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

- [Instructor] Un músculo se contrae

cuando la superposición de los filamentos

delgados y gruesos aumenta

haciendo que la longitud
del sarcómero disminuya.

A nivel molecular, la
contracción se produce

cuando el ATP, unido a la región de la

cabeza globular de la miosina,

se hidroliza a ADP, convirtiendo
la cabeza de miosina

a un estado de alta energía
en el que se une a la actina

y crea un puente cruzado.

La liberación de ADP provoca
que la cabeza de miosina

vuelva a un estado de baja
energía, lo que mueve la actina

hacia el centro del sarcómero.

Une una nueva molécula de
ATP a la cabeza de miosina

y luego la disocia de la actina.

La próxima vez que esta cabeza
de miosina se una a la actina

sucederá en la parte que
esté más cerca de la línea Z.

Este proceso de unión es controlado

por dos proteínas reguladoras,

la tropomiosina y la troponina,

y por la concentración de calcio,

que se almacena y luego se libera

desde el retículo sarcoplasmático.

La tropomiosina cubre el sitio de unión

de la miosina en la actina

y la troponina se une al
calcio cuando está disponible,

alejando a la tropomiosina

desde el sitio de unión de
la miosina sobre la actina.

En esta confirmación se puede
formar un puente cruzado

y el músculo se contrae.

Este ciclo continúa hasta
que el calcio y el ATP

ya no están presentes
en la fibra muscular.

Guellich, Aziz, Elisa Negroni, Valérie Decostre, Alexandre Demoule y Catherine Coirault. "Propiedades alteradas de puentes cruzados en distrofias musculares esqueléticas". Frontiers in Physiology 5 (14 de octubre de 2014). [<a href="https://doi.org/10.3389/fphys.2014.00393" target="__blank">Fuente</a>]

Debold, Edward P. "Conocimientos recientes sobre la fatiga muscular en el nivel de puente cruzado". Frontiers in Physiology 3 (1 de junio de 2012). [<a href="https://doi.org/10.3389/fphys.2012.00151" target="__blank">Fuente</a>]

Rall, Jack A. "¿Qué hace que el músculo esquelético esté estriado? Descubrimientos en el citoesqueleto endosarcomérico y exosarcomérico." Avances en Educación en Fisiología 42, no. 4 (15 de noviembre de 2018): 672–84. [<a href="https://doi.org/10.1152/advan.00152.2018" target="__blank">Fuente</a>]

ciclo de puente cruzado

A medida que el músculo se contrae, aumenta la superposición entre los filamentos finos y gruesos, lo que disminuye la longitud del sarcómero,la unidad contráctil del músculo, utilizando energía en forma de ATP. A nivel molecular, se trata de un proceso cíclico de varios pasos que implica la unión e hidrólisis del ATP y el movimiento de la actina por la miosina. Cuando el ATP, que está adherido a la cabeza de miosina, se hidroliza a ADP, la miosina pasa a un estado de alta energía unida a la actina, creando un puente cruzado. Cuando se libera ADP, la cabeza de miosina pasa a un estado de baja energía, moviendo la actina hacia el centro del sarcómero. La unión de una nueva molécula de ATP disocia la miosina de la actina. Cuando este ATP se hidroliza, la cabeza de miosina se unirá a la actina, esta vez en una porción de actina más cercana al extremo del sarcómero. Las proteínas reguladoras troponina y tropomiosina, junto con el calcio, trabajan juntas para controlar la interacción miosina-actina. Cuando la troponina se une al calcio, la tropomiosina se aleja del sitio de unión de la miosina en la actina, lo que permite que la miosina y la actina interactúen y se produzca la contracción muscular. <h4>Calcio</h4> Como regulador de la contracción muscular, la concentración de calcio está muy controlada en las fibras musculares. Las fibras musculares están en estrecho contacto con las neuronas motoras. Los potenciales de acción en las neuronas motoras provocan la liberación del neurotransmisor acetilcolina en las proximidades de las fibras musculares. Esto genera un potencial de acción (despolarización) en la célula muscular, que se transporta a lo largo de la membrana plasmática y a través de invaginaciones de la membrana plasmática llamadas túbulos transversales o T. Los túbulos T se adentran profundamente en el músculo y están adyacentes a orgánulos especializados del retículo endoplásmico llamados retículo sarcoplásmico o SR. El calcio secuestrado dentro del SR se libera cuando los canales iónicos dependientes de voltaje (canales iónicos que se abren y cierran según las cargas locales) se abren en respuesta a la despolarización, lo que permite que los iones de calcio ingresen al citoplasma y que los músculos se contraigan. Cuando se detiene la señalización de las neuronas motoras, comienza la relajación del músculo a medida que el calcio se bombea de regreso al SR, lo que disminuye los niveles citoplasmáticos de calcio y repone las reservas de calcio del SR en preparación para la siguiente contracción. <h4>Degeneración muscular</h4> El músculo sano puede contraerse, pero el músculo enfermo a menudo pierde esta capacidad. Enfermedades como la miastenia gravis impiden la estimulación de las neuronas motoras del músculo, lo que provoca atrofia muscular y disminución de la masa muscular. La esclerosis lateral amiotrófica (ELA o enfermedad de Lou Gehrig) hace que las neuronas motoras se degeneren, lo que de manera similar conduce a la degeneración y atrofia muscular.

Ciclo de puente cruzado

A medida que el músculo se contrae, la superposición entre los filamentos delgados y gruesos aumenta, disminuyendo la longitud del sarcómero, la unidad contráctil del ...

Education

Educación

JoVE Core

Biology

Biología

Human Biology

Biología Humana

Musculoskeletal System

Sistema musculoesquelético

KEY TERMS AND CONCEPTS

TÉRMINOS Y CONCEPTOS CLAVE

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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