page_title: Muscle contraction
section_title: Excitation-contraction coupling
hierarchical_section_title: Muscle contraction / Vertebrates / Cardiac muscle / Excitation-contraction coupling
caption_attribution_description: English: Cartoon showing the key proteins involved in cardiac calcium cycling and excitation contraction coupling
context_page_description: Muscle contraction is the activation of tension-generating sites within muscle fibers. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length, such as when holding a heavy book or a dumbbell at the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.
  Muscle contractions can be described based on two variables: length and tension. A muscle contraction is described as isometric if the muscle tension changes but the muscle length remains the same. In contrast, a muscle contraction is isotonic if muscle tension remains the same throughout the contraction. If the muscle length shortens, the contraction is concentric; if the muscle length lengthens, the contraction is eccentric. In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner. Therefore, neither length nor tension is likely to remain the same in muscles that contract during locomotor activity.
context_section_description: Unlike skeletal muscle, excitation–contraction coupling in cardiac muscle is thought to depend primarily on a mechanism called calcium-induced calcium release. Though the proteins involved are similar, the L-type calcium channels and ryanodine receptors (RyRs) are not physically coupled. Instead, RyRs are activated by a calcium trigger, which is brought about by the flow of Ca²⁺
  through the L-type calcium channels. Furthermore, cardiac muscle tend to exhibit diad (or dyad) structures, rather than triads.
  Excitation-contraction coupling in cardiac muscle cells occurs when an action potential is initiated by pacemaker cells in the sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions. The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes extracellular Ca²⁺
   to enter the cell via L-type calcium channels and possibly sodium-calcium exchanger (NCX) during the early part of the plateau phase. This Ca²⁺
   influx causes a small local increase in intracellular Ca²⁺
  . The increase in Ca²⁺
   is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum, which releases Ca²⁺
   in a positive feedback physiological response. This positive feedback is known as calcium-induced calcium release and gives rise to calcium sparks (Ca²⁺
   sparks). The spatial and temporal summation of ~30,000 Ca²⁺
   sparks gives a cell-wide increase in cytoplasmic calcium concentration. The increase in cytosolic calcium following the flow of calcium through the cell membrane and sarcoplasmic reticulum is moderated by calcium buffers, which bind a large proportion of intracellular calcium.  As a result, a large increase in total calcium leads to a relatively small rise in free Ca²⁺
  .
  The cytoplasmic calcium binds to Troponin C, moving the tropomyosin complex off the actin binding site allowing the myosin head to bind to the actin filament. From this point on, the contractile mechanism is essentially the same as for skeletal muscle (above). Briefly, using ATP hydrolysis, the myosin head pulls the actin filament toward the centre of the sarcomere.
  Following systole, intracellular calcium is taken up by the sarco/endoplasmic reticulum ATPase (SERCA) pump back into the sarcoplasmic reticulum ready for the next cycle to begin. Calcium is also ejected from the cell mainly by the sodium-calcium exchanger (NCX) and, to a lesser extent, a plasma membrane calcium ATPase.  Some calcium is also taken up by the mitochondria. An enzyme, phospholamban, serves as a brake for SERCA. At low heart rates, phospholamban is active and slows down the activity of the ATPase so that Ca²⁺
   does not have to leave the cell entirely. At high heart rates, phospholamban is phosphorylated and deactivated thus taking most Ca²⁺
   from the cytoplasm back into the sarcoplasmic reticulum.  Once again, calcium buffers moderate this fall in Ca²⁺
  concentration, permitting a relatively small decrease in free Ca²⁺
  concentration in response to a large change in total calcium. The falling Ca²⁺
  concentration allows the troponin complex to dissociate from the actin filament thereby ending contraction.  The heart relaxes, allowing the ventricles to fill with blood and begin the cardiac cycle again.
caption: Key proteins involved in cardiac calcium cycling and excitation-contraction coupling
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