Welcome to the World of Muscle and Motility (HL Focus!)

Hello Biologist! This chapter, Muscle and Motility, is where we dive deep into how animals move. You've already learned that muscles are essential for movement (part of the "Form and Function" section), but now, as HL students, we are going to break down the incredible molecular machinery that powers every twitch and stride.

Don't worry if this seems tricky at first—we are moving from the macro level (how the arm bends) to the nano level (what proteins slide past each other). We will use simple analogies to make the complex process of muscle contraction crystal clear!

1. The Antagonistic Muscle System

Before diving into the microscopic structure, let's quickly review how muscles are organized in the body.

Antagonistic Pairs: Pulling the Strings

Skeletal muscles are attached to bones and cause movement at joints. However, muscles can only contract (pull); they cannot actively push. Because of this limitation, muscles work in opposing or antagonistic pairs.

  • Flexor: A muscle that bends a limb (decreases the angle of the joint). Example: The Biceps brachii.
  • Extensor: A muscle that straightens a limb (increases the angle of the joint). Example: The Triceps brachii.

Analogy: Imagine two people pulling on a seesaw. When one contracts (pulls), the other must relax to allow movement. To move the limb back, the roles must switch.

Key Takeaway: Movement requires coordinated action where one muscle contracts (the agonist) while the opposing muscle relaxes (the antagonist).

2. The Structure of Striated Muscle (HL Depth)

We focus primarily on striated muscle (skeletal muscle), which appears striped under a microscope. This striped pattern is key to its function and comes from its organized internal structure.

From Muscle to Myofibril

Skeletal muscle is highly organized:

  1. A whole muscle is made up of bundles of Muscle Fibers (which are single, large, multi-nucleated cells).
  2. Each Muscle Fiber contains many cylindrical organelles called Myofibrils.
  3. Myofibrils are the parts that actually contract, and they are made up of repeating functional units called Sarcomeres.

The Sarcomere: The Functional Unit of Contraction

The sarcomere is the smallest part of the muscle that can contract. It is defined by the structure of two types of protein filaments:

1. Thin Filaments: Composed mainly of the protein Actin.
2. Thick Filaments: Composed mainly of the protein Myosin.

The way these filaments overlap creates the characteristic banding pattern:

  • Z-lines (or Z-discs): Mark the boundary between adjacent sarcomeres. (Mnemonic: Z is the end of the sarcomere.)
  • I-band: The area containing only Actin (thin filaments). This area shortens during contraction.
  • A-band: The area containing Myosin (thick filaments). It includes the area where thick and thin filaments overlap. This area does not shorten during contraction.
  • H-zone: The area in the center of the A-band containing only Myosin (thick filaments). This area shortens during contraction.
  • M-line: The structure in the very center of the H-zone that holds the Myosin filaments together.

Quick Review of Sarcomere Bands:

Band/Line Composition Changes during Contraction?
Z-line Boundary Gets Closer Together
I-band Only Actin Shortens
H-zone Only Myosin Shortens
A-band All Myosin (including overlap) Constant Length

3. The Mechanism: Sliding Filament Theory (HL)

Contraction occurs when the Actin filaments slide past the Myosin filaments, pulling the Z-lines closer together. Critically, the filaments themselves do not change length; their overlap changes.

The Role of Myosin Heads

Myosin filaments have globular myosin heads which act like little levers or oars. They bind to sites on the actin filament, pivot (the power stroke), and detach, using ATP in a cyclical process.

Step-by-Step: The Cross-Bridge Cycle

This cycle requires two key components: ATP (for energy and detachment) and Calcium ions (\(\text{Ca}^{2+}\)) (for activation, covered in Section 4).

Phase 1: ATP Hydrolysis (Cocking the Head)

  • The Myosin head contains an active site for ATP.
  • ATP is hydrolyzed (broken down) into ADP and inorganic phosphate (\(P_\text{i}\)).
  • The energy released "cocks" the myosin head, moving it into a high-energy, resting position, ready to bind to actin.

Phase 2: Cross-Bridge Formation (Binding)

  • The cocked myosin head binds to the exposed binding site on the Actin filament, forming a cross-bridge.

