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Sliding Filament Theory
Contraction Cycle

Explore how actin and myosin interact at the molecular level to produce muscle contraction through the cross-bridge cycle.

Anatomy & Physiology

What Is Muscle Contraction?

Muscle contraction is the process by which muscle fibers generate tension through the interaction of contractile proteins. Every movement you make: walking, breathing, even your heartbeat: depends on this fundamental mechanism.

The Sarcomere: Functional Unit

Z-line Z-line M-line Actin (thin) Myosin (thick) One Sarcomere

Key Contractile Proteins

Myosin
Thick filament with globular heads that bind to actin and act as molecular motors, powered by ATP hydrolysis.
Actin
Thin filament with binding sites for myosin heads. When exposed, cross-bridges can form and sliding occurs.
Tropomyosin
Regulatory protein that wraps around actin, physically blocking myosin-binding sites at rest.
Troponin
Calcium-sensitive complex bound to tropomyosin. When \( \text{Ca}^{2+} \) binds, it shifts tropomyosin away, exposing binding sites.

The Sliding Filament Theory

Proposed by Huxley and Hanson in 1954, the Sliding Filament Theory states that muscle contraction occurs when thin filaments (actin) slide past thick filaments (myosin), shortening the sarcomere without any change in filament length.

Sarcomere Band Changes

Relaxed I-band A-band H-zone I-band Contracted I A-band (same) H-zone (gone) I

Excitation-Contraction Coupling

Before the cross-bridge cycle can begin, the muscle fiber must receive a signal from a motor neuron. This process links the electrical signal to the mechanical contraction.

1
Action potential arrives at the neuromuscular junction; acetylcholine (ACh) is released into the synaptic cleft.
2
ACh binds to receptors on the sarcolemma, triggering an action potential that spreads across the muscle fiber membrane.
3
The action potential travels down the T-tubules deep into the muscle fiber.
4
The sarcoplasmic reticulum (SR) releases stored \( \text{Ca}^{2+} \) ions into the sarcoplasm.
5
\( \text{Ca}^{2+} \) binds to troponin, causing tropomyosin to shift and expose myosin-binding sites on actin.

The Cross-Bridge Cycle

1 Bind 2 Pull 3 Release 4 Re-cock Myosin binds actin Power stroke ATP binds, myosin detaches ATP hydrolysis re-cocks head Cross-Bridge Cycle

Cross-Bridge Cycle: Four Steps

1
Cross-bridge formation: The energized myosin head (carrying \( \text{ADP} + \text{P}_\text{i} \)) binds to the exposed binding site on actin, forming a cross-bridge.
2
Power stroke: The myosin head pivots, pulling the actin filament toward the M-line. \( \text{ADP} \) and \( \text{P}_\text{i} \) are released. This is the force-generating step.
3
Cross-bridge detachment: A new molecule of ATP binds to the myosin head, causing it to release from actin. Without ATP, the head stays locked (rigor).
4
Myosin reactivation: \( \text{ATP} \) is hydrolyzed to \( \text{ADP} + \text{P}_\text{i} \), providing energy to "re-cock" the myosin head back to its high-energy position. The cycle repeats.

Role of ATP and \( \text{Ca}^{2+} \)

ATP Functions
1. Energizes the myosin head (hydrolysis to \( \text{ADP} + \text{P}_\text{i} \)).
2. Detaches myosin from actin after the power stroke.
3. Powers the \( \text{Ca}^{2+} \) pump that returns \( \text{Ca}^{2+} \) to the SR.
\( \text{Ca}^{2+} \) Functions
1. Binds to troponin, triggering the tropomyosin shift.
2. Exposes myosin-binding sites on actin.
3. Removal of \( \text{Ca}^{2+} \) causes relaxation (tropomyosin re-covers sites).

Contraction vs. Relaxation

Contraction Relaxation
\( \text{Ca}^{2+} \) Level High in sarcoplasm Low (pumped back to SR)
Troponin \( \text{Ca}^{2+} \) bound \( \text{Ca}^{2+} \) released
Tropomyosin Shifted: sites exposed Blocking: sites covered
Cross-bridges Actively cycling No binding occurring
Sarcomere Shortened Returns to resting length
ATP Used For Power stroke + detach \( \text{Ca}^{2+} \) pump (active transport)

How to Trace the Pathway

Use this checklist to walk through the entire sequence from nerve signal to muscle contraction:

1
Nerve impulse: Motor neuron fires, ACh released at the neuromuscular junction.
2
Depolarization: Sarcolemma action potential travels down T-tubules.
3
\( \text{Ca}^{2+} \) release: SR releases \( \text{Ca}^{2+} \) into sarcoplasm.
4
Troponin shift: \( \text{Ca}^{2+} \) binds troponin, tropomyosin moves, binding sites exposed.
5
Cross-bridge cycling: Myosin binds, pulls, detaches, re-cocks (repeat).
6
Relaxation: \( \text{Ca}^{2+} \) pumped back to SR, tropomyosin re-covers sites, contraction ends.

Example: Identifying Band Changes

Scenario: A sarcomere is observed under a microscope before and after stimulation. Which bands change width?

I-Band
Decreases. As actin slides inward over myosin, the region of actin alone (not overlapping myosin) shrinks.
H-Zone
Decreases/disappears. The region of myosin alone narrows as actin slides over it.
A-Band
Stays the same. This represents the full length of the myosin filament, which does not change.

Example: What Happens Without ATP?

Scenario: A researcher applies a chemical that blocks all ATP production in a muscle fiber. Predict the outcome.

Example: Curare Poisoning

Scenario: Curare is a toxin that blocks ACh receptors on the sarcolemma. Predict the effect on muscle contraction.

1
The motor neuron fires normally and releases ACh into the synaptic cleft.
2
ACh cannot bind to blocked receptors. No action potential is generated on the sarcolemma.
3
No signal reaches the T-tubules, so the SR does not release \( \text{Ca}^{2+} \).
4
Tropomyosin remains in place, binding sites stay covered: no contraction occurs.

Common Mistakes

✕ Filaments Shorten
Actin and myosin do not shorten. They slide past each other. The sarcomere shortens, but individual filaments stay the same length.
✕ ATP Only for Contraction
ATP is also needed for relaxation: detaching myosin from actin and pumping \( \text{Ca}^{2+} \) back into the SR.
✕ A-Band Changes
The A-band stays constant during contraction. Only the I-band and H-zone decrease. The A-band = myosin length, which is fixed.

Question 1 of 5

During muscle contraction, which band of the sarcomere remains constant in width?

Question 2 of 5

What is the direct role of \( \text{Ca}^{2+} \) in initiating the cross-bridge cycle?

Question 3 of 5

A muscle cell is treated with a drug that prevents ATP from binding to myosin. What is the most likely result?

Question 4 of 5

Which structure is responsible for storing and releasing \( \text{Ca}^{2+} \) during excitation-contraction coupling?

Question 5 of 5

During the power stroke of the cross-bridge cycle, what happens to \( \text{ADP} \) and \( \text{P}_\text{i} \)?