muscles 1 Flashcards
Cardiac muscle
- 200-300 micro metres long
- Single nucleus
- Striated
- Involuntary
- Responsible for contraction of the heart
- Has intercalated disks
intercalated disks
○ Cardiac muscle cells branch and are interconnected by intercalated disks
○ Connected by gap junctions - electrically connected
Smooth muscle
- Involuntary
- Lines internal structures eg. Digestive tract, veins/arteries, respiratory passage ways
- Small elongated, thin spindle shaped cells
- Single nucleus
- Non-striated - smooth
Muscle fibre
- Surrounded by endomysium
- Contains myofibrils
- The cell
Myofibrils
- Surrounded by sarcoplasmic reticulum
- Consists of sarcomeres
- Thing inside the cell (100s of em)
Sarcomere
- Contains
○ thick filaments
○ Thin filaments
actin is attached to
Z disk
actin is attached to Z disc by
a-actinin
myosin thick filament is attached to
Z disk
myosin thick filament is attach to Z disc by
titin
how is tension created in the sarcomere
actin and myosin pull on each other
Actin (thin) filaments
- Double helix of polymerised G-actin (F-actin)
- Tropomyosin and troponin complexes are embedded in the cleft of the twisted chains
Tropomyosin
○ Tropomyosin is filamentous and spans the lengths of the filament
Myosin (thick) filaments
- Thick filaments are comprised of many myosin molecules
○ 1.6 micro metres long x 12nm wide
Sarcomeres change during contraction
- Shorted
- I bands and H zone shorten
- A bands do not change in length
A bands
length of myosin thick filaments
I bands
distance between mysosin thick filaments
H bands
distance between actin think filaments
4 steps of actin myosin cross bridge
- Myosin binds actin
- Myosin head attached reversibly to high affinity active sites on the actin thin filament- Myosin ‘power stroke’ pulls actin filament, contracting sarcomere
- ADP released, freeing ATP-binding site
- ATP binding releases myosin from actin
- Conformational change
- ATP hydrolysis drives re-cocking of myosin to high energy state, but is not required for power stroke
- Myosin ‘power stroke’ pulls actin filament, contracting sarcomere
Sliding filament model
- The lever movement pulls on the actin filament relative to the myosin head (~5nm) producing force
- Thick and thin filaments interdigitate and slide relative to each other
tension is proportional to
○ Proportional to the number of actin-myosin crossbridges
○ Ie. Amount of overlap
- Length-tension curve
○ The tension generated by a sarcomere can be predicted from sarcomere length ie. Overlap
In relaxed muscle
§ Tropomyosin ™ blocks the myosin binding site on actin filaments preventing crossbridge formation
§ Tropomyosin is regulated by the tropomyosin complex
troponin complex
Tn-T, Tn-I, Tn-C
Tn-T binds to
tropomyosin
Tn-I binds to
Tn-C and actin
Tn-C binds to
Ca ions
how does troponin work
○ When Tn binds Ca its conformation changes pulling tropomyosin out of the myosin binding site so myosin thick filament can bind
How is Ca regulated
- Action potential -> opens dihydropyridine receptor (DHPR) -> opens ryanodine receptor (RyR) -> releases Ca2+ from the sarcoplasmic reticulum
sarcoplasmic reticulum
endoplasmic reticulum and muscle
surrounds each myofibril
SERCA
calcium ATPases / calcium pumps
on the sarcoplasmic reticulum
sequesters calcium to cause relaxation
dihydropyridine receptor
on the outside of the cell
voltage gated
ryanodine receptor
mechanically gated calcium channel
gated by dihydropyridine receptor
on the sarcoplasmic reticulum inside the cell
DHPR does
voltage gated
mechanically pushes the RyR receptor
T tubule
part of the plasma membrane that brings the action potential closer to the interior of the muscle fibre
numero muscular junction
where the nerve talks to muscle
motor end plate
cholinergic synapse
motor neurone secretes
acetyl choline
Nicotinic Ach receptor
§ Ionotropic - ligand-gated Na+ channel
§ Always excitatory
lets sodium into the cell to cause an action potential which travels down the T tubule
How does contraction stop
- Motorneuron AP stops
- Ach degraded at the synapse by AChE
- Muscle AP stops - DHPR - RyR close
- Ca -ATPase pumps remove cytoplasmic Ca so calcium sequestered back into the sarcoplasmic reticulum
- Troponin-tropomyosin complex blocks cross bridges, causing relaxation (if ATP is present)
excitation/contraction event called
- This whole event is called a twitch
latent period
time between action potential and coupling
excitation contraction coupling
Because a twitch is slow, theres time for >1 AP
Wave summation progressively increases [Ca2+] which increases tension
maximum tension
- Maximum tension (tetanus) Is reached when all actin + myosin are forming crossbridges