Phase 3: Power Stroke (Pulling)

  • The release of ADP and \(P_\text{i}\) triggers the power stroke.
  • The myosin head pivots and pulls the actin filament toward the center of the sarcomere (the M-line).

Analogy: This is like rowing a boat. The myosin head acts as the oar, pulling the actin filament (the water) towards the center.

Phase 4: Cross-Bridge Detachment (Resetting)

  • A new ATP molecule binds to the myosin head.
  • The binding of new ATP causes the myosin head to release the actin filament, breaking the cross-bridge.
  • The cycle repeats as the new ATP is hydrolyzed (back to Phase 1).

Did you know? Rigor mortis (stiffening after death) occurs because there is no ATP left to bind to the myosin heads, meaning they cannot detach from the actin filaments, locking the muscles in place.

Key Takeaway: The continuous repetition of the cross-bridge cycle (binding, pivoting, detaching) pulls the thin filaments towards the center, shortening the sarcomere and causing contraction. This requires a constant supply of ATP.

4. Control of Contraction: Nerves and Calcium (HL)

For muscle contraction to occur, the myosin binding sites on the actin filaments must be exposed. This crucial step is controlled by two other proteins found on the thin filament, and by the nervous system.

The Molecular Switch: Tropomyosin and Troponin

In a resting muscle:

  • Tropomyosin is a long filament-like protein that wraps around the actin filament.
  • It physically blocks the myosin binding sites on actin, preventing the cross-bridge cycle.
  • Troponin is a complex of three proteins attached to the tropomyosin strand. This is the molecule that acts as the switch.

The Electrical Signal: The Neuromuscular Junction

Contraction begins when a motor neuron sends an electrical signal:

  1. An action potential arrives at the neuromuscular junction (the synapse between the motor neuron and the muscle fiber).
  2. The neuron releases the neurotransmitter Acetylcholine (ACh) into the synaptic cleft.
  3. ACh binds to receptors on the muscle fiber membrane (the sarcolemma), generating a new action potential in the muscle cell.

The Role of Calcium (\(\text{Ca}^{2+}\))

The electrical signal must now be transmitted deep into the muscle fiber:

  1. The action potential travels rapidly along the sarcolemma and down specialized infoldings called T-tubules.
  2. This signal causes the adjacent Sarcoplasmic Reticulum (SR)—a specialized endoplasmic reticulum that stores \(\text{Ca}^{2+}\)—to release large amounts of stored calcium ions into the cytoplasm (sarcoplasm).
  3. \(\text{Ca}^{2+}\) binds to Troponin.
  4. This binding causes Troponin to change its shape, which in turn pulls the attached Tropomyosin molecule away from the myosin binding sites on the actin filament.
  5. The sites are now exposed, allowing the Myosin heads to form cross-bridges and begin the sliding filament cycle. Contraction begins!
Stopping the Contraction

For the muscle to relax, the nerve stimulation must stop, and the \(\text{Ca}^{2+}\) must be removed from the sarcoplasm.

  • Special calcium pumps in the SR membrane actively transport \(\text{Ca}^{2+}\) back into the SR store.
  • As the \(\text{Ca}^{2+}\) concentration in the sarcoplasm drops, the ions detach from Troponin.
  • Tropomyosin moves back, covering the binding sites on the actin filament.
  • Cross-bridges can no longer form, and the muscle relaxes (lengthens passively via external forces, like gravity or an antagonistic muscle).

Common Mistake to Avoid!

Do not say that the Myosin or Actin filaments shorten. They only slide past each other. The Z-lines, H-zone, and I-band shorten, but the A-band and the filaments themselves remain the same length!


Key Takeaway: Muscle contraction is initiated by a nerve impulse that triggers the release of \(\text{Ca}^{2+}\). \(\text{Ca}^{2+}\) acts as the key, unlocking the binding sites on the actin filament by moving the regulatory proteins (Troponin and Tropomyosin) out of the way.

Summary Review: Molecular Muscle Movement

You've successfully tackled the toughest part of motility! Remember the chain of events:

Nerve Impulse -> ACh Release -> Muscle AP -> SR releases \(\text{Ca}^{2+}\) -> \(\text{Ca}^{2+}\) binds to Troponin -> Tropomyosin moves -> Actin sites exposed -> Myosin forms cross-bridges (using ATP) -> Sarcomere Shortens.