Muscle Structure, Function, and Contraction Mechanism Study Notes

Understanding muscle function hinges on the specifics of muscle types and their components.

Myofibrillary Unit: The principal structural and functional units of muscle fibers.
- Composition: Made up of myofilaments.
- Types of Myofilaments:
- Contractile: Responsible for muscle contraction (Primary focus).
- Regulatory: Control the interaction between actin and myosin.
- Structural: Support the overall framework of the muscle fibers (Less emphasis).

Thick Filaments:
- Composed of Myosin only.
Thin Filaments:
- Composed of Actin, Tropomyosin, and Troponin:
- Actin: Contains binding sites for myosin heads.
- Troponin and Tropomyosin: Regulatory proteins controlling actin's availability to myosin for binding.

When muscle fibers contract:
- Myosin heads attach to actin's binding sites.
- Requires ATP to initiate movement of the myosin heads.
Action of Myosin Heads:
- Described as "golf clubs" that can pivot and pull actin inwards during contraction.

Sarcomere:
- Basic unit of muscle structure containing myofilaments.
- Light Bands: Composed only of thin filaments (Actin).
- Dark Bands: Contain both thick (Myosin) and thin (Actin) filaments.
- Striations are observed under a microscope due to these organized bands.

As the muscle contracts:
- Sarcomeres shorten, resulting in tighter striations.
- Myosin heads move and pull actin filaments towards the center of the sarcomere, which visually appears as a contraction of the muscle (Striations seem smaller).

Dystrophin: A structural protein essential for muscle fiber integrity, connecting sarcolemma to cytoskeleton.
- Duchenne Muscular Dystrophy (DMD):
- A degenerative disorder caused by defective dystrophin gene.
- Primarily affects males as it is X-linked (sex-linked disorder).
- Leads to muscle degeneration, resulting in severe disability and early mortality (usually by age 20).
Symptoms start between ages 2-6, with loss of mobility leading to wheelchair dependence.

Describes how thin and thick filaments slide over each other to produce muscle contraction.
Important characteristics:
- Actin and myosin do not change length; only their overlap changes as they slide past each other.
- Relaxation of muscles involves elongation of sarcomeres by antagonistic muscle contractions.

Ex: Biceps and Triceps:
- Contracting the biceps (flexion) requires relaxation of the triceps (extension).
- Antagonistic muscles facilitate movement through relaxation and contraction.

Overstretching can lead to muscle injuries as the myosin heads cannot effectively attach to actin if too far apart.
Downhill movements increase injury risk due to the greater stretch on muscles.

Electrophysiology: Focuses on electrical charges and physiological processes in muscle cells.
Resting Membrane Potential:
- Results from a distribution of ions across membranes (negative inside, positive outside).
- Essential for muscle cells to remain ready for contraction.
Action Potentials: Involve depolarization and repolarization of the membrane, necessary for muscle contraction initiation.

Sodium-Potassium Pump: An active transport mechanism crucial for maintaining resting membrane potential.
- Pumps 3 sodium ions out and 2 potassium ions into the cell, requiring ATP.
- Essential for keeping muscle cells ready for depolarization.

Action Potential Phases:
- Depolarization: Opening of sodium channels allows sodium influx, making the inside less negative.
- Repolarization: Closing of sodium channels and opening of potassium channels restores the negative charge.
All-or-None Principle: Once an action potential is initiated, it propagates along the sarcolemma without loss in strength.

Components of NMJ:
- Axon Terminal: Contains synaptic vesicles filled with acetylcholine (ACh).
- Synaptic Cleft: The gap between motor neuron and muscle fiber.
- Motor End Plate: Receptor-rich area on the muscle fiber's sarcolemma.

Excitation Phase: Triggered by ACh from the motor neuron.
- Action potential reaches axon terminal causing calcium ion influx.
- ACh release leading to depolarization of muscle fiber.
Excitation-Contraction Coupling: Transmits excitation throughout the muscle fiber, involves calcium release for contraction.
Contraction Phase: Actual sliding filament activity occurs leading to muscle shortening.

Muscle contraction requires repeated action potentials to maintain tension and facilitate contraction cycles through continued ACh release.
Acetylcholinesterase rapidly degrades ACh to prevent continuous stimulation and allow muscle relaxation after contraction.

Blocking sodium-potassium pumps can hinder action potential generation, illustrating the critical nature of these pumps in functional muscle physiology.
Botulism: Affects neurotransmitter release, consequently stopping muscle contractions, illustrating the impact of specific toxins on neuromuscular functioning.