Skeleton and Muscle

Core Explanation

Types of Skeletons

A skeleton provides structural support, protects internal organs, and serves as a framework for muscle attachment enabling movement. Three major types have evolved:

Skeletal Muscle Structure

Skeletal muscle is organized hierarchically:

Muscle → fascicles → muscle fibers (cells) → myofibrils → sarcomeres → myofilaments

• A muscle fiber is a single, long, multinucleated cell containing hundreds of myofibrils.
• Each myofibril is composed of repeating sarcomeres — the functional contractile units.
• Each sarcomere contains:
  • Thin filaments: Primarily actin, plus the regulatory proteins troponin and tropomyosin.
  • Thick filaments: Myosin — each myosin molecule has a long tail and a globular head that binds actin and hydrolyzes ATP.

Sarcomere structure (bands and zones):

• Z-lines: Boundaries of each sarcomere; thin filaments are anchored here.
• I-band: Region containing only thin filaments (light appearance); shortens during contraction.
• A-band: Region containing thick filaments (dark appearance); length remains constant during contraction.
• H-zone: Central region of A-band containing only thick filaments; shortens during contraction.
• M-line: Center of the sarcomere; thick filaments are linked here.

During contraction, the Z-lines move closer together, the I-band and H-zone narrow, but the A-band does not change length — confirming that filaments slide past each other rather than shorten.

The Sliding Filament Model

Muscle contraction is explained by the sliding filament model — thick and thin filaments slide past each other, shortening the sarcomere without changing filament lengths.

The Cross-Bridge Cycle:

1. ATP binding: ATP binds to the myosin head, causing it to release from actin.
2. ATP hydrolysis: ATP → ADP + Pi; the myosin head "cocks" into a high-energy, extended position.
3. Cross-bridge formation: The energized myosin head binds to actin (this step is blocked in resting muscle by tropomyosin covering the myosin-binding sites on actin).
4. Power stroke: Pi is released; the myosin head pivots, pulling the thin filament toward the center of the sarcomere. ADP is released.
5. The cycle repeats as long as ATP and Ca²⁺ are available.

Rigor mortis illustrates the cycle: after death, ATP is depleted, so myosin heads cannot detach from actin — muscles remain rigidly contracted until proteins decompose.

Excitation-Contraction Coupling

1. Motor neuron releases acetylcholine (ACh) at the neuromuscular junction.
2. ACh binds to nicotinic receptors on the muscle fiber membrane (sarcolemma), opening Na⁺ channels → depolarization.
3. The action potential propagates along the sarcolemma and into T-tubules (invaginations of the membrane that penetrate deep into the fiber).
4. Depolarization of T-tubules triggers the sarcoplasmic reticulum (SR) to release stored Ca²⁺ into the cytoplasm.
5. Ca²⁺ binds to troponin, causing a conformational change that moves tropomyosin away from the myosin-binding sites on actin — exposing them.
6. Cross-bridge cycling begins → contraction.
7. When the motor neuron stops firing, Ca²⁺ is actively pumped back into the SR (Ca²⁺-ATPase), tropomyosin re-covers binding sites, and the muscle relaxes.

Key players:

• Ca²⁺ is the trigger for contraction — without it, tropomyosin blocks the binding sites.
• ATP is required for both contraction (power stroke) AND relaxation (detaching myosin from actin, pumping Ca²⁺ back into SR).

Muscle Types

Cardiac muscle has intercalated discs containing gap junctions that electrically couple cells — an action potential in one cell spreads to all, coordinating heart contraction as a functional syncytium. Cardiac muscle also has a long refractory period (~250 ms compared to ~1–2 ms in skeletal muscle), preventing tetanic contractions that would stop the heart from filling.

Smooth muscle lacks the regular sarcomere organization of striated muscle but still uses actin, myosin, and Ca²⁺-dependent contraction. It is found in blood vessel walls, the digestive tract, bladder, uterus, and respiratory passages. Smooth muscle can maintain sustained contractions with relatively little ATP consumption — important for functions like maintaining blood vessel tone.

Common Misconceptions and Exam Traps

• "Actin and myosin filaments shorten during contraction." The filaments themselves do NOT shorten — they SLIDE past each other. The sarcomere (the distance between Z-lines) shortens.
• "ATP is only needed for contraction." ATP is needed for RELAXATION too — to detach myosin from actin and to pump Ca²⁺ back into the SR. Rigor mortis demonstrates this: no ATP = permanent contraction.
• "Skeletal muscle, cardiac muscle, and smooth muscle contract by fundamentally different mechanisms." All three use actin, myosin, and Ca²⁺-dependent regulation, but they differ in structural organization, Ca²⁺ sources, control, and speed.