Class 17 - Muscle Tissue pt. 2 Flashcards
4 major phases of contraction and relaxion
- Excitation
- Excitation-contraction coupling
- Contraction
- Relaxation
Excitation-contraction coupling
Events that link the action potentials on the sarcolemma to activation of the myofilaments, preparing them to contract
Stages of muscle fiber excitation (4)
- Nerve signal opens calcium channels, releasing calcium into NMJ
- Calcium causes release of AcH into synaptic cleft
- ACh binds to ACh receptors in sarcolemma, opening them and allowing Na+ in and K+ out.
- Voltage change opens voltage-gated ion channels, allowing more Na+ in and K+ out
Stages of excitation-contraction coupling of a muscle fibers (3)
- Voltage change enters T-tubules and triggers opening of Ca2+ channels, releasing calcium from terminal cisterns
- Calcium binds troponin
- Troponin shifts tropomyosin, exposing active sites of actin
Stages of contraction of muscle fibers (4)
- ATP on myosin head hydrolyzes, straightening the head
- Straightened head binds to actin active site, forming myosin-actin cross-bridge
- ADP and P dissociate from myosin head, recocking the head and causing a power stroke which slides thin filament over thick
- A new ATP binds to myosin head, breaking the cross-bridge between it and actin
Stages of relaxation of muscle fibers (4)
- Nervous stimulation and ACh release ceases
- Acetylcholinesterase breaks down ACh in NMJ.
- SR resorbs calcium ions, and calcium ions detach from troponin
- Troponin moves tropomyosin back onto active sites
Length-tension relationship + what happens if muscle too short or stretched
The idea that the amount of tension generated by a muscle depends on how stretched or shortened it was before stimulation
Too short - Thick filaments butt against Z-discs; weak contraction
Too stretched - Minimal overlap between filaments results in minimal cross-bridge formation; weak contraction
Muscle tone
Maintenance of partial contraction of muscle at rest to ensure optimum resting length (and therefore strongest contraction)
Stages causing rigor mortis (4)
- Deteriorating SA releases Ca2+ and deteriorating sarcolemma allows Ca2+ to enter cytosol.
- Ca2+ activates myosin-actin cross-bridge formation and muscle contraction
- Lack of ATP production after death prevents muscle relaxation (cross-bridges can’t dissociate)
- Fibers remain contracted until myofilaments decay
Muscle twitch + measuring method
A quick cycle of contraction and relaxation when a muscle is directly stimulated with an electrode
Measured using a myogram
3 phases of muscle twitch
- Latent period - Delay just after muscle stimulation; time required for excitation-contraction coupling and tensing elastic components. Generates internal tension
- Contraction phase - External tension generated and load moved as muscle fiber shortens
- Relaxation phase - Sarcoplasmic calcium levels fall as calcium is reabsorbed into SR; tension declines
Threshold
Minimum voltage that causes a muscle twitch.
5 Reasons different stimuli cause varying twitch strengths (even if same voltage)
- Muscles starting length influences tension
- Muscles fatigue after continual use
- Warmer muscles’ enzymes work more quickly
- Muscle cell’s hydration levels influence cross-bridge connections
- Increasing frequency of stimulus delivery increases tension output
Max contraction = optimal muscle tone, rested, warmed, hydrated, continual impulses
How higher voltages produce stronger contractions
Excite more nerve fibers which stimulate more motor units to contract
Recruitment or multiple motor unit summation + size principle
Process of bringing more motor units into play with stronger stimuli
Size principle - Weak stimuli recruit small units, strong stimuli rector small and large units for powerful movements
