Musculoskeletal system Flashcards
Muscle fibre - internal structures
- T-tubules : extension of sarcolemma, excitable (maintain membrane potential), allow APs/electrical activity to travel deep into the muscle fibre
- Sarcoplasmic reticulum : contains Ca2+ ions (essential for contraction)
Dystrophin
- One end of dystrophin protein is linked to the actin of a myofilament
- Other end is linked to a peripheral protein on the inside of the sarcolemma
- Dystrophin transfers the force of the myofilament movement to the basal lamina, endomysium and other extracellular parts of the muscle
- Overall, it transmits the tension created by contraction
Muscle fibre components
- Actin strand : 2 actin molecules, tropomyosin (covering actin binding sites), troponin (bound to tropomyosin, holding it in place)
- Myosin strand : globular head (enzymatic; can break down ATP to ADP+Pi), alpha-helical tail, 2 hinges
Sliding filament theory
- At rest; myosin head unattached, actin binding site covered
- AP arrives, Ca2+ released from SpR and bind to troponin
- Troponin pulls tropomyosin, revealing binding sites on actin
- Myosin head attaches to the binding sites on actin (facilitated by hinge)
- ADP+Pi released from myosin head, releasing energy
- Myosin head pivots, pulling the actin filaments over the myosin, shortening the sarcomere
- It is necessary to detach cross-bridge, so ATP binds to myosin head, causing its release from the actin
- Enzymatic activity (myosin ATPase) of myosin head hydrolyses ATP to form ADP+Pi
- That energy released adds tension back to myosin head; back in original position, ready for next attachment
Active tension
- At full resting length, overlap between actin and myosin is greatest, so probability of cross-bridging is greatest and therefore greatest tension is developed
- If sarcomere shortens beyond certain length, actin are overlapping and so sites for cross-bridging are shielded; tension declines
- If sarcomere lengthens beyond certain length, cross-bridge formation cannot occur; tension declines
ATP
- Only substrate used to produce energy required for contraction
- Limited amounts available in muscle
- All other energy stores eg. carbohydrates, fats, proteins, creatine phosphate, ultimately produce ATP
Excitation-contraction coupling
- AP arrives at motor end plate (excitatory impulse down alpha-motor nerve)
- Causes release of Ach, which diffuses across synapse and binds to receptors
- Receptors are ion channels which allow influx of Na+; if enough Na+ floods in, AP is generated in sarcolemma (sarcolemma is depolarised)
- AP propagates deep into muscle via T-tubules
- When AP arrived in vicinity of SpR, Ca2+ channels are activated and Ca2+ released from SpR
- Ca2+ exposes actin binding sites, cross-bridges form and contraction proceeds
Slow twitch fibres (type 1)
- Slow oxidative
- Smaller fibres
- Innervated by smaller nerve fibres
- More extensive blood vessel system
- Increased numbers of mitochondria
- Large amounts of myoglobin
- Red colour
Fast fibres (type IIb)
- Fast glycolytic
- Large fibres
- Extensive sarcoplasmic reticulum
- Large amounts of glycolytic enzymes
- Less extensive blood supply
- Fewer mitochondria
- White colour
Fast-twitch oxidative fibres (type IIa)
- Fast oxidative glycolytic
- Intermediate type
- Fast contraction and increased force
- Can utilise oxidative processes
- Red colour
The motor unit
- Nerve cell bodies in ventral horn of spinal cord
- Alpha motor neurone exits the ventral root of the spinal cord and innervates 10-1000 muscle fibres
- Muscles with fine control = less fibres attached to motor neurone (1:10)
- Muscles with course control = more fibres (1:1000)
- Motor unit = alpha motor neurone + all motor fibres it innervates
- Fibres that are innervated by 1 motor neurone are evenly spread throughout the muscle so as to avoid potential damage if fibres were concentrated in one area; tension is distributed throughout the muscle
- Each motor unit contains only 1 type of fibre
How is force of contraction regulated?
MUSCLE FIBRE RECRUITMENT
To generate small forces and fine control of movement:
- Small numbers of motor units are recruited
- Motor command coming down spinal cord from motor areas of the brain will excite smaller cell bodies of slow twitch motor units first are more excitable, and generate smaller forces
To generate larger forces:
- With more force required, stimulus strength increases and there is an increased size of motor units recruited
- Fast twitch fibres are innervated and a greater amount of tens in generated
CHANGE FREQUENCY OF APs
- As frequency increases, recovery from the previous contraction is less complete
- Contractions begin to summate and this leads to tetany
Neuromuscular transmission
- AP depolarises terminal pre-synaptic axon
- Ca2+ diffuses into terminal button via voltage-gated calcium channels
- Secretory vesicles fuse with plasma membrane and Ach is released into neuromuscular cleft via exocytosis
- Ach binds to nicotinic receptors on the MEP
- Causes opening of voltage-gated cation channels in post-synaptic membrane
- Sarcolemma is depolarised; AP continues to propagate along T-tubules to reach deep into the muscle fibre
- Acetylcholinesterase (attached to MEP membrane) releases Ach from receptors by breaking it down into acetate and choline
- MEP repolarises and neuromuscular transmission is complete
Neuromuscular blockers: Curare
- Group of several active compounds
- Nicotinic Ach receptor blocker
- Turbocurarine used in surgery as muscle relaxant
- Decreases levels of anaesthesia required
- Allows easy intubation under general anaesthetic
Neuromuscular blockers: Botulinum toxin
- Produced by Clostridium botulinum bacteria
- LD50 of roughly 0.005-0.05 micrograms/kg
- Prevents fusion of Ach vesicles with synaptic membrane