Name: calcium control in muscle contraction
Uploaded: 2025-10-23T11:47:01.000Z
Duration: 1 min 26 s
Channel: JoVE

K12 Standards

Florida Department of Education

High School

Life Science

SC.912.L.14

SC.912.L.14.17

Cross-bridge Cycle

Ein Muskel zieht sich zusammen, wenn die Überlappung der dünnen und dicken Filamente zunimmt, wodurch die Länge des Sarkomers abnimmt.
 Auf molekularer Ebene tritt eine Kontraktion auf, wenn ATP, das an die globuläre Kopfregion von Myosin gebunden ist, zu ADP hydrolysiert wird, wodurch das Myosinköpfchen in einen Zustand hoher Energie umgewandelt wird, in dem er an Actin bindet und eine Kreuzbrücke bildet.
 Durch die Freisetzung von ADP kehrt das Myosinköpfchen in einen Zustand niedriger Energie zurück und bewegt Aktin in Richtung des Zentrums des Sarkomers.
 Die Bindung eines neuen ATP-Moleküls an das Myosinköpfchen trennt es dann von Actin.
 Wenn dieses Myosinköpfchen das nächste Mal an Actin bindet, befindet es sich an einem Abschnitt, welcher näher an der Z-Linie liegt.
 Dieser Bindungsprozess wird durch zwei regulatorische Proteine, Tropomyosin und Troponin und die Kalziumkonzentration gesteuert, die im sarkoplasmatischen Retikulum gespeichert ist und aus diesem auch freigesetzt wird.
 Tropomyosin bedeckt die Myosin-Bindungsstelle auf Actin und Troponin bindet an Calcium, wenn es verfügbar ist, wodurch Tropomyosin von der Myosin-Bindungsstelle auf Actin wegbewegt wird.
 In dieser Bestätigung kann sich eine Kreuzbrücke bilden und der Muskel kontrahiert.
 Dieser Zyklus setzt sich fort, bis Calcium und ATP nicht mehr in der Muskelfaser vorhanden sind.

Guellich, Aziz, Elisa Negroni, Valérie Decostre, Alexandre Demoule und Catherine Coirault. "Veränderte Cross-Bridge-Eigenschaften bei Skelettmuskeldystrophien." Frontiers in Physiology 5 (14. Oktober 2014). [<a href="https://doi.org/10.3389/fphys.2014.00393" target="__blank">Quelle</a>]

Debold, Edward P. "Jüngste Einblicke in die Muskelermüdung auf der Cross-Bridge-Ebene." Frontiers in Physiology 3 (1. Juni 2012). [<a href="https://doi.org/10.3389/fphys.2012.00151" target="__blank">Quelle</a>]

Rall, Jack A. "Was macht die Skelettmuskulatur quergestreift? Entdeckungen im endosarkomerischen und exosarkomerischen Zytoskelett." Fortschritte in der physiologischen Ausbildung 42, Nr. 4 (15. November 2018): 672–84. [<a href="https://doi.org/10.1152/advan.00152.2018" target="__blank">Quelle</a>]

querbrückenzyklus

Wenn sich ein Muskel kontrahiert, vergrößert sich die Überlappung der dünnen und dicken Filamente, wodurch die Länge der Sarkomers, die kontraktile Einheit des Muskels, unter Verwendung von Energie in Form von ATP verringert wird. Auf molekularer Ebene ist dies ein zyklischer, mehrstufiger Prozess, der die Bindung und Hydrolyse von ATP sowie die Bewegung von Aktin durch Myosin involviert.
 
 Wenn das am Myosinkopf haftende ATP zu ADP hydrolysiert wird, geht das Myosin in einen hochenergetischen Zustand in dem es an Aktin gebunden über und eine Querbrücke entsteht. Wenn ADP freigesetzt wird, bewegt sich der Myosinkopf in einen niedrigen Energiezustand und das Aktin wird zum Zentrum des Sarkomers bewegt. Durch die Bindung eines neuen ATP-Moleküls wird das Myosin vom Aktin dissoziiert. Wenn dieses ATP hydrolysiert wird, bindet der Myosinkopf an einem Teil des Aktins der sich näher am Ende des Sarkomers befindet. Die regulatorischen Proteine Troponin und Tropomyosin arbeiten zusammen mit Kalzium, um die Myosin-Aktin-Interaktion zu kontrollieren. Wenn Troponin Kalzium bindet, wird Tropomyosin von der Myosin-Bindungsstelle auf dem Aktin entfernt. Wodurch Myosin und Aktin wieder interagieren können und eine Muskelkontraktion stattfinden kann.
 
 <h4>Kalzium</h4>
 
 Als Regulator der Muskelkontraktion wird die Konzentration des Kalziums in den Muskelfasern sehr genau kontrolliert. Die Muskelfasern liegen nah an den Motoneuronen. Aktionspotentiale in den Motoneuronen bewirken die Freisetzung des Neurotransmitters Acetylcholin nah der Muskelfasern. Dadurch wird in der Muskelzelle ein Aktionspotential (Depolarisation) erzeugt, das entlang der Plasmamembran und der Einstülpungen in der Plasmamembran transportiert wird. Diese Einstülpungen bezeichnet man als transversale oder T-Tubuli.
 
 Die T-Tubuli verlaufen tief in den Muskel und grenzen an spezialisierte endoplasmatische Retikulumorganellen, die sarkoplasmatisches Retikulum oder SR genannt werden. Das Kalzium im Inneren des SR wird freigesetzt, wenn sich die spannungsgesteuerten Ionenkanäle (Ionenkanäle, die sich aufgrund lokaler Ladungen öffnen und schließen) durch die Depolarisation öffnen. Dadurch treten Kalzium-Ionen in das Zytoplasma ein und die Muskeln kontrahieren.
 
 Wenn die Signale der Motoneuronen aufhören, beginnt die Entspannung des Muskels, indem das Kalzium zurück in das SR gepumpt wird. Dadurch senkt sich der Kalziumspiegel im Zytoplasma und die Kalziumspeicher des SR werden in Vorbereitung auf die nächste Kontraktion wieder aufgefüllt.
 
 <h4>Muskel-Degeneration</h4>
 
 Gesunde Muskeln können sich zusammenziehen, jedoch verlieren kranke Muskeln diese Fähigkeit oft. Krankheiten wie Myasthenia gravis verhindern die Stimulation des Muskels durch die Motorneuronen, was zu Muskelschwund und zu einer Abnahme der Muskelmasse führt. Amyotrophe Lateralsklerose (ALS oder Lou-Gehrigs-Krankheit) führt zu einer Degeneration der Motoneuronen, was ebenfalls zu Muskeldegeneration und-atrophie führt.

Querbrückenzyklus

Wenn sich der Muskel zusammenzieht, nimmt die Überlappung zwischen den dünnen und dicken Filamenten zu, wodurch sich die Länge des Sarkomers verringert – die kontraktile Einheit des Sarkomers ...

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calcium control in muscle contraction

Calcium control in muscle contraction depends on ATP, motor neurons, and the sliding action of actin and myosin. As a muscle contracts, the thin and thick filaments overlap more, and the sarcomere, which is the contractile unit of the muscle, becomes shorter. This process uses energy from ATP and happens in a repeating cycle at the molecular level.

Myosin drives the movement of actin through a cross-bridge cycle. When ATP attached to the myosin head is hydrolyzed to ADP, myosin shifts into a high-energy state and binds actin. This forms a cross-bridge. When ADP is released, the myosin head moves to a lower-energy state and pulls actin toward the center of the sarcomere. A new ATP molecule then binds to myosin and causes it to detach from actin. After that ATP is hydrolyzed, myosin can bind again, this time to a new site on actin closer to the end of the sarcomere.

Troponin, tropomyosin, and calcium regulate this interaction. When troponin binds calcium, tropomyosin moves away from the myosin-binding site on actin. That shift lets myosin and actin interact, and muscle contraction can occur. Calcium concentration in muscle fibers is tightly controlled so this switch can happen at the right time.

Motor neurons start the process by signaling nearby muscle fibers. Their action potentials trigger release of the neurotransmitter acetylcholine near the muscle cell. This produces an action potential, or depolarization, in the muscle cell membrane. The signal travels along the plasma membrane and through T-tubules, which are inward folds of the membrane that carry the signal deep into the muscle. T-tubules sit next to the sarcoplasmic reticulum, or SR, a specialized endoplasmic reticulum that stores calcium.

When depolarization reaches the SR, voltage-gated ion channels open and release calcium into the cytoplasm. The rise in calcium allows the muscle to contract. When signaling from the motor neuron stops, relaxation begins. Calcium is pumped back into the SR, which lowers calcium in the cytoplasm and restores the SR calcium supply for the next contraction.

Healthy muscle can contract, but diseased muscle may lose that ability. Myasthenia gravis can prevent motor neuron stimulation of muscle, which can lead to muscle atrophy and a decrease in muscle mass. Amyotrophic lateral sclerosis, or ALS, also called Lou Gehrig's disease, causes motor neurons to degenerate. That loss of motor neurons can likewise lead to muscle degeneration and atrophy.

Calcium Control in Muscle Contraction

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cross-bridge cycle

Calcium control in muscle contraction depends on ATP, motor neurons, and the sliding action of actin and myosin. As a muscle contracts, the thin and thick filaments overlap more, and the sarcomere, which is the contractile unit of the muscle, becomes shorter. This process uses energy from ATP and happens in a repeating cycle at the molecular level. Myosin drives the movement of actin through a cross-bridge cycle. When ATP attached to the myosin head is hydrolyzed to ADP, myosin shifts into a...

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key terms and concepts

Learn how calcium, troponin, tropomyosin, and ATP control muscle contraction, from motor neuron signaling to relaxation and muscle degeneration.

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Calcium Control in Muscle Contraction

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