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KIN 3600

lec 19

Transverse Tubules (T-Tubules) extensions of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells.
Cardiac muscle 1 t-tubule
Skeletal muscle 2 t-tubule
T-Tubules Average diameter 0.04mm (40nm)
T-tubules network @ every A-I band junction
Sarcoplasmic reticulum specialized type of smooth ER that regulates the calcium ion concentration in the cytoplasm of striated muscle cells
The sliding filament theory Thin pulls thick over center sarcomere which is pulling the z-disc along
What is doing the pulling for the thin myofibril? What is the molecular motor? Head of myosin molecule
How are the thin filaments pulled over along thick filaments, what structures generate the force, there is the molecular motor? Myosin head pulls with attached actin & brings the heads closer together
Cross Bridges Form between thick and thin filaments Actin and myosin head attach
Length-tension relationship Force developed by muscle depends on lengthn
Power stroke Formation of strong bond (contracted muscle) with thin filament
Strong bond o Release inorganic phosphate o Formation of weak bond
When muscle is relaxed o Cross bridges are waiting & energized o Utilized before
Cross bridge recycling during muscular contraction o Formation of weak bond o Re-energized cross bridges o Repeating the cycle
Cross bridges Duration of cycling 50ms
Since skeletal muscle can shorten by 40% means cross-bridges must recycle many times o Asynchronous cycling of cross bridges
Rigor Mortis (“death”): muscle remains contracted and cannot resynthesize ATP for relaxation (locked state)
About 50% of all the cross-bridges are in strong bond s
Both range & velocity of muscle shortening depends on length (# of sarcomere) of muscle
The longer is the muscle fiber greater its range & velocity of contractions
What determines force? How many arranged side by side / How thick the muscle is
If myosin binding site on thin filament is exposed the cross bridge will recycle continuously
Relaxation is caused by deactivation of myosin binding sites on thin filament -Turn on and off contraction: o Role of troponin-tropomyosin complex
Excitation-Contraction coupling Voltage-regulated Ca++ gates
Voltage-regulated Ca++ gates -ATP -Calcium rushes out (100,000 fold different in Ca concentration) -Troponin C binds calcium -Something else -Unblock myosin binding sites -Pumping Ca++ back into the SR
Created by: rmart11



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