Essay on Contraction And Relaxation Of Cardiac Fibers

  • Introduction

    The contractile unit of the cardiac muscle fiber is the sarcomere which contains actin, myosin, troponin and tropomyosin. Also known as the thin and thick filaments respectively, actin and myosin interact to enable the shortening and lengthening of the sarcomere. Troponin and tropomyosin are regulator proteins that allow the sarcomere to shorten in the presence of calcium ions (Ca2+) and lengthen in the absence of calcium ions. The interaction of the thin and thick filaments can occur through the sliding filament theory or the cross bridge theory. The contraction and relaxation of the cardiac fibers is a complex process involving influx and outflow of Ca2+ in the myocyte.

    Contraction and Relaxation of Cardiac Fibers

    A cell membrane known as sarcolemma surrounds cardiac fibers or myocytes. In the myocyte, sarcoplasmic reticulum which is similar to the endoplasmic reticulum present in other types of cells surrounds the filaments and regulator proteins. The cardiac myocyte has a membrane structure known as transverse tubule or T tubule that has a continuous lumen and transmits action potential. Extracellular fluid surrounds the myocyte and intercalated disks join adjacent cardiac myocytes.

    According to Indu Khurana, the contraction of cardiac muscles requires a raised intracellular concentration of calcium ions (Ca2+) following an action potential.  The influx of Ca2+ leads to further increase of Ca2+ from the sarcoplasmic reticulum through calcium release channels. The T tubules have voltage gated calcium channels that undergo conformational change when the T tubules conduct action potential. This causes calcium release channels to open releasing Ca2+ into the cytoplasm. The free intracellular Ca2+ bind to troponin causing a conformational change in the troponin/tropomyosin complex. The change leads to actin interacting with myosin and the sarcomere shortens resulting in contraction.

    The relaxation of the cardiac fiber occurs when the levels of Ca2+ reduce in the myocyte. As a result, Ca2+ dissociate from troponin resulting in relaxation. Cardiac fiber relaxation is an active process that requires ATP. Consequently, a carrier system in the sarcolemma that transports Ca2+ in exchange of two sodium ions (Na+) pumps Ca2+ out of the myocyte. According to JeremyPinnell, Turner Simon, and Howell Simon, calcium transport out of the cytosol also occurs through the Ca2+-ATPase in the sarcoplasmic reticulum, Ca2+-ATPase in the sarcolemma and throughmitochondrial Ca2+ uniport.

    In the sliding filament theory, the thin and thick filaments slide past each other leading to the shortening of the sarcomere. The myofibrils shorten but both the thin and thick filaments remain the same during cardiac fiber contraction. The filaments slide past each other through asynchronous lashes of myosin cross bridges that pull the thin filaments over the thick filaments. In the cross bridges theory, the thin and thick filaments slide past each other through various cross bridges that extend from the thick filaments to the thin filaments. The cross bridges are part of myosin proteins that form globular heads where actin and ATP can bind.

    Once the myosin head binds to ATP, ATP hydrolysis to ADP and inorganic phosphate occurs and this activates the myosin head to bind with actin. Binding of actin to the myosin head leads to the release of inorganic phosphate causing the bridge to form a power stroke. This force pulls the thin filaments causing muscle contraction and ADP is released. A new ATP molecule binds to the myosin head and the process repeats itself. In a relaxed muscle, intracellular concentration of Ca2+ is very low and tropomyosin blocks the attachment of actin to cross bridges. During contraction, Ca2+ increase and attach to troponin causing a conformational change in troponin/tropomyosin complex such that the cross bridges can bind to actin.


    In conclusion, the contraction and relaxation of the cardiac muscle fiber depend on the action potential in the myocyte membrane. During stimulation, Ca2+ are released into the cytoplasm where they bind with troponin causing contraction. In the absence of action potential, Ca2+ is actively transported back to the sarcoplasmic reticulum causing relaxation. The sliding filament and cross bridge theories explain how attachment of Ca2+ to and from troponin causes contraction and relaxation of cardiac muscle fibers.

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