Contraction of Cardiac Muscle - Podcast Version 0:00 / 0:00 1x 0.25x 0.5x 0.75x 1x 1.25x 1.5x 1.75x 2x Like skeletal muscle, cardiac myocytes contract according to the sliding filament theory of muscle contraction. In this article, we will look at the process of calcium-induced calcium release and the electrical coupling of cardiac myocytes. Pro Feature - 3D Model You've Discovered a Pro Feature Access our 3D Model Library Explore, cut, dissect, annotate and manipulate our 3D models to visualise anatomy in a dynamic, interactive way. Learn More Calcium-Induced Calcium Release Calcium can be released from the sarcoplasmic reticulum (SR) in 2 ways: Via IP3 Gq-protein coupling facilitates the release of Ca2+ from the sarcoplasmic reticulum. This is particularly important in muscle types that require calcium-induced calcium release (e.g. in cardiac muscle). Gq activates the effector: Phospholipase C enzyme Phospholipase C breaks down PIP2 (phosphatidylinositol 4,5-biphosphate), into IP3 + DAG IP3 then binds to the IP3 receptor on the SR DAG acts on various proteins (e.g PKC) Ca2+ channels on the SR open and Ca2+ is released. Action is then terminated by IP3 phosphatase (IP3 is cleaved to IP2) Via Ryanodine receptors (RyR): these are a family of Ca2+ releasing channels found on intracellular organelles that store or release Ca2+. Membrane depolarisation opens voltage-operated calcium channels (VOCCs) in the T-tubule system and calcium is released. Calcium binds to RyR on the sarcoplasmic reticulum. This induces conformational changes in a Ca2+ channel which is closely associated with RyR. RyR is activated and opens to release Ca2+ from the SR stores. This is known as the ‘calcium spark’. Released calcium leads to a calcium spike. Calcium binds to troponin C thus activating the cross-bridge cycling mechanism for contraction. By TeachMeSeries Ltd (2026) Fig 1Diagram showing the process of Calcium Induced Calcium Release (CICR). Pathway of Contraction Pacemaker cells in the SA and AV nodes initiate an action potential which is conducted around the heart via gap junctions. The action potential travels down the T-tubules between sarcomeres resulting in an influx of calcium ions into the sarcoplasm through VOCCs. When calcium enters the sarcoplasm (through VOCCs and ryanodine receptors) it binds to cardiac troponin-C which moves the tropomyosin away from the actin-binding site thus exposing it and initiating cross-bridge binding. Sliding Filament Model of Contraction Cardiac muscle contraction occurs via the sliding filament model of contraction, much like skeletal muscle. Once calcium is bound to troponin-C and the conformational change of tropomyosin has occurred, myosin heads can bind to actin. Following this ADP and inorganic phosphate are released from the myosin head so the power stroke can occur. In this the myosin head pivots and bends, pulling on the actin and moving it, causing muscle contraction. After this occurs a new molecule of ATP binds to the myosin head, causing it to detach from the actin. Finally, the ATP is hydrolysed into ADP and inorganic phosphate. Following this, the cycle can begin again and further contraction can occur. By OpenStax [CC BY 4.0 (http://creativecommons.org/licenses/by/4.0)], via Wikimedia Commons Fig 2Diagram showing the sliding filament model of muscle contraction. Removal of Calcium After the stimulus is removed, intracellular calcium is then reduced in two ways: By entering the sarcoplasmic reticulum for storage via a SERCA (sarco(endo)plasmic reticulum calcium-ATPase) channel at the expense of an ATP molecule. Through an NCX (sodium-calcium exchange) channel which extrudes a calcium ion and admits a sodium ion when membrane repolarisation starts. Calcium is no longer bound to troponin C and the actin-binding site is covered up, ending contraction and relaxing the muscle. Clinical Relevance Troponin Assays Some subtypes of troponin can be used as very specific and sensitive markers of damage to the cardiac muscle, particularly troponin I and T. They are typically measured in the blood to differentiate between unstable angina and myocardial infarctions, as they may present with similar symptoms. The cardiac troponin levels in a patient suffering from a myocardial infarction would typically be hugely elevated. These elevated troponin levels would not be seen in unstable angina. Depending on the onset of the myocardial infarction, troponin levels peak a few hours following injury and can remain high for up to two weeks after the event. However, it is important to note that troponin release is not specific to myocardial infarction and only indicates cardiac muscle damage. As such, they may also be elevated in conditions such as heart failure, pericarditis, and amyloidosis. In addition to this, non-cardiac diseases such as sepsis or renal failure can also elevate troponins. Do you think you’re ready? Take the quiz below Pro Feature - Quiz Contraction of Cardiac Muscle Question 1 of 3 Submitting... Skip Next Rate question: You scored 0% Skipped: 0/3 More Questions Available Upgrade to TeachMePhysiology Pro Challenge yourself with over 2100 multiple-choice questions to reinforce learning Learn More Frequent questions What is calcium-induced calcium release in cardiac muscle? Calcium-induced calcium release is a process where calcium ions are released from the sarcoplasmic reticulum, primarily triggered by the binding of calcium to ryanodine receptors. This mechanism is essential for initiating contraction in cardiac myocytes. How does the sliding filament theory explain cardiac muscle contraction? The sliding filament theory describes cardiac muscle contraction as the interaction between actin and myosin filaments, facilitated by calcium binding to troponin C. This binding causes tropomyosin to shift, allowing myosin heads to attach to actin and produce muscle contraction. What role do pacemaker cells play in cardiac muscle contraction? Pacemaker cells in the SA and AV nodes generate action potentials that propagate through the heart via gap junctions. This electrical activity triggers calcium influx, leading to the contraction of cardiac muscle. How is calcium removed from the sarcoplasm after cardiac contraction? Calcium is removed from the sarcoplasm by being transported back into the sarcoplasmic reticulum via the SERCA channel and by the sodium-calcium exchange mechanism. This reduction in calcium levels leads to muscle relaxation as troponin C releases calcium and the actin-binding site is covered. Why are troponin levels clinically significant in diagnosing cardiac conditions? Troponin levels, particularly troponin I and T, serve as sensitive markers for cardiac muscle damage, helping to distinguish between conditions like unstable angina and myocardial infarction. Elevated troponin levels indicate myocardial injury and can remain elevated for days, but they may also rise in other non-cardiac conditions. Rate This Article