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

Мышца контрактирует, когда увеличивается перекрывание тонких и толстых филаментов, из-за чего уменьшается длина саркомера. На молекулярном уровне сокращение происходит, когда АТФ, связанная с шаровидным головным регионом миозина гидролизуется в АДФ, преобразовывая головку миозина в высокоэнергетическом состоянии, в котором он связывается с актином и создаёт перекрёстный мостик. Выпуск АДФ заставляет головку миозина вернуться в состояние низкого энергопотребления, в сторону центра саркомера.Связывание новой молекулы АТФ с миозиновой головкой приводит к её диссоциации от актина. Когда в следующий раз головка миозина свяжется с актином, это произойдёт в какой-то части, которая ближе к линии Z.Этот процесс привязки контролируется двумя регуляторными белками, тропомиозином и тропонином, и концентрацией кальция, который хранится и выпускается из саркоплазматического ретикулума. Тропиомиозин покрывает сайт привязки миозина на актине, и тропонин связывается с кальцием, когда он доступен, передвигая тропомиозин с сайта привязки миозина во время действий.В этой связи может образоваться перекрёстный мостик, и мышцы сжимаются. Этот цикл продолжается до тех пор, пока в мышечном волокне не закончатся кальций и АТФ.

Геллич, Азиз, Элиза Негрони, Валери Декостр, Александр Демуль и Катрин Койро. «Измененные свойства поперечного моста при дистрофии скелетных мышц». Frontiers in Physiology 5 (14 октября 2014 г.). [<a href="https://doi.org/10.3389/fphys.2014.00393" target="__blank">Источник</a>]

Деболд, Эдвард. "Последние сведения о мышечной усталости на уровне поперечного моста." Frontiers in Physiology 3 (1 июня 2012 г.). [<a href="https://doi.org/10.3389/fphys.2012.00151" target="__blank">Источник</a>]

Ралл, Джек А. «Что делает скелетные мышцы поперечно-полосатыми? Открытия в эндосаркомериальном и экзосаркомерном цитоскелете." Успехи в образовании в области физиологии 42, No4 (15 ноября 2018 г.): 672–84. [<a href="https://doi.org/10.1152/advan.00152.2018" target="__blank">Источник</a>]

Цикл миозиновых (поперечных) мостиков

По мере сокращения мышцы перекрытие между тонкими и толстыми нитями увеличивается, уменьшая длину саркомера - сократительной единицы мышцы, использующей энергию в виде АТФ. На молекулярном уровне это циклический, многоступенчатый процесс, который включает связывание и гидролиз АТФ и перемещение актина миозином. 

 Когда АТФ, прикрепленный к головке миозина, гидролизуется до АДФ, миозин переходит в высокоэнергетическое состояние, связанный с актином, создавая поперечный мостик. Когда АДФ высвобождается, головка миозина переходит в состояние низкой энергии, перемещая актин к центру саркомера. Связывание новой молекулы АТФ отделяет миозин от актина. Когда этот АТФ гидролизуется, миозиновая головка связывается с актином, на этот раз с частью актина ближе к концу саркомера. Регулирующие белки тропонин и тропомиозин, наряду с кальцием, работают вместе, чтобы контролировать взаимодействие миозин-актин. Когда тропонин связывается с кальцием, тропомиозин отодвигается от сайта связывания миозина на актине, позволяя миозину и актину взаимодействовать и происходить сокращение мышц. 

<h4> Кальций </h4>

 Как регулятор сокращения мышц, концентрация кальция в мышечных волокнах очень строго контролируется. Мышечные волокна находятся в тесном контакте с мотонейронами. Потенциалы действия в двигательных нейронах вызывают высвобождение нейромедиатора ацетилхолина в непосредственной близости от мышечных волокон. Это создает потенциал действия (деполяризацию) в мышечной клетке, который переносится вдоль плазматической мембраны и через инвагинации плазматической мембраны, называемые поперечными, или Т-канальцами. 

 Т-канальцы проходят глубоко в мышцу и соседствуют со специализированными органеллами эндоплазматической сети, называемыми саркоплазматической сетью, или SR. Кальций, секвестрированный внутри SR, высвобождается, когда управляемые напряжением ионные каналы (ионные каналы, которые открываются и закрываются в зависимости от локальных зарядов) открываются в ответ на деполяризацию, позволяя ионам кальция проникать в цитоплазму и сокращать мышцы. 

 Когда сигнал от мотонейронов прекращается, начинается расслабление мышцы, поскольку кальций перекачивается обратно в SR, снижая цитоплазматические уровни кальция и пополняя запасы кальция SR в рамках подготовки к следующему сокращению. 

<h4> Дегенерация мышц </h4>

 Здоровая мышца может сокращаться, но больная мышца часто теряет эту способность. Такие заболевания, как миастения, препятствуют стимуляции двигательных нейронов мышц, что приводит к атрофии мышц и уменьшению мышечной массы. Боковой амиотрофический склероз (БАС или болезнь Лу Герига) вызывает дегенерацию мотонейронов, что аналогичным образом приводит к дегенерации и атрофии мышц.

По мере сокращения мышц перекрытие между тонкими и толстыми нитями увеличивается, уменьшая длину саркомера — сократительной единицы ...

Education

JoVE Core

Biology

Биология

Human Biology

Биология человека

Musculoskeletal System

Опорно-двигательная система

KEY TERMS AND CONCEPTS

ОСНОВНЫЕ ТЕРМИНЫ И ПОНЯТИЯ

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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The human skeleton is a living framework made of 206 bones in adults. Bones connect with cartilage, tendons, and ligaments. This system gives the body support, protects organs, and helps with movement and locomotion. The skeleton has two main parts: the axial skeleton and the appendicular skeleton. The axial skeleton has 80 bones and includes the skull, the vertebral column, and the rib cage. The cranium, or upper skull, has eight bones that enclose the brain, while the lower part of the skull...

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Muscle Fibers, Tendons, and Contraction

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classification of skeletal muscle fibers

Skeletal Muscle Fiber Speed and Energy

Skeletal muscle fibers can be grouped by how fast they contract and how they make ATP, the energy cells use for movement. These differences also shape their physical features. Most human muscles contain all three fiber types, but in different amounts. Slow oxidative fibers, also called slow-twitch fibers, appear red because they have many capillaries and high levels of myoglobin, an oxygen-storing protein. They also contain more mitochondria, which make ATP through oxidative phosphorylation,...

muscle contraction

Nerve Signals That Trigger Muscle Contraction

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

How Motor Units Control Muscle Movement

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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.

Calcium Control in Muscle Contraction | JoVE K12

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Calcium Control in Muscle Contraction

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