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

근육의 수축은 가는 섬유와굵은 섬유의 중복이 증가하여근절 길이가 줄어들 떄 일어난다분자 수준에서의 수축은미오신의 구상 머리 부분에 결합된 ATP가ADP로 가수 분해 되어 미오신 머리를고에너지 상태로 만들고 그래서 액틴에 결합하여연결 다리를 만들어낼 때 일어난다ADP의 방출로 미오신 머리가저에너지 상태로 돌아오게 만들고액틴을 근절의 중앙으로 가게 만든다새로운 ATP 분자가 미오신에 결합하면액틴에서 분리가 된다다음 번에 이 미오신 머리가 액틴에 결합하면Z 선에 더 가까운 부분 위에 있게 된다이 결합 과정은 두 개의 규제 단백질인트로포닌과 토로포마이오신 그리고칼슘 농도에 의해서 통제되는데칼슘은 근 소포체에저장되고 방출된다토로포마이오신은 액틴 위의 미오신 결합 부위를커버하고 트로포닌은 칼슘에 결합하여액틴 위의 미오신 결합 부위로부터토로포마이오신을 멀어지게 한다이 과정에서 연결 고리가 형성되고근육이 축소한다이 순환은 칼슘과 ATP가 근육 섬유에더 이상 존재하지 않을 때까지 계속된다

Guellich, Aziz, Elisa Negroni, Valérie Decostre, Alexandre Demoule 및 Catherine Coirault. "골격근 이영양증의 변경된 교차 다리 특성." Frontiers in Physiology 5 (2014년 10월 14일). [<a href="https://doi.org/10.3389/fphys.2014.00393" target="__blank">소스</a>]

Debold, Edward P. "Cross-bridge level에서 근육 피로에 대한 최근 통찰력." Frontiers in Physiology 3 (2012년 6월 1일). [<a href="https://doi.org/10.3389/fphys.2012.00151" target="__blank">소스</a>]

Rall, Jack A. "골격근을 줄무늬로 만드는 것은 무엇입니까? Discoveries in the Endosarcomeric and Exosarcomeric Cytoskeleton(내육종 및 외육종 세포골격의 발견)."Advances in Physiology Education 42, no. 4 (2018년 11월 15일): 672–84. [<a href="https://doi.org/10.1152/advan.00152.2018" target="__blank">출처</a>]

교차 결합 주기

근육이 수축하면서 얇은 필라멘트(filament; 미세섬유)와 두꺼운 필라멘트 사이의 겹침이 증가하여 아데노신삼인산(ATP) 형태의 에너지를 사용하는 근육의 수축 단위인 근섬유분절(sarcomere; 근분절)의 길이가 짧아집니다. 분자 수준에서 이것은 ATP의 결합과 가수분해(hydrolysis), 그리고 미오신(myosin; 마이오신)에 의한 액틴(actin)의 이동을 포함하는 주기적인 다단계 과정입니다.
 
 미오신 머리에 붙어 있는 ATP가 ADP로 가수분해되면 미오신은 액틴과 결합해 높은 에너지 상태로 전환하여 교차 결합(cross-bridge)을 형성합니다. ADP가 방출되면, 미오신 머리는 낮은 에너지 상태로 전환하여 근섬유분절의 중앙을 향해 움직입니다. 새로운 ATP 분자의 결합은 미오신과 액틴을 분리합니다. 이 ATP가 가수분해되면, 미오신 머리는 액틴과 결합합니다. 그러면 이번에는 액틴의 일부분이 근섬유분절의 끝에 가까워지게 됩니다. 조절 단백질(regulatory protein) 트로포닌(troponin)과 트로포미오신(tropomyosin; 트로포마이오신)은 칼슘과 함께 미오신-액틴 상호작용을 조절합니다. 트로포닌이 칼슘과 결합하면, 트로포미오신은 액틴의 미오신 결합 자리(myosin-binding site)에서 멀어져 미오신과 액틴이 상호작용하고 근육 수축이 일어나도록 합니다.
 
 <h4>칼슘</h4>
 
 근육 수축의 조절자(regulator)로서, 칼슘 농도는 근육 섬유에서 매우 엄격하게 조절됩니다. 근육 섬유는 운동 뉴런과 밀접하게 접촉합니다. 운동 뉴런의 활동전위(action potential)는 근육 섬유 근처에서 신경전달물질(neurotransmitter)인 아세틸콜린(acetylcholine)의 방출을 일으킵니다. 이는 근육 세포에서 활동전위를 생성(탈분극(depolarization))하는데, 이 활동전위는 원형질막(plasma membrane)을 따라 그리고 원형질막의 함입(invagination), 즉 횡소관(transverse tubule, 줄여서 T-tubule)을 따라 전파됩니다.
 
 횡소관은 근육 깊숙이 뻗어있으며 근소포체(sarcoplasmic reticulum, 줄여서 SR)이라고 불리는 특수한 소포체(endoplasmic reticulum)에 인접해 있습니다. 근소포체 내부에 격리된 칼슘은 탈분극에 따라 전위의존성 이온 채널(voltage-gated ion channel; 국소 전하를 기반으로 개폐되는 이온 채널)이 열리면 방출되고, 이 칼슘 이온이 세포질(cytoplasm)로 들어가서 근육이 수축합니다.
 
 운동 뉴런의 신호가 멈추면, 칼슘이 근소포체로 다시 펌프질 되어 칼슘의 세포질 수치를 낮추고 다음 수축에 대비하여 근소포체 칼슘 저장고를 보충하면서 근육의 이완이 시작됩니다.
 
 <h4>근육 퇴화</h4>
 
 건강한 근육은 수축할 수 있지만, 병든 근육은 종종 이 능력을 잃습니다. 중증근무력증(myasthenia gravis)과 같은 질병은 근육에 가는 운동 뉴런 자극을 막아 근육 위축과 근육 질량의 감소를 초래합니다. 근위축성 축삭경화증(amyotrophic lateral sclerosis, 줄여서 ALS; Lou Gehrig’s disease; 루게릭병)은 운동 뉴런의 퇴화를 유발해 근육의 퇴화와 위축으로 이어집니다.

근육이 수축함에 따라 얇은 필라멘트와 두꺼운 필라멘트 사이의 겹침이 증가하여 sarcomere의 길이가 감소합니다.

Education

교육

JoVE Core

Biology

생물학

Human Biology

인체 생물학

Musculoskeletal System

근골격계

KEY TERMS AND CONCEPTS

주요 용어 및 개념

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.

Calcium Control in Muscle Contraction | JoVE K12

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Explain the significance of genetic factors, environmental factors, and pathogenic agents to health from the perspectives of both individual and public health.

SC.912.L.14.6

A. Cells have characteristic structures and functions that make them distinctive.

B. Processes in a cell can be classified broadly as growth, maintenance, reproduction, and homeostasis.

C. Life can be organized in a functional and structural hierarchy ranging from cells to the biosphere.

D. Most multicellular organisms are composed of organ systems whose structures reflect their particular function.

Calcium Control in Muscle Contraction

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