Skeletal muscle

Structrure of striated muscle

Thin and thick filaments make up the sarcomere——> group of sarcomere———>group of myofibril——→ group of muscle fibre———> muscle fasciles.

Note:

  • Sarcoplasmic reticulum is the endoplasmic reticulum in the muscle cells.

  • It is responsible for calcium storage.

  • It has two parts:

  • 1. Longitudinal tubules. 2.Terminal cisternea. SEE DIAGRAM BELOW

  • Sarcolemma is the plasma membrane of the muscle cell.

  • The sarcolemma has T tubules (Transverse tubule). T-tubules are invaginations (foldings) of the sarcolemma that dive deep into the muscle fiber.

Electro-Mechanical Coupling Steps

  1. Neuromuscular Junction (NMJ) Stimulation

    • A stimulus arrives via a motoneuron.

    • Acetylcholine (ACh) is released at the NMJ, binding to receptors on the sarcolemma, initiating a muscle action potential.

  2. Action Potential Propagation

    • The action potential spreads along the sarcolemma and dives into the T-tubules.

    • Voltage-sensitive DHPR (dihydropyridine receptors) in the T-tubules detect the depolarization. DHPR is a volatage gated calcium channel.

  3. Calcium Release from the Sarcoplasmic Reticulum (SR)

    • DHPRs mechanically interact with RyR (ryanodine receptors) on the SR membrane. DHPR and RyR are coupled with each other.

    • RyR opens, causing calcium ions (Ca²⁺) to flood into the cytosol.

  4. Activation of Contractile Proteins → Contraction

    • Calcium binds to troponin (Tc subunit), causing a conformational change that moves tropomyosin off actin binding sites.

    • Myosin heads bind to actin, and cross-bridge cycling occurs → muscle contraction.

  5. Calcium Reuptake → Relaxation

    • Calcium is actively pumped back into the SR via SERCA (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase).

    • Cytosolic calcium decreases, troponin-tropomyosin complex blocks actin sites, and the muscle relaxes.

NOTE: Contraction of a muscle without an action potential is called a contracture.

  • A triad is a T-tubule and two neighbouring Terminal cisternae of the sarcoplasmic reticulum.

Differences between the skeletal muscle and cardiac muscle:

  • The skeletal muscle has a triad while cardica muscle has a diad

  • Extracellular calcium is not needed for skeletal muscle contraction rather, calcium is released from the sarcoplasmic reticulum while for cardiac muscle, extracellular calcium is needed for contraction.

The contactile protein

  • Thick: myosin

  • Thin: actin+tropomysosin+troponin

Sarcomere us the basic functional unit of the muscle. It shortens during contraction.

In the presence of calcium, calcium Binds to Troponin C

  1. Ca²⁺ binds to Troponin C (TnC) on the thin filament.

  2. Troponin changes shape, moving tropomyosin away from myosin-binding sites on actin.

  3. This exposes the binding sites so myosin heads can attach.

Note: Troponin has 3 subunits:

Subunit

Main Function

Action

TnC

Calcium binding

Triggers conformational change → moves tropomyosin.

TnI

Inhibition

Blocks actin–myosin binding when Ca²⁺ is low.

TnT

Tropomyosin binding

Anchors troponin to thin actin filament.

Actin myosin cycle

This is also called Cross-Bridge Formation (Contraction).

  1. Myosin heads bind to actin → forming cross-bridges.

  2. Myosin performs a power stroke:

    • ADP + Pi is released from myosin.

    • Actin filament slides toward the center of the sarcomere.

  3. ATP binds to myosin → myosin releases actin.

  4. ATP is hydrolyzed → myosin head is “re-cocked” for another stroke.

  5. This cycle repeats as long as Ca²⁺ and ATP are present → sarcomere shortens → muscle contracts

  • The force generated by the muscle depends on the length of the muscle.

  • The number of cross bridges determines the strength of the contraction. If there are more cross bridges, the strength of contraction would be stronger.

  • The number of cross bridges depends in the relative postition of thin and thick filaments.

  • Maximum tension is between 2.2-2.5 micrometres

  • The contraction lasts longer than the refactory period so another AP can start and fuse with the previous one.

Great notes! 👍 Let’s organize and expand them into a clear overview of Characteristics of Muscle Contraction II so it’s easier to study.

Characteristics of Muscle Contraction II

1. Motor Unit

  • Definition: A motor unit = one motor neuron + all the muscle fibers it innervates.

  • Within a motor unit, all fibers contract together when the neuron fires.

  • Contraction is typically tetanic (sustained, maximal force), not single twitches.

Regulation of Force and Precision

  • Force regulation: Depends on the number of active motor units recruited.

  • Precision of movement: Depends on the number of fibers per motor unit.

    • Small motor unit (few fibers) → fine control (e.g. eye, fingers).

    • Large motor unit (many fibers) → powerful contraction (e.g. quadriceps).

  • Recruitment: Sequential activation of motor units to increase force.

  • Fatigue: Prolonged activity reduces the ability to generate force.

  • Paralysis/Atrophy: Loss of neural input leads to muscle wasting.

2. Elastic Elements in Muscle

  • Series elastic elements: Tendons and cross-bridges (in line with the contractile elements).

  • Parallel elastic elements: Connective tissue around fibers (endomysium, perimysium).

  • Role: They store elastic energy and contribute to smooth, efficient movement.

3. Clinical Conditions

  • Hypocalcemic Tetany:

    • Low extracellular Ca²⁺ → increased excitability of nerves → sudden, painful contractions.

  • Denervation Hypersensitivity:

    • If nerve supply is lost, nAChRs spread outside the end-plate region, making the muscle overly sensitive to ACh or drugs.

4. Muscle Diseases

  • Myasthenia Gravis

    • Autoimmune disease → antibodies attack nAChRs at NMJ.

    • Leads to muscle weakness, worsens with activity.

  • Myotonias

    • Defective relaxation after contraction (ion channel mutations).

  • Muscular Dystrophies

    • Progressive degeneration of muscle fibers (e.g., Duchenne dystrophy).

  • Malignant Hyperthermia

    • Genetic disorder of RyR calcium channels.

    • Triggered by certain anesthetics → excessive Ca²⁺ release, hypermetabolism, dangerous rise in body temperature.

  • Central Core Disease

    • Congenital myopathy → defects in RyR → muscle weakness and structural abnormalities in fibers.