Copy of Lab 11 Mini Lesson Learning Guides

Homeostasis Role: Skeletal muscles maintain homeostasis by:
- Generating heat (shivering).
- Enabling movement and posture.
- Assisting in venous return of blood to the heart.
- Regulating metabolism and glucose uptake.

Hierarchy of Structure (From largest to smallest):
- Muscle (Organ) → Fascicle → Muscle Fiber (Cell) → Myofibrils → Sarcomeres → Myofilaments (Actin & Myosin).
- Skeletal muscle is striated and voluntary, meaning it's under conscious control.
Thick and Thin Filament Composition:
- Thick filaments: Made of myosin, with heads that form cross-bridges for contraction.
- Thin filaments: Composed of actin, along with tropomyosin and troponin (which regulate contraction).
Sarcomere Structure:
- Z-line (Z-disk): Boundaries of a sarcomere.
- M-line: Center of the sarcomere, anchoring thick filaments.
- A-band: Dark region containing thick filaments (myosin) and overlapping thin filaments.
- I-band: Light region containing only thin filaments (actin).
- H-zone: Region within the A-band that contains only thick filaments.
- Titin: Elastic protein that helps with structural integrity.
T-Tubules & Sarcoplasmic Reticulum (SR):
- T-Tubules: Extensions of the sarcolemma that transmit action potentials deep into the muscle fiber.
- SR & Terminal Cisternae: Store and release calcium for muscle contraction.
Thin Filament Regulation & Calcium’s Role:
- Calcium binds to troponin, causing tropomyosin to move and expose binding sites on actin.
- Myosin heads bind actin, triggering contraction (power stroke).

Steps at the Neuromuscular Junction:
- Action potential arrives at axon terminal of an alpha motor neuron.
- Voltage-gated Ca²⁺ channels open, allowing Ca²⁺ influx.
- Ca²⁺ triggers vesicles to release acetylcholine (ACh) into the synaptic cleft.
- ACh binds to receptors on the motor end plate, generating an end-plate potential (EPP).
- EPP depolarizes the sarcolemma, triggering an action potential in the muscle fiber.
- ACh is broken down by acetylcholinesterase, stopping the signal.
End-Plate Potential (EPP) & Action Potential Initiation:
- EPP is a localized depolarization at the motor end plate.
- If strong enough, it triggers a full muscle fiber action potential.
Effects of Disruptions:
- Botulinum toxin (Botox): Blocks ACh release → Paralysis.
- Curare: Blocks ACh receptors → No muscle contraction.
- Organophosphates: Inhibit acetylcholinesterase → Prolonged contraction.
- Succinylcholine: Mimics ACh but doesn’t degrade quickly → Temporary paralysis.

Action Potential Timing vs. Muscle Contraction:
- Muscle action potential occurs before contraction.
- A slight delay exists due to calcium release and cross-bridge cycling.
Key Proteins & Their Roles:
- Dihydropyridine Receptor (DHPR): Voltage sensor in T-tubules, linked to RyR.
- Ryanodine Receptor (RyR): Calcium release channel in SR.
- SERCA Pump: Pumps Ca²⁺ back into SR, stopping contraction.
Sliding Filament Mechanism:
- Myosin heads bind actin, forming cross-bridges.
- Power stroke moves thin filaments inward, shortening sarcomere.
- Regions that change:
  - I-band & H-zone shorten.
  - A-band remains constant.
Cross-Bridge Cycle:
- Step 1: Myosin binds actin (cross-bridge formation).
- Step 2: Power stroke occurs (ADP + Pi released).
- Step 3: ATP binds myosin, detaching it from actin.
- Step 4: ATP hydrolysis resets myosin head.
Rigor Mortis:
- No ATP after death → Myosin remains bound to actin → Stiff muscles.
Cytosolic Ca²⁺ & Contraction Timing:
- Ca²⁺ rises quickly after AP but lags slightly behind.
- Ca²⁺ removal by SERCA takes time, leading to a gradual relaxation phase.
ATP Functions in Contraction:
- Energizes myosin for cross-bridge cycling.
- Detaches myosin from actin.
- Powers Ca²⁺ pumps for relaxation.