Cardiac muscle is found only in the heart, where it forms a muscular bag the myocardium in the atria and in the ventricle. The cells are uninucleate cylinders, 10-20 µm diameter (c. ¼ skeletal). They are short (50-100 µm) but are often branched, and joined to each other end-to-end to form an interlacing meshwork. The junctions between cells (intercalated discs) are partly tight junctions for strong adherence, and partly low resistance gap junctions which allow free spread of small molecules and electrical currents (ions) between fibres. The fibres are cross-striated like skeletal muscle fibres. This muscle gives spontaneous, forcible contractions, repetitively throughout life.

For cardiac muscle time to peak contraction may be about 150 ms.  Time to peak in skeletal muscle is 7.5 ms to about 90 ms and for smooth muscle, of the order of 500 ms. Cardiac muscle behaves like very slow skeletal muscle. It is rich in mitochondria and myoglobin and highly dependent on a good oxygen supply.  The differential speeds of contraction are related to differences in (1) the potency of the myosin ATPase isozyme in the muscle, (2) in smooth muscle, the attachment time of the myosin heads - which may be quite prolonged at low Ca²⁺ levels (latch mechanism), and (3) the abundance of SR and the potency of the Ca²⁺-Mg²⁺-ATPase and/or (in cardiac and smooth muscle) the potency of Na⁺-Ca²⁺ exchanger in the sarcolemma.  Item (3) determines relaxation rate as well as contraction rate.  Items (1) and (2) determine cycling time for the myosin heads, and thereby, speed of contraction.

In cardiac muscle, the mechanism of contraction is essentially the same as in skeletal, but the excitation-contraction coupling mechanism differs slightly.  T-tubules invaginate at the level of the Z-lines.  The SR is relatively poorly developed (cisternae are small or absent - in most EM sections 'diads' and not 'triads' are seen), and provides insufficient Ca²⁺ to fully activate the contractile apparatus.  Unlike those in skeletal muscle the ryanodine channels in cardiac muscle are activated by Ca²⁺ in the cytosol (calcium activated calcium release) and Ca²⁺ entry through the dihydropyridine channels is an important trigger of Ca²⁺ release.  Significant amounts of Ca²⁺ enter the fibre from the ECF during the AP, which consequently has a long plateau phase caused by slowly inactivating Ca²⁺ channels in the sarcolemma, prolonging AP (c. 200 ms).  Ca²⁺ is also released from sub-sarcolemmal binding sites during the AP.  Because the AP lasts almost as long as the twitch, heart muscle cannot be tetanized. 

After contraction, Ca²⁺ is pumped back into the SR by a Ca²⁺-Mg²⁺-ATPase pump (relatively weak), and back to the extra-cellular fluid by a Na⁺-dependent Ca²⁺ pump in the sarcolemma (these two pumps compete with each other).  The calcium ion in the SR is the more readily available, and the greater the amount of Ca²⁺ in the SR is the more fully activated will the contractile apparatus be, on each contraction.  Poisoning the Na⁺/K⁺ pump with digitalis, and reducing the extra/intra-cellular Na⁺ gradient, can therefore actually enhance contraction of the heart muscle.  Because the extracellular Ca²⁺ is necessary however, cardiac contractility (see below) is significantly affected by extracellular Ca²⁺ levels (not so in skeletal muscle).

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