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

Un muscolo si contrae
quando la sovrapposizione

dei filamenti sottili e spessi aumenta,

facendo diminuire la
lunghezza del sarcomero.

A livello molecolare, la
contrazione si verifica

quando l'ATP legato alla
testa globosa della miosina

viene idrolizzato in ADP,
convertendo la testa della miosina

in uno stato di alta energia
in cui si lega all'actina

e crea un ponte.

Il rilascio di ADP fa ritornare
la testa della miosina

a uno stato di bassa energia,

spostando l'actina verso
il centro del sarcomero.

Il legame di una nuova molecola
di ATP alla testa della

miosina si dissocia dall'actina.

La prossima unione della
testa di miosina all'actina,

sarà su una porzione
più vicina alla linea z.

Questo processo di legame è controllato

da due proteine regolatrici,
la tropomiosina e la troponina

e la concentrazione di calcio,

che viene immagazzinata e rilasciata

dal reticolo sarcoplasmatico.

La tropomiosina copre il legame
della miosina sull'actina

e la troponina si lega al
calcio quando è disponibile,

spostando la tropomiosina dal

sito di legame della miosina sull'actina.

In questa conferma, si
può formare un ponte

e il muscolo si contrae.

Questo ciclo continua
fino a quando calcio e ATP

non sono più presenti
nella fibra muscolare.

Guellich, Aziz, Elisa Negroni, Valérie Decostre, Alexandre Decostre, Alexandre Demule e Catherine Coirault. "Proprietà alterate del ponte trasversale nelle distrofie muscolari scheletriche". Frontiers in Physiology 5 (14 ottobre 2014). [<a href="https://doi.org/10.3389/fphys.2014.00393" target="__blank">Sorgente</a>]

Debold, Edward P. "Recenti intuizioni sull'affaticamento muscolare a livello di ponte trasversale". Frontiers in Physiology 3 (1 giugno 2012). [<a href="https://doi.org/10.3389/fphys.2012.00151" target="__blank">Sorgente</a>]

Rall, Jack A. "Cosa rende striato il muscolo scheletrico? Scoperte nel citoscheletro endosarcomico ed esosarcomerico. Advances in Physiology Education 42, n. 4 (15 novembre 2018): 672–84. [<a href="https://doi.org/10.1152/advan.00152.2018" target="__blank">Sorgente</a>]

ciclo dei ponti trasversali

Mentre il muscolo si contrae, la sovrapposizione tra i filamenti sottili e spessi aumenta, diminuendo la lunghezza del sarcomero, l'unità contrattile del muscolo, utilizzando l'energia sotto forma di ATP. A livello molecolare, questo è un processo ciclico e multifase che coinvolge il legame e l'idrolisi dell'ATP e il movimento dell'actina da parte della miosina.

Quando ATP, che è attaccato alla testa di miosina, è idrolizzato ad ADP, la miosina si muove in uno stato ad alta energia destinato ad actina, creando un ponte incrociato. Quando ADP viene rilasciato, la testa della miosina si sposta in uno stato di bassa energia, muovendo l'actina verso il centro del sarcomero. Il legame di una nuova molecola ATP dissocia la miosina dall'actina. Quando questo ATP è idrolizzato, la testa della miosina si legherà all'actina, questa volta su una porzione di actina più vicina alla fine del sarcomero. Proteine regolatorie troponina e tropomiosina, insieme al calcio, lavorano insieme per controllare l'interazione tra miosina-actina. Quando la troponina si lega al calcio, la tropomiosina viene allontanata dal sito legante della miosina sull'actina, consentendo alla miosina e all'actina di interagire e di verificarsi la contrazione muscolare.

<h4>Calcio</h4>

Come regolatore della contrazione muscolare, la concentrazione di calcio è strettamente controllata nelle fibre muscolari. Le fibre muscolari sono a stretto contatto con i motoneuroni. Potenziali di azione nei motoneuroni causano il rilascio del neurotrasmettitore acetilcolina in prossimità di fibre muscolari. Questo genera un potenziale d'azione (depolarizzazione) nella cellula muscolare, che viene trasportato lungo la membrana plasmatica e attraverso invaginazioni della membrana plasmatica chiamata trasversale, o tubuli T.

I tubuli T corrono in profondità nel muscolo e sono adiacenti a organelli di reticolo reticolo endoplasmatico specializzati chiamati reticolo sarcoplasmico, o SR. Il calcio sequestrato all'interno del SR viene rilasciato quando i canali ionici "voltage-gated" (canali ionici che si aprono e si chiudono in base alle cariche locali) si aprono in risposta alla depolarizzazione, permettendo agli ioni di calcio di entrare nel citoplasma e ai muscoli di contrarsi.

Quando la segnalazione da neuroni motori si ferma, il rilassamento del muscolo inizia come calcio viene pompato di nuovo nella SR, diminuendo i livelli citoplasmatici di calcio e ricostituire i depositi di calcio SR in preparazione per la successiva contrazione.

<h4>Degenerazione muscolare</h4>

Muscolo sano può contrarsi, ma il muscolo malato spesso perde questa capacità. Malattie come la mioasthenia gravis impediscono la stimolazione del motoneurone del muscolo che si traduce in atrofia muscolare e una diminuzione della massa muscolare. La sclerosi laterale amiotrofica (SLA o malattia di Lou Gehrig) fa degenerare i motoneuroni, il che porta in modo simile alla degenerazione muscolare e all'atrofia.

Ciclo dei ponti trasversali

Man mano che il muscolo si contrae, la sovrapposizione tra i filamenti sottili e spessi aumenta, diminuendo la lunghezza del sarcomero, l'unità contrattile del ...

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KEY TERMS AND CONCEPTS

TERMINI E CONCETTI CHIAVE

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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Muscle Fibers, Tendons, and Contraction

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muscle contraction

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Nerve signals trigger muscle contraction in both skeletal and smooth muscle, but the two muscle types use different control systems. In skeletal muscle, the signal begins at the motor end plate, which is the synapse between a motor neuron and a muscle fiber. In smooth muscle, contraction is controlled by the autonomic nervous system and happens without conscious control. In skeletal muscle, motor nerve terminals release acetylcholine. This neurotransmitter binds to receptors on the sarcolemma,...

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...

motor units

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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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