Muscle Physiology Flashcards
sarcolemma
“sarco-“ = pertaining to muscle
sarcolemma = muscle plasma membrane
sarcoplasma = muscle cytoplasm
etc
which type of muscle does NOT acquire calcium for contraction from an extracellular source?
skeletal muscle: intracellular calcium source (stored in sarcoplasmic reticulum)
cardiac and smooth: extra and intracellular calcium sources
muscle strength vs power
strength = max force/torque that is generated during a max voluntary contraction
power = work performed per unit time
what are the components of actin and myosin, respectively, that allow them to participate in muscle contraction?
actin: filamentous double-helix F actin
- troponin I: anchors to actin
- troponin C: Ca2+ binding
- troponin T: shields tropomyosin
- tropomyosin: myosin binding domain
myosin: 2 heavy chains (tail) + 4 light chains (head)
- ATPase
describe the mechanism calcium release from the sarcoplasmic reticulum of cardiac and skeletal muscle cells to initiate contraction
- action potentials conducted along T-tubules
- DHPR (dihydropyridine receptor) on SR are activated (voltage-gated)
- activated DHPR activates RyR (ryanodine receptor) on SR
- activated RyR are Ca2+ channels in SR
- Ca2+ floods out of the SR due to concentration gradient
what is the role of calsequesterin?
calsequesterin: located in the sarcoplasmic reticulum, binds Ca2+ and maintains it in low energy state while housed in the SR
describe the structure of a sarcomere
A band = overlapping thick (myosin) and thin (actin) filaments
I band = thin (actin) filaments
H band = thick (myosin) filaments, centrally located
Z band = end boundaries of each sarcomere, actin anchored to Z discs
after calcium is released from the SR, how is skeletal and cardiac muscle contraction initiated?
- Ca2+ floods out of SR and binds troponin C on actin, causing conformational change
- tropomyosin (myosin binding site) is released
- high energy myosin head (which during rest hydrolyzed ATP with intrinsic ATPase in light chains) binds actin
- conformational change is induced which causes myosin head to pull actin closer (power-stroke, shortening of sarcomere via overlap)
- ADP+Pi is released by power stroke, and when ATP binds myosin head again it causes myosin to dissociate from actin (and cycle begins again)
what is the determining factor of whether muscle contraction will continue cycling or cease?
concentration of sarcoplasmic Ca2+
when sarcoplasmic (read: cytoplasm of myocytes) calcium drops below threshold, muscle contraction ceases
what is the function of SERCA and NCX?
both function in facilitating muscle relaxation by lowering concentration of sarcoplasmic Ca2+
SERCA (sarco/endoplasmic reticulum Ca2+ ATPase): in membrane of SR, pumps Ca2+ against its concentration back into SR
NCX (Na+/Ca2+ exchanger): in plasma membrane of CARDIOmyocytes, secondary active transporter that exchanges extracellular Na+ for intracellular Ca2+, very important to help cardiac muscle relax in between contractions
preload vs afterload
preload = force potential a muscle can generate
afterload = anything resisting muscle contraction
preload must overcome afterload to cause movement (displacement of load - isotonic)
what is different about the amount of force that can be generated by a skeletal muscle vs a cardiac muscle fiber?
skeletal muscle has a set/given amount of force it can generate (if more force is needed, more motor units are recruited)
cardiac muscle contractive force is dependent on the concentration of intracellular calcium
what is the preload and afterload of heart contraction?
preload = force potential a muscle can generate = myocardial contractile force
afterload = anything resisting muscle contraction = blood pressure (the “weight”)
fill in the following equations:
BP = ____ x ____
MAP = ____ x ____
BP = CO x TPR
where TPR = total peripheral resistance (via vascular smooth muscle)
MAP = CO x TPR
where MAP = mean arterial pressure
these are the same equations, the MAP is just a more accurate way of describing this relationship
what are beta blockers used for?
beta blockers = beta1 antagonists
antagonize beta1 adrenal receptors expressed in myocardium of SA node (activated by nor/epinephrine to increase HR) —> slow down HR and CO, used to lower blood pressure
[recall BP = CO x TPR]