Excitation contraction coupling Flashcards
Myasthenia gravis
Autoimmune response to ash receptors
- results in muscle fatigability
- edrophonium chloride
- -cholinesterase inhibitor– increases Ach in NMJ
Triad in skeletal muscle
2-sarcoplasmic reticulum
1- transverse tubule
Dihydropyridine (DHP) receptors
L-type Ca channels
-Depolarization of t-tubule membrane
-induces change in the structure of the DHP receptors
this opens Ca channel gate in the ryanodine receptor in the SR
-causes Ca release into the sarcoplasm- triggering contraction
Ryanodine
Higher concentration of ryanodine
-closes ryanodine receptors
Ca induced Ca release
rapid release of Ca from SR
Ryanodine receptors
-stimulated to open by the presence of cytoplasmic Ca
This triggers adjacent ryanodine receptors to open and release Ca and so on….
SERCA
Uses energy from ATP to pump Ca back into SR
- then binds to Ca binding proteins- Calreticulin and Calsequesterin
2 mechanisms of Ca removal that do extrude Ca into the ECF
PMCA- uses ATP- pumps 1 Ca out at expense of 1 ATP
NCX- Lets 3 Na in and removes 1 Ca from the cell
Treppe
No summation occurs
- each twitch relaxes to zero tension before the next twitch
- Ca release may exceed Ca uptake- get left over Ca causing greater tension
Motor unit
Somatic motor neuron and all the muscle fibers (myofibers) it innervates
Muscle Pain
due to lactic acid buildup
Delayed onset muscle soreness (DOMS)
Occurs days after and is due to muscle damage
-inflammatory response
Muscle Fatigue
Is NOT caused by ATP depletion
High frequency fatigue
Accompanying high intensity, short duration exercise is due to failure in the conduction of AP in the T-tubule
-recovery is rapid
Low Frequency fatigue
Low intensity, long duration exercise
- build up of lactic acid and phosphates
- change conformation of muscle protein
- recovery is slow
