Cardiac Muscle Mechanics

Question 1

what is the functional syncytium made of?

Answer 1

two synctytia: atrial and ventricular

Question 2

differences in cardiomycete structure from skeletal muscles

Answer 2

1. T-tubules only at Z lines

2. endfeet (triad) not observed, but the ryanodine receptors and L-type Ca++ channels are still associated

Question 3

what does cardiac muscle use to open ryanodine receptors?

Answer 3

only small amount of Ca++ influx via L-type Ca++ channels, but they also open Ryanodine receptors then allow greater CICR (calcium induced calcium release) to cause muscle contraction

Question 4

what phases of a cardiac AP correspond to absolute refractory period?

Answer 4

phases 1 and 2
1 = transient outward current
2 = L-type Ca++ current in, K+ current out

Question 5

Ca++ dynamics during contraction phase

Answer 5

during depolarization; Ca++ enters sarcoplasm via L-type Ca++ channels (20% of twitch) and opens ryanodine receptors via CICR (80% of twitch)
-NCX may work in reverse, exchanging 1 Ca++ into the cell for 3 Na+ out

Question 6

Ca++ dynamics during relaxation phase

Answer 6

during relaxation; as L-type Ca++ channels inactivate, SERCA (80%), NCX (normal operation; 15%) and PMCA (5%) remove Ca++ from sarcoplasm, back into sarcolemma

Question 7

what does the trans-sarcolemmal influx of Ca++ mean for cardiac muscle?

Answer 7

much more sensitive to extracellular Ca++ than skeletal muscle
-also more sensitive to L-type Ca++ channel blockers

Question 8

cardiac muscle contraction

Answer 8

use troponin C and tropomyosin movement to initiate crossbridge cycle (like in skeletal), BUT twitches don’t have summation/tetanus or recruitment b/c of their long refractory period

Question 9

how can tension of cardiac muscle be affected?

Answer 9

1. sarcoplasmic [Ca++] is altered (by inotropic agents)

2. Ca++ sensitivity of myofilaments is altered

Question 10

how is heart rate increased and decreased?

Answer 10

increase: sympathetic activation via NE release
decrease: parasympathetic (vagal) activation via ACh release
both primarily realized by changing K+ conductances at SA node

Question 11

why does the ejection fraction increase with ventricle filling?

Answer 11

NOT because of thick/thin filament overlap, b/c this happens at normal thick/thin overlap

• direct consequence of effect of increasing load on a single muscle fiber
• increases affinity of troponin C for Ca++, increasing contractile force (increase in sensitivity)

Question 12

at what initial sarcomere length is maximal force generated?

Answer 12

2.2 micrometers (rarely exceeded in normal heart)

Question 13

effects of greater initial length on cardiac muscle function

Answer 13

• increased Po (maximum load) at same Vmax
• velocity of shortening increases
• amount of shortening increases
• work of heart increases
• power delivered by the heat increases

Question 14

what does inotropic intervention (w/ NE) do to cardiac twitch?

Answer 14

increases tension development and Ca++ levels

• increases contractility (force of contraction)
• shorten duration of contraction

Question 15

coordinated response of heart to beta-adrenergic stimulation

Answer 15

increase in intracellular cAMP, causing increased influx of Ca++ across sarcolemma during AP, so increased release of Ca++ by SR
-cAMP activates protein kinase to phosphorylate phospholamban regulatory PRO in SR membrane to increase sensitivity of SR Ca++ pump, increasing Ca++ rate of uptake, to decrease duration of muscle contraction

Question 16

does Po (maximum load) increase, decrease, or stay the same at all muscle lengths, and if NE is applied?

Answer 16

it increases in all cases

Question 17

how is muscle shortening affected by NE addition?

Answer 17

it can be have a greater length of shortening compared to weight added
ex: if initial is 13 mm muscle, w/o NE will go to 12 mm (1 mm movement), but w/ NE will go to 11 mm (2 mm movement)