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Muscular System
Structure & Contraction

Master the sliding filament model, sarcomere anatomy, and muscle contraction mechanisms for the MCAT.

MCAT Biological Foundations

Three Types of Muscle Tissue

Skeletal
Voluntary, striated, multinucleated. Attached to bones for movement.
Cardiac
Involuntary, striated, branched with intercalated discs. Found only in the heart.
Smooth
Involuntary, non-striated, spindle-shaped. Lines organs and blood vessels.

Skeletal Muscle Hierarchy

Muscle Fascicle Muscle Fiber (Cell) Myofibril Sarcomere Myofilaments Actin & Myosin Epimysium Perimysium Endomysium

The Sarcomere: Functional Unit

Z-line Z-line M-line I Band A Band I Band H Zone Actin (thin) Myosin (thick)

Key Contractile Proteins

Myosin
Thick filament with globular heads that have ATPase activity and bind actin during cross-bridge cycling.
Actin
Thin filament: G-actin monomers polymerize into F-actin. Contains myosin-binding sites.
Tropomyosin
Wraps around actin, blocking myosin-binding sites in resting muscle.
Troponin
Regulatory complex that binds \( \text{Ca}^{2+} \), shifting tropomyosin to expose binding sites.

The Sliding Filament Model

During contraction, thin filaments slide over thick filaments, pulling Z-lines closer together. The filaments themselves do not shorten: the sarcomere shortens.

Relaxed Full sarcomere length → Contracted Shortened sarcomere What changes during contraction? I band shortens ✓ H zone shortens ✓ Sarcomere shortens ✓ What stays the same? A band: constant ✓ Filament lengths: constant ✓

The Cross-Bridge Cycle

1. ATP Binding Myosin releases actin 2. ATP Hydrolysis Myosin head cocks 3. Cross-Bridge Myosin binds actin 4. Power Stroke ADP + Pi released Cross-Bridge Cycle ATP binds
\( \text{ADP}+\text{P}_i \) on head
\( \text{Ca}^{2+} \) required
\( \text{ADP}+\text{P}_i \) released
Net: 1 ATP hydrolyzed per cycle \( \text{ATP} \rightarrow \text{ADP} + \text{P}_i + \text{mechanical work} \)

Excitation-Contraction Coupling

1
Action potential travels along the motor neuron to the neuromuscular junction (NMJ).
2
Acetylcholine (ACh) is released into the synaptic cleft and binds nicotinic receptors on the sarcolemma.
3
Depolarization spreads along the sarcolemma and into T-tubules.
4
T-tubule signal triggers sarcoplasmic reticulum (SR) to release \( \text{Ca}^{2+} \).
5
\( \text{Ca}^{2+} \) binds troponin C, shifting tropomyosin and exposing myosin-binding sites on actin.
6
Cross-bridge cycling begins: contraction occurs as long as \( \text{Ca}^{2+} \) and ATP are available.

Muscle Relaxation

Relaxation is not passive: it requires active transport of \( \text{Ca}^{2+} \) back into the sarcoplasmic reticulum.

1
ACh is degraded by acetylcholinesterase (AChE) in the synaptic cleft.
2
SERCA pump (a \( \text{Ca}^{2+} \)-ATPase) actively transports \( \text{Ca}^{2+} \) back into the SR, using ATP.
3
Tropomyosin re-covers the myosin-binding sites. Cross-bridge cycling stops.

Comparing Muscle Types

Feature Skeletal Cardiac Smooth
Control Voluntary Involuntary Involuntary
Striations Yes Yes No
Nuclei Multinucleated 1-2 per cell 1 per cell
T-tubules Yes (at A-I junction) Yes (at Z-lines) None (caveolae)
Pacemaker No Yes (SA node) Some (slow waves)
Gap junctions No Yes (intercalated discs) Yes
Regulation Troponin-tropomyosin Troponin-tropomyosin Calmodulin-MLCK

Smooth Muscle: Calmodulin Pathway

Smooth muscle lacks troponin. Instead, contraction is regulated by the calmodulin-MLCK pathway:

1
\( \text{Ca}^{2+} \) enters the cytoplasm (from SR and extracellular sources).
2
\( \text{Ca}^{2+} \) binds calmodulin, forming a \( \text{Ca}^{2+} \)-calmodulin complex.
3
The complex activates myosin light-chain kinase (MLCK).
4
MLCK phosphorylates the myosin head, enabling it to bind actin and contract.

Motor Units and Recruitment

Motor Unit
A single motor neuron plus all the muscle fibers it innervates. The smallest functional unit of motor control.
Recruitment
Activating more motor units increases force. Small units fire first (size principle), then larger ones.

Muscle Fiber Types

Type I (Slow Oxidative)
Red fibers, rich in myoglobin and mitochondria. Fatigue-resistant: marathons, posture.
Type IIa (Fast Oxidative)
Intermediate: moderate mitochondria, moderate fatigue resistance. Middle-distance running.
Type IIb (Fast Glycolytic)
White fibers, few mitochondria, rapid fatigue. High force: sprinting, weightlifting.

Example: Band Changes During Contraction

Question: A muscle fiber contracts. Which bands/zones change in width?

Structure Change? Why? I Band (actin only) Shortens More overlap H Zone (myosin only) Shortens Actin slides in A Band (full myosin) No change Myosin is fixed

Example: Summation and Tetanus

Force Time Single twitch Unfused tetanus Fused tetanus ↑ ↑↑↑ ↑↑↑↑↑

Common Mistakes

✕ A band shortens
The A band remains constant during contraction. Only the I band and H zone shorten.
✕ Filaments contract
Filaments slide past each other: they do not shorten or compress. The sarcomere shortens, not the filaments.
✕ Relaxation is passive
Relaxation requires ATP for the SERCA pump to resequester \( \text{Ca}^{2+} \) into the SR. It is an active process.
✕ Smooth = troponin
Smooth muscle uses calmodulin-MLCK, not troponin-tropomyosin. This is a frequent MCAT trap.
✕ ATP for power stroke
ATP is used for detachment and re-cocking the myosin head. The power stroke is driven by release of \( \text{ADP} + \text{P}_i \).

Question 1 of 5

During skeletal muscle contraction, which of the following remains constant in width?

Question 2 of 5

What is the immediate trigger for tropomyosin to shift and expose myosin-binding sites on actin?

Question 3 of 5

In smooth muscle, contraction is initiated when \( \text{Ca}^{2+} \) binds to which molecule?

Question 4 of 5

A patient is exposed to a toxin that blocks the SERCA pump. What is the most likely immediate effect on skeletal muscle?

Question 5 of 5

Which of the following correctly describes the role of ATP in the cross-bridge cycle?