Muscle

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Structure of a skeletal muscle fibre

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  • The ends of the tubes of the sarcoplasmic reticulum, terminal cisternae, abut closely to the membranes of the T tubules, forming triads.
  • A triad is part of a T-tubule and the terminal cisternae on either side and is the site of excitation-contraction coupling.
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Motoneuron action potential to muscle contraction

  • T-tubules are extensions of plasma membrane in contact with the sarcoplasmic reticulum, allowing for coordinated contraction of striated muscles.
  • In the sarcomere, the H zone and the I band regions get shorter during contraction.
  • Each myosin molecule consists of two heavy alpha-helical protein chains, wound together to form a rod-like tail, and two tadpole-like heads, S1, each connected to a flexible neck, S2.
    • The S1 portion contains the active site that reacts with actin and the S2 portion allows movement of the head by a stroke-like action. The molecules are wound together in such a way that the S1 heads are clustered at each end of the thick filament, resulting in the central portion being just a bundle of myosin tails.
  • Actin molecule is a globular protein (G-actin) and is polymerized (F-actin) to form filaments, and two filaments wound together form a thin filament. Each “bead” of G-actin in the filament has a binding site for a myosin S1 head.
  • Tropomyosin is an elongated protein polymer wrapped around the actin filament and partly obscures the myosin S1-binding sites.
  • Troponin is a complex of three proteins associated with tropomyosin. Troponin I is inhibitory, troponin T binds to tropomyosin and troponin C binds reversibly to Ca2+
  • Calcium ion binding pulls tropomyosin away from the myosin-binding sites allowing binding of the myosin S1 heads can bind and execution of the power stroke.
  • During muscle contraction, myosin cross-bridges pull the thin filaments toward the center of each sarcomere, thus shortening the myofibril and the entire muscle fiber
  1. Action potential opens presynaptic voltage-gated Ca²⁺ channels, inducing acetylcholine (ACh) release.
  1. Postsynaptic ACh binding leads to muscle cell depolarization at the motor end plate.
  1. Depolarization travels over the entire muscle cell and deep into the muscle via the T-tubules.
  1. Membrane depolarization induces conformational changes in the voltage-sensitive dihydropyridine receptor (DHPR) and its mechanically coupled ryanodine receptor (RR) → Ca²⁺ release from the sarcoplasmic reticulum (buffered by calsequestrin) into the cytoplasm.
  1. Tropomyosin is blocking myosin-binding sites on the actin filament. Released Ca²⁺ binds to troponin C (TnC), shifting tropomyosin to expose the myosin-binding sites.
  1. Myosin head binds strongly to actin (crossbridge). Pᵢ released, initiating power stroke.
  1. During the power stroke, force is produced as myosin pulls on the thin filament A. Muscle shortening occurs, with shortening of H and I bands and between Z lines (HI, I'm wearing shortZ). The A band remains the same length (A band is Always the same length). ADP is released at the end of the power stroke.
  1. Binding of new ATP molecule causes detachment of myosin head from actin filament. Ca²⁺ is resequestered.
  1. ATP hydrolysis into ADP and Pᵢ results in myosin head returning to high-energy position (cocked). The myosin head can bind to a new site on actin to form a crossbridge if Ca²⁺ remains available.
  1. Recapture of calcium by sarco(endo)plasmic reticulum Ca²⁺ ATPase (SERCA) → muscle relaxation.
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Muscle proprioceptors

  • Specialised sensory receptors that relay information about muscle dynamics.
  • Both information are carried by the dorsal spinocerebellar tracts at 120 m/ to the brain
Muscle stretch/spindle receptors
Muscle stretch/spindle receptors
  • Muscle spindle
    • Detects length and velocity of change in the length of the muscle.
    • In parallel with the muscle fibers and is stimulated by stretching.
    • Increases firing with muscle stretch and decreases firing with muscle contraction
PATHWAY
↑ length and speed of stretch → via dorsal root ganglion (DRG) → Activation of inhibitory interneuron and α motor neuron → Simultaneous inhibition of antagonist muscle (prevents overstretching) and activation of agonist muscle (contraction).
LOCATION/ INNERVATION
Body of muscle/type Ia and II sensory axons
ACTIVATION BY
↑ muscle stretch. Responsible for deep tendon reflexes
Golgi tendon organ
Golgi tendon organ
PATHWAY
↑ tension → via DRG → activation of inhibitory interneuron → inhibition of agonist muscle (reduced tension within muscle and tendon)
LOCATION/ INNERVATION
Tendons/type Ib sensory axons
ACTIVATION BY
↑ muscle tension
 

Type of muscle fibres

Type
1
2
Contraction velocity
Slow
Fast
Fatigue
Resistant
Prone
Fiber colour
Red
White
Metabolism
Oxidative phosphorylation
Anaerobic glycolysis
Mitochondria, myoglobin content
High
Low
Type of training
Endurance training
Weight/resistance training, sprinting
2A fast fatigue resistant fibers, generate rapid contractions that can be maintained for several minutes.
 
2B fast fatigable fibers, large amounts of glycogen, cannot sustain contraction forces due to the rapid accumulation of lactic acid

Images

Banding patterns seen in striated muscle. Image from Wareham, AC, Physiology, Muscle, Anaesthesia & Intensive Care Medicine, 2014, 15(6); 279-281.
Banding patterns seen in striated muscle. Image from Wareham, AC, Physiology, Muscle, Anaesthesia & Intensive Care Medicine, 2014, 15(6); 279-281.
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Image from Wareham, AC, Physiology, Muscle, Anaesthesia & Intensive Care Medicine, 2014, 15(6); 279-281.
Image from Wareham, AC, Physiology, Muscle, Anaesthesia & Intensive Care Medicine, 2014, 15(6); 279-281.
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  • The nuclear bag fibers transmit though Ia fibers not Ib as written in the mindmap
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