muscle must contract repetitively for a lifetime, and hence it requires a continuous supply of O2. Cardiac muscle is therefore very rich in mitochondria. The large number of mitochondria (see
Fig. 13.1
B), which have the enzymes necessary for oxidative phosphorylation, allows rapid oxidation of substrates and synthesis of ATP and thus sustains the myocardial energy requirements.
CHAPTER 16 Elements of Cardiac Function
To provide adequate O2 and substrate for its metabolic machinery, the myocardium is also endowed with a rich capillary supply, approximately one capillary per fiber. Thus diffusion distances are short, and O2, CO2, substrates, and waste material can move rapidly between the myocardial cell and capillary. The transverse (T) tubular system within myocardial cells participates in this exchange of substances between capillary blood and myocardial cells (as described later, the T tubule system also plays a key role in excitation-contraction coupling). The T tubular system is absent or poorly developed in the atrial cells of many mammals.