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

השריר מתכווץ כאשר החפיפה בין הפילמנטים הדקים והעבים גדלה, מה שגורם להיקצרות הסרקומר. ברמה המולקולרית, ההתכווצות מתרחשת הקשור ATP כאשר לראש הכדורי של מיוזין, ADP-עובר הידרוליזה ל ומעביר את ראש המיוזין למצב של אנרגיה גבוהה שבו הראש נקשר לאקטין ויוצר גשר רוחב. גורם לראש המיוזין ADP שחרור לחזור למצב של אנרגיה נמוכה, מה שמניע את אקטין אל מרכז הסרקומר.ATP קישור מולקולת חדשה לראש המיוזין מנתק אותו מהאקטין. בפעם הבאה שראש המיוזין יקשר לאקטין, זה יהיה על החלק Z-הקרוב יותר לקו ה. תהליך קישור זה מבוקר על-ידי שני חלבוני בקרה, טרופומיוזין וטרופונין, ועל-ידי ריכוז הסידן אשר מאוחסן ומשוחרר מהרשתית הסרקופלסמית.טרופומיוזין מכסה את אתרי הקישור למיוזין שעל אקטין, והטרופונין נקשר לסידן כאשר הוא זמין, מה שמרחיק את הטרופומיוזין מאתר הקישור למיוזין שעל אקטין. סידור מרחבי זה מאפשר לגשר רוחב להיווצר ולשריר להתכווץ. מחזור זה נמשך עד שהסידן כבר לא נוכחים בסיבי השריר ATP-וה.

גליך, עזיז, אליסה נגרוני, ואלרי דקוסטרה, אלכסנדר דמול וקתרין קוארו. "שינוי תכונות גשר חוצה ניוון שרירי השלד." Frontiers in Physiology 5 (14 באוקטובר 2014). [<a href="https://doi.org/10.3389/fphys.2014.00393" target="__blank">מקור</a>]

Debold, Edward P. "תובנות אחרונות על עייפות שרירים ברמת גשר חוצה גשרים." גבולות בפיזיולוגיה 3 (יוני 1, 2012). [<a href="https://doi.org/10.3389/fphys.2012.00151" target="__blank">מקור</a>]

ראל, ג'ק א. "מה גורם לשרירי השלד להיות מתוחים? תגליות בשלד הציטוסרקומרי והאקסוסרקומרי." התקדמות בחינוך לפיזיולוגיה 42, מס '4 (15 בנובמבר 2018): 672–84. [<a href="https://doi.org/10.1152/advan.00152.2018" target="__blank">מקור</a>]

מחזור גשרי הרוחב

<div style="direction:rtl">כאשר השריר מתכווץ, החפיפה בין הפילמנטים הדקים והעבים גדלה, ומקטינה את אורך הסרקומר יחידת ההתכווצות של השריר באמצעות אנרגיה בצורה של ATP. ברמה המולקולרית, זהו תהליך מחזורי רב-שלבי הכולל קישור והידרוליזה של ATP, ותנועה של אקטין על ידי מיוזין. כאשר ATP, המחובר לראש המיוזין, עובר הידרוליזה ל-ADP, המיוזין עובר למצב אנרגיה גבוהה הקשור לאקטין, ויוצר גשר רוחבי. כאשר ADP משתחרר, ראש המיוזין עובר למצב של אנרגיה נמוכה, ומניע את האקטין לכיוון מרכז הסרקומר. קשירה של מולקולת ATP חדשה מנתקת את המיוזין מהאקטין. כאשר ATP זה עובר הידרוליזה, ראש המיוזין ייקשר לאקטין, הפעם על חלק של אקטין קרוב יותר לקצה הסרקומר. חלבונים רגולטוריים טרופונין וטרופומיוזין, יחד עם סידן, פועלים יחד כדי לשלוט באינטראקציה של מיוזין-אקטין. כאשר טרופונין נקשר לסידן, הטרופומיוזין מתרחק מהאתר הקישור למיוזין על האקטין, מה שמאפשר מיוזין ואקטין לתקשר ולהתרחש התכווצות שרירים. <h4>סידן</h4> ריכוז הסידן, מווסת של התכווצות שרירים, נשלט מאוד בסיבי השריר. סיבי השריר נמצאים במגע הדוק עם נוירונים מוטוריים. פוטנציאל פעולה בנוירונים מוטוריים גורמים לשחרור הנוירוטרנסמיטר אצטילכולין בקרבת סיבי השריר. שחרור זה יוצר פוטנציאל פעולה (דה-פולריזציה) בתא השריר, הנישא לאורך קרום הפלזמה ודרך פלישות של קרום הפלזמה הנקראים transverse, או צינוריות T. צינוריות T עוברות עמוק לתוך השריר וצמודות לאברוני רטיקולום אנדופלזמיים מיוחדים הנקראים סרקופלזמי רטיקולום, או SR. סידן שנסגר בתוך ה-SR משתחרר כאשר תעלות יונים תלויות מתח (תעלות יונים שנפתחות ונסגרות על סמך מטענים מקומיים) נפתחות בתגובה לדה-פולריזציה, מה שמאפשר ליוני סידן להיכנס לציטופלזמה ולשרירים להתכווץ. כאשר האותות מנוירונים מוטוריים מפסיקים, הרפיית השריר מתחילה כאשר סידן נשאב בחזרה ל-SR, מפחית את רמות הציטופלזה של סידן וממלא את מאגרי הסידן SR כהכנה להתכווצות הבאה. <h4>ניוון שרירים</h4> שריר בריא יכול להתכווץ אך שרירים חולים מאבדים לעיתים קרובות את היכולת הזו. מחלות כמו מיאסטניה גרביס מונעות גירוי נוירון מוטורי של השריר שגורם לניוון שרירים וירידה במסת השריר. טרשת צדדית אמיוטרופית (ALS או מחלת לו גריג) גורמת לנוירונים מוטוריים להתנוון, מה שמוביל באופן דומה לניוון שרירים ולאטרופיה.</div>

ככל שהשריר מתכווץ, החפיפה בין החוטים הדקים והעבים גדלה, ומקטינה את אורך הסרקומרה - יחידת ההתכווצות של ...

Education

JoVE Core

Biology

ביולוגיה

Human Biology

ביולוגיה אנושית

Musculoskeletal System

מערכת השלד והשרירים

KEY TERMS AND CONCEPTS

מונחים ומושגים מרכזיים

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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skeletal muscle anatomy

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

Motor units control skeletal muscle movement. A motor unit includes one efferent motor neuron, which carries signals away from the central nervous system, and all of the muscle fibers it innervates. A single motor neuron can connect with multiple muscle fibers, but each muscle fiber is innervated by only one motor neuron. Lower motor neurons are the efferent neurons that control skeletal muscle, the most abundant type of muscle in the body. Their cell bodies are found in the spinal cord or...

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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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