systole. after emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. a normally performing heart must be fully expanded before it can efficiently pump again. the rest phase is considered polarized. the resting potential during this phase of the beat separates the ions such as sodium, potassium, and calcium. myocardial cells possess the property of automaticity or spontaneous depolarization. this is the direct result of a membrane which allows sodium ions to slowly enter the cell until the threshold is reached for depolarization. calcium ions follow and extend the depolarization even further. once calcium stops moving inward, potassium ions move out slowly to produce repolarization. the very slow repolarization of the cmc membrane is responsible for the long refractory period. however, the mechanism by which calcium concentrations within the cytosol rise differ between skeletal and cardiac muscle. in cardiac muscle, the action potential comprises an inward flow of both sodium and calcium ions. the flow of sodium ions is rapid but very short-lived, while the flow of calcium is sustained and gives the plateau phase characteristic of cardiac muscle action potentials. the comparatively small flow of calcium through the l-type calcium channels triggers a much larger release of calcium from the sarcoplasmic reticulum in a phenomenon known as calcium-induced calcium release. in contrast, in skeletal muscle, minimal calcium flows into the cell during action potential and instead the sarcoplasmic reticulum in these cells is directly coupled to the surface membrane. this difference can be illustrated by the observation that cardiac muscle fibers require calcium to be present in the solution surrounding the cell to contract, while skeletal muscle fibers will contract without extracellular calcium. during contraction of a cardiac muscle cell, the long protein myofilaments oriented along the length of the cell slide over each other in what is known as the sliding filament theory. there are two kinds of myofilaments, thick filaments composed of the protein myosin, and thin filaments composed of the proteins actin, troponin and tropomyosin. as the thick and thin filaments slide past each other the cell becomes shorter and fatter. in a mechanism known as cross-bridge cycling, calcium ions bind to the protein troponin, which along with tropomyosin then uncover key binding sites on actin. myosin, in the thick filament, can then bind to actin, pulling the thick filaments along the thin filaments. when the concentration of calcium within the cell falls, troponin and tropomyosin once again cover the binding sites on actin, causing the cell to relax. regeneration dog cardiac muscle (400x) it was commonly believed that cardiac muscle cells could not be regenerated. however, this was contradicted by a report published in 2009. olaf bergmann and his colleagues at the karolinska institute in stockholm tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. by using dna samples from many hearts, the researchers estimated that a 4-year-old renews about 20% of heart muscle cells per year, and about 69 percent of the heart muscle cells of a 50-year-old were generated after he or she was born. one way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process. in the 2000s, the discovery of adult endogenous cardiac stem cells was reported, and studies were published that claimed that various stem cell lineages, including bone marrow stem cells were able to differentiate into cardiomyocytes, and could be used to treat heart failure. however, other teams were unable to replicate these findings, and many of the original studies were later retracted for scientific fraud. differences between atria and ventricles the swirling musculature of the heart ensures effective pumping of blood. cardiac muscle forms both the atria and the ventricles of the heart. although this muscle tissue is very similar between cardiac chambers, some differences exist. the myocardium found in the ventricles is thick to allow forceful contractions, while the myocardium in the atria is much thinner. the individual myocytes that make up the myocardium also differ between cardiac chambers. ventricular cardiomyocytes are longer and wider, with a denser t-tubule network. although the fundamental mechanisms of calcium handling are similar between ventricular and atrial cardiomyocytes, the calcium transient is smaller and decays more rapidly in atrial myocytes, with a corresponding increase in calcium buffering capacity. the complement of ion channels differs between chambers, leading to longer action potential durations and effective refractory periods in the ventricles. certain ion currents such as ik(ur) are highly specific to atrial cardiomyocytes, making them a potential target for treatments for atrial fibrillation. clinical significance further information: cardiomyopathy diseases affecting cardiac muscle, known as cardiomyopathies, are the leading cause of death in developed countries. the most common condition is coronary artery disease, in which the blood supply to the heart is reduced. the coronary arteries become narrowed by the formation of atherosclerotic plaques. if these narrowings become severe enough to partially restrict blood flow, the syndrome of angina pectoris may occur. this typically causes chest pain during exertion that is relieved by rest. if a coronary artery suddenly becomes very narrowed or completely blocked, interrupting or severely reducing blood flow through the vessel, a myocardial infarction or heart attack occurs. if the blockage is not relieved promptly by medication, percutaneous coronary intervention, or surgery, then a heart muscle region may become permanently scarred and damaged. a specific cardiomyopathy, can cause heart muscle to become abnormally thick (hypertrophic cardiomyopathy), abnormally large (dilated cardiomyopathy), or abnormally stiff (restrictive cardiomyopathy). some of these conditions are caused by genetic mutations and can be inherited. heart muscle can also become damaged despite a normal blood supply. the heart muscle may become inflamed in a condition called myocarditis, most commonly caused by a viral infection but sometimes caused by the body's own immune system. heart muscle can also be damaged by drugs such as alcohol, long standing high blood pressure or hypertension, or persistent abnormal heart racing. many of these conditions, if severe enough, can damage the heart so much that the pumping function of the heart is reduced. if the heart is no longer able to pump enough blood to meet the body's needs, this is described as heart failure. significant damage to cardiac muscle cells is referred to as myocytolysis which is considered a type of cellular necrosis defined as either coagulative or colliquative.