Cardiac muscle cell

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Cardiac muscle cell
Latin cardiomyocytus; myocytus cardiacus
Code TH H2.
Anatomical terminology
Illustration of a myocardiocyte, including organelles and cell membrane functions

Cardiac muscle cells or cardiomyocytes (also known as myocardiocytes[1] or cardiac myocytes[2]) are the muscle cells (myocytes) that make up the cardiac muscle. Each myocardial cell contains myofibrils, which are specialized organelles consisting of long chains of sarcomeres, the fundamental contractile units of muscle cells. Cardiomyocytes show striations similar to those on skeletal muscle cells, but unlike multinucleated skeletal cells, they contain only one nucleus. Cardiomyocytes have a high mitochondrial density, which allows them to produce adenosine triphosphate (ATP) quickly, making them highly resistant to fatigue.

Two types of cells[edit]

There are two types of cells within the heart: the cardiomyocytes and the cardiac pacemaker cells. Cardiomyocytes make up the atria (the chamber in which blood enters the heart) and ventricles (where blood is pumped out of the heart) of the heart. These cells must be able to shorten and lengthen their fibers and the fibers must be flexible enough to stretch. These functions are critical to the proper form during the beating of the heart.[3]

Cardiomyocytes can contain vimentin and desmin.[4] Vimentin is a substance in mesenchymal cells that is responsible for holding the organelles in the cytosol. It is also responsible for adding flexibility to the cell and keeps them from being too delicate. The exact nature of desmin is not known. It is purported to have a similar function as vimentin although the levels of each vary at different points during cardiac muscle growth. Desmin is more readily available during early growth whereas vimentin is predominate in later stages.

Cardiac pacemaker cells carry the impulses that are responsible for the beating of the heart. They are distributed throughout the heart and are responsible for several functions. First, they are responsible for being able to spontaneously generate and send out electrical impulses. They also must be able to receive and respond to electrical impulses from the brain. Lastly, they must be able to transfer electrical impulses from cell to cell.[5]

All of these cells are connected by cellular bridges. Porous junctions called intercalated discs form junctions between the cells. They permit sodium, potassium and calcium to easily diffuse from cell to cell. This makes it easier for depolarization and repolarization in the myocardium. Because of these junctions and bridges the heart muscle is able to act as a single coordinated unit.[6][7]

Depolarization/repolarization cycle[edit]

The cardiac action potential consists of two cycles, a rest phase and an active phase. The rest phase is considered polarized. The resting potential during this phase of the beat separates the ions such as sodium, potassium and calcium. The electrical cell will then generate an impulse. The ions will then cross the cell membrane causing depolarization. The movement of these ions through the sodium, potassium and calcium channels causes the contraction of the heart muscle. The depolarization and contraction together cause a wave of movement to pass through the heart muscle. The ions will then return to their regular resting state and the heart muscle relaxes. This is called repolarization. And ECG (electrocardiogram) measures the strength of these cycles. The length of time between depolarization and repolarization is long (relatively speaking.) This period of time is called the refractory period. The refractory period is about the same amount of time between the contraction and relaxation of the heart muscle. Because of this, the cardiac muscle does not tire as easily. 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.[8][9]

Myocardial infarction[edit]

Myocardial infarction, commonly known as a heart attack, occurs when the heart's supplementary blood vessels are obstructed by an unstable build-up of white blood cells, cholesterol, and fat. With no blood flow, the cells die causing whole portions of cardiac tissue to die. Once these tissues are lost, they cannot be replaced, thus causing permanent damage. Current research indicates, however, that it may be possible to repair damaged cardiac tissue with stem cells.[10]

Growth and renewal[edit]

Humans are born with a set number of heart muscle cells, or cardiomyocytes, which increase in size as our heart grows larger during childhood development. Recent evidence suggests that cardiomyocytes are actually slowly turned over as we age, but that less than 50% of the cardiomyocytes we are born with are replaced during a normal life span.[11] The growth of individual cardiomyocytes not only occurs during normal heart development, it also occurs in response to extensive exercise (athletic heart syndrome), heart disease, or heart muscle injury such as after a myocardial infarction. A healthy adult cardiomyocyte has a cylindrical shape that is approximately 100μm long and 10-25μm in diameter. Cardiomyocyte hypertrophy occurs through sarcomerogenesis, the creation of new sarcomere units in the cell. During heart volume overload, cardiomyocytes grow through eccentric hypertrophy.[12] The cardiomyocytes extend lengthwise but have the same diameter, resulting in ventricular dilation. During heart pressure overload, cardiomyocytes grow through concentric hypertrophy.[12] The cardiomyocytes grow larger in diameter but have the same length, resulting in heart wall thickening.

See also[edit]


  1. ^ Wolfgang Kühnel (1 January 2003). Color atlas of cytology, histology, and microscopic anatomy. Thieme. pp. 172–. ISBN 978-3-13-562404-4. Retrieved 18 April 2010. 
  2. ^ Julian Seifter; Austin Ratner; David Sloane (1 October 2005). Concepts in medical physiology. Lippincott Williams & Wilkins. pp. 201–. ISBN 978-0-7817-4489-8. Retrieved 18 April 2010. 
  3. ^ Severs, Nicholas. "The Cardiac Muscle Cell". Retrieved 2012. 
  4. ^ Sampayo-Reyes A, Narro-Juárez A, Saíd-Fernández S, et al. (2006). "Effect of clofibric acid on desmin and vimentin contents in rat cardiomyocytes". Int. J. Toxicol. 25 (5): 403–8. doi:10.1080/10915810600846989. PMID 16940012. 
  5. ^ "Anatomy and Physiology of the Heart". Retrieved 2012. 
  6. ^ "American Heart Association: How the Heart Works". Retrieved 2012. 
  7. ^ Martini, Frederic. "The Fundamentals of Anatomy and Physiology: Chapter 10 Cardiac Muscle Tissue". 
  8. ^ Klabunde, Richard. "Cardiovascular Physiology= Cardiac muscle Concept". Retrieved 2012. 
  9. ^ "Cells Alive: Pumping Myocytes". Retrieved 2012. 
  10. ^ "Stem Cell Research News". Retrieved 2012. 
  11. ^ Bergmann, O.; Bhardwaj, R. D., Bernard, S., Zdunek, S., Barnabe-Heider, F., Walsh, S., Zupicich, J., Alkass, K., Buchholz, B. A., Druid, H., Jovinge, S., Frisen, J. (3 April 2009). "Evidence for cardiomyocyte renewal in humans". Science 324 (5923): 98–102. doi:10.1126/science.1164680. PMC 2991140. PMID 19342590. 
  12. ^ a b Göktepe, S; Abilez, OJ, Parker, KK, Kuhl, E (2010-08-07). "A multiscale model for eccentric and concentric cardiac growth through sarcomerogenesis". Journal of Theoretical Biology 265 (3): 433–42. doi:10.1016/j.jtbi.2010.04.023. PMID 20447409.