Cytology · MU Sofia

62. Striated skeletal muscle tissue. Mechanism of muscle contraction.

Walks through how a nerve impulse becomes muscle contraction, from acetylcholine release at the neuromuscular junction through T-tubule spread and calcium release from the sarcoplasmic reticulum at triads. It then follows the cross-bridge cycle with troponin, tropomyosin and ATP, explains relaxation and rigor mortis, lists which sarcomere bands change during shortening, and closes with how whole-muscle force is graded by motor units.

Inside: 1 section · 3 labelled pictures · 13 flashcards · 4 min

Topic 62 of 127 in the MU Sofia syllabus for Cytology (Dental Medicine, Year 1). The free AceMed note covers it in 1 section, about 508 words (4 min of reading), with 13 flashcards.

In this note

  1. Mechanism of Muscle Contraction (Striated Skeletal Muscle Tissue)

Mechanism of Muscle Contraction (Striated Skeletal Muscle Tissue)

Skeletal muscle contraction is a complex, energy-dependent process that converts a neural signal into mechanical force, primarily by the sliding of actin and myosin filaments.

  • Fundamental Principle: Muscle contraction is the activation of tension-generating sites within muscle fibers. It occurs when thick (myosin) and thin (actin) filaments slide past one another, shortening the sarcomere without the filaments themselves changing length. This is known as the Sliding Filament Model.
  • 1. Initiation at the Neuromuscular Junction (NMJ):
  • Skeletal muscle contraction begins with a conscious effort from the brain.
  • An electrical signal (action potential) travels through a motor neuron to its terminal, the synaptic knob.
  • At the synaptic knob, the neurotransmitter Acetylcholine (ACh) is released into the synaptic cleft.
  • ACh binds to receptors on the muscle fiber's membrane, the sarcolemma (specifically at the motor end plate), initiating a muscle action potential.
  • Acetylcholinesterase quickly removes ACh from the synaptic cleft to prevent continuous stimulation.
  • 2. Excitation-Contraction Coupling:
  • The muscle action potential spreads rapidly along the sarcolemma and delves deep into the muscle fiber via T-tubules (transverse tubules).
  • T-tubules are invaginations of the sarcolemma that encircle myofibrils at the A-I band junctions.
  • At structures called triads (one T-tubule flanked by two terminal cisterns of the sarcoplasmic reticulum), the action potential triggers the release of calcium ions (Ca2+) from the sarcoplasmic reticulum (SR) into the sarcoplasm. The SR is specialized for Ca2+ sequestration and release.
  • 3. The Cross-Bridge Cycle (Molecular Mechanism):
  • Ca2+ binds to troponin on the thin (actin) filaments.
  • This binding causes troponin to change shape, which in turn moves tropomyosin, thereby exposing the myosin-binding (active) sites on the actin filaments.
  • Myosin heads (which have already hydrolysed ATP into ADP + Pi and are in a high-energy, "cocked" position) then bind to the exposed active sites on actin, forming crossbridges.
  • The myosin heads pivot (the "power stroke"), pulling the actin filaments towards the center of the sarcomere, causing the sarcomere to shorten. ADP and inorganic phosphate are released during this step.
  • A new ATP molecule binds to the myosin head, causing it to detach from actin.
  • The ATP is again hydrolysed, re-cocking the myosin head, and the cycle repeats as long as Ca2+ and ATP are available, continuously shortening the sarcomeres and contracting the muscle.
  • 4. Muscle Relaxation:
  • When the nerve impulse ceases, the SR actively pumps Ca2+ back into its cisternae.

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