Physiology Objectives 5
1.
ICa-L (DHP) receptor in skeletal muscle:
a.
Location: In the t-tubule mechanically connected to the Ca2+ release
channel (ryanodine) of the sarcoplasmic reticulum
b.
Role: to allow release of Ca2+ into cell from extracellular space as well as
release Ca2+ into cell from sarcoplasmic reticulum
c.
Interactions: interacts with the aforementioned ryanodine receptor
Action potential timing/Ca-transient/tension:
Force development vs. Ca2+ availability:
2.
Sarcomere:
Major components of the myofilament:
a.
Actin (thin filament): major component of sarcomere
a. Tropomyosin: stabilizes actin, blocks myosin binding site in Ca2+ poor
state
b. Troponin: binds Ca2+ to move troponin and allow myosin binding
b.
Myosin (thick filament): major component of sarcomere
Roles of Ca2+ and ATP in cross-bridge cycling:
a.
Ca2+: binds to troponin so that cross-bridge can be formed
b.
ATP: binds to myosin and allows myosin to release actin
Stages of cross-bridge cycling:
1.
Resting muscle: myosin is cocked and bound to ADP
2.
Cross-bridge formation: Ca2+ binds troponin and myosin binds actin
3.
Power stroke: Release of Pi
4.
Rigor state: Release of ADP
5.
Release of rigor state: ATP binds myosin and releases myosin from actin
6.
Back to resting muscle: ATP is hydrolyzed by myosin ATPase
3.
Tension vs. length:
Relationship to the “sliding-filament” model of muscle contraction: if muscle
is stretched too far it can not contract optimally; similarly, after it has contracted it
can not contract optimally (thin and thick filaments are too far apart or too close
together, respectively)
4.
Strategies used by CNS to regulate active cross-bridges:
a.
Regulation of frequency: summation can cause tetanus and increase the
number of active cross-bridges
b.
Recruitment: motor units can be recruited to increase the number of active
cross-bridges