Heart Muscle

Question 1

Sarcomere

Answer 1

one Z line to another Z line
middle is H zone or M line
thin;I abnd and thick filaments: A band
length 1.6-2.2 micro m : determines contraction force
basic contractile unit
made of
-myosin: 300 bundled for thick filaments, site of myosin ATPase
-actin: chain make a thin filament. tropomyosin strand is a chan of 7 actin
- tropomyosin regulatory complex

Question 2

M line

Answer 2

line when contracted, the H zone disapears and the 2 I bands (actin) join
middle of sarcomere

Question 3

H zone

Answer 3

when sarcomere relaxed, middle

thick filament without overlaping actin (I band)

Question 4

A band

Answer 4

length of a single thick filament, middle of sarcome, makes the H zone, in between thin filaments

Question 5

I band

Answer 5

thin filaments in sarcomere

actin, titin, …

Question 6

Z line

Answer 6

anchor the actin filaments

Question 7

Cardiac Myocyte

Answer 7

1 nucleus
25 micro m, 100 micro m (shorter skeletal muscle)
atrial myocyte smaller than ventricular
made of myofibrils: made of myofilaments: actin and myosin
found in syncytium
transfer tubules (t-tubules): extend surface area of cardiac myocyte
sarcoplasmic reticulum: ryonodine receptors (Ca2+), store intracellular Ca2+

Question 8

Functionaly syncytium

Answer 8

group of myocytes interconnected by intercalated disks. Membranes have gap junctions for Ca2+ ions to flow.
Desmosomes hold cells together with contractions

Question 9

Myosin

Answer 9

2 heads

titin: myosin connection to Z lines
elastic: passive mechanic

Question 10

Tropomyosin regulatory complex

Answer 10

attached to tropomyosin 
troponin T (TN-T) : attaches to tropomyosin
troponin C (TN-C): binding site Ca2+ for excitation contraction coupling
troponin I (TN-I): inhibits myosin binding to actin -> prevent binding of myosin heads to acting Ca2+ binds to TN-C -> myosin head can access acting

myocite die -> release TN-T & TN-I : biomarkers

Question 11

Frank Starling Mechanism

Answer 11

Make the pressure volume loop larger: more volume not more pressure. More EDV (end diastolic volume) but thus also more venous return

Venous return up -> ventricular filling up -> pressure up -> preload up -> myocyte stretch up -> force generation up -> stroke volume up
Balance the right and left ventricular output
venous return up right -> right stroke volume up -> venous return left up -> stroke volume left up

venous return up -> passive filling up -> EDV up -> SV up

inotropy up (interdependent with preload and afterload) -> force velocity up -> stroke volume up -> frank starling up

Question 12

ESPVR, EDPVR

Answer 12

ESPVR: end systolic pressure volume relation
max pressure ventricle can reach for a given value
pressure volume loop doesnt cross it in inotropic state
EDPVR: end diastolic pressure volume relation
filling phase moves along this line: describes the compliance

Question 13

Excitation Contraction coupling

Answer 13

coupling of myocyte action potential and contraction

Ca2+ ->(gap junction)-> depolarization cardiomyocyte -> threshold membrane potential -> Na+ (sodium) channels open

Calcium induced calcium release: Acetylcholine → nicotinic acetylcholine → AP T tubules to SR
T-tubule release calcium → L type Ca2+ channels →
ryonodine receptor activated → sarcoplasmic reticulum
release Ca2+ → activate myofilaments
actin & myosin)

Ca2+→ binds to troponin C (tn-c) → tropomyosin slides → binding sites accesible
to myosin heads → cross-bridge → pulls Actin over myosin (ADP consumed) → muscle(sarcomere) shortened

SERCA pump: ion transporters (use ATP and concentration gradient) → remove Ca2+ → Ca2+ back in sarcoplasmic reticulum → troponin slides back (original length)→ cross-bridge blocked

Question 14

Contractility

Answer 14

depends on Ca2+ levels
modulated by sympathetic and parasympathetic
↳ positive inotropy

Question 15

Inotropy

Answer 15

Contractility up
Length independent

sympathetic stimulation: norepinephrine → beta 1 receptors on myocytes
stimulatory G- protein → adenyl cyclase up → hydralization ATP-> CAMP → phosphorylation
↳ active PK-A phosphorylates → up sarcoplasmic
reticulum Ca2+-release
↳ Pk-A phosphorylation → inhibitory
effects of phospho lamban down on
SERCA → Ca2+ uptake / storage up
↳ L-type Ca2+ channels
permeability up → up extracellular
Ca2+ entry in myocytes

TN-C binding calcium affinity → force generation up

Parasympathetic stimulation down:
↳ decrease SA node firing -> HR down
↳ decrease contractility
inhibitory G-protein → adenyl cyclase down → cAMP down → M2 muscarinic receptors activated → inhibition of Ca2+ channels → Ca2+ in cell down → Ca2+ released by sarcoplasmic reticulum. Acetylcholine

HR up → AP up → Ca2+ up→ Sarcoplasmic reticulum accumulates ca2+ → contractility increase

Question 16

Phospholamban

Answer 16

Ca2+ pumps from cytoplasm to sarcoplasmic reticulum
regulate ATPase
on sarcoplasmic reticulum membrane

Question 17

Lusitropy

Answer 17

Myocyte relaxation
Reduce intracellular Ca2+ → Ca2+ unbind from TN-C→ troponin-tropomyosin complex inactivated
rate the calcium enters
rate calcium leaves cell with sarcolemmal calcium pump and Na+/Ca2+ exchange pump
Activity of SERCA pump

Question 18

Dromotropy

Answer 18

conduction velocity

negative: vagal activation → conduction velocity down

Question 19

Chronotropy

Answer 19

Heart rate
positive: influence pacemaker firing
increase slope of phase 4, lower treshold voltage of phase 0, alter hyperpolarization degree
negative: vagal activation → SA