muscle contraction

• sliding filament theory(1)


  1.Action potential arrives at the neuromuscular junction

  2.calcium ions are released from the sarcoplasmic recticulum

  3.ca+ bind to troponin(on actin filament) causing them to change shape

  4.this causes both troponin and tropomyosin proteins to change position on the actin filament

  5.myosin binding sites on the actin filament are now exposed

  6. globular heads of myosin bind with these sites forming cross bridges between 2 types of filaments
• sliding filament theory(2)


  7.formation of cross bridges causes myosin heads to bend, releasing ADP+PI- pulling actin towards the centre of sarcomere

  8.ATP binds to myosin head=change in shape causing myosin head to release from actin filament

  9.ATPase hydrolyses ATP into ADP+PI causing myosin head to move back to its original position

  10. myosin head then able to bind to new binding sites on the actin filament, closer to the Z disc

  • this repeats for as long as stimulation is still occuring
• once stimulation stops

  • CA+ leave their binding sites on troponin molecules
  • they actively transported back to the sarcoplasmic recticulum
  • troponin molecules return to OG shape, pulling tropomyosin molecules in a position that blocks actin-myosin binding sites
  • no cross bridges can form=no muscle contractions
  • sarcomere lengthens as actin filament slides back to relaxed position