All Access Pass - 3 FREE Months!
Institutional email required, no credit card necessary.
Muscle Excitation/Contraction (E/C Coupling)

Muscle Excitation/Contraction (E/C Coupling)

Start 3-Month Free Access!
No institutional email? Start your 1 week free trial, now!
skeletal muscle excitation and contraction coupling
Summary
Key Structures of the muscle cell
  • The sarcolemma (its plasma membrane).
  • A myofibril.
    • The A band refers to the length of the thick filaments, "think "A" for d-a-rk – they are aniosotropic (or birefringent) in polarized light.
    • The I band is the region along the thin filaments (between the thick filaments). Think "I" for L-i-ght: they are "isotropic" (do not alter polarized light).
  • Sarcoplasmic reticulum (SR)
    • Form web-like rows.
    • Store calcium.
    • Are a key component to coupling muscle cell excitation to myofibril contraction.
  • Terminal cisternae (aka lateral cisternae) of the sarcoplasmic reticulum.
    • Flank the transverse tubules (T-Tubules)
  • Transverse tubules (T-Tubules)
    • Are tubular invaginations of sarcolemma.
  • Sarcoplasm
    • The muscle cell cytoplasm.
    • Muscle cell nuclei lie within the periphery of the cell.
    • During development, the nuclei transition from a central location to a peripheral one.
    • Muscle cells comprise numerous mitochrondria: they are the energy powerhouses of the cell – the site of aerobic respiration, which by definition requires oxygen but is capable of generate the most amount of ATP.
  • The synaptic terminal (aka terminal bouton, terminal button, synaptic bouton) of a typical motor nerve.
    • Within it are molecules of acetylcholine.
Key aspects of myofilaments
Thin filaments
  • Actin
    • Spherical molecules joined in pairs of strands (like beads on a string). It is referred to as F-actin for filamentous actin, and comprises a polymer of G-actin monomers that are arranged in a double helix.
Tropomyosin
  • Threadlike strands
Troponin
  • Protein complexes that bind tropomyosin, actin, and also calcium (show their calcium-binding sites).
Thick filaments
  • Comprise myosin molecules, which form a golfclub shape, and comprise two heavy chains and two light chains.
Excitation
Acetylcholine binds a post-synaptic receptor on muscle.
  • This triggers an action potential, which proceeds along the T Tubule to a dihydropyridine receptor (it is blocked by dihydropyridine, hence its name).
  • Depolarization of the dihydropyridine receptor activates the ryanodine receptor (aka foot proteins, calcium-release channels) within the terminal cisternae,
  • This triggers the release of calcium into the cytosol.
Calcium binds troponin.
  • This causes a shift in tropomyosin, moving it away from its blocking position along actin, which allows myosin to bind actin.
Myosin binds actin and proceeds through thin filament sliding (muscle contraction).
Drawing at the end.
Tropomyosin shift
  • Once the action potentials cease, calcium releases from troponin and returns to the cytoplasm, tropomyosin then shifts, again, and once again myosin is unable to bind actin, and the contractions cease.
Huxley Sliding-Filament Model
See: Huxley Sliding-Filament Model.
The rigor state.
  • The myosin head is bound to the thin filament.
  • Calcium is bound to troponin.
    Calcium binding to troponin allows myosin access to its binding site on actin.
ATP induces release of actin.
  • Myosin has ATP bound to its head.
  • The actin molecules are separated from (no longer bound to) the myosin.
  • ATP is required to move out of the rigor state.
  • If ATP is absent, which occurs after death, rigor will persist, called rigor mortis.
ATP is hydrolyzed to ADP and Inorganic phosphate (Pi).
  • The myosin head rotates on the neck: it is now "cocked" – it's in its high-energy state.
  • The "cocked" state causes the thin and thick filaments to again bind via their cross-bridge.
  • ADP and inorganic phosphate (Pi) are still bound to the myosin head.
Pi release initiates the power stroke for the myosin head to release its energy.
  • Accordingly, the thin filament begins its slide.
The myosin returns to its uncocked, low energy state.
  • At some point after the power stroke, ADP is released.
  • Note that this is an area of intertextual variation, some authors instead write that ADP is released at the same time as phosphate to initiated the power stroke.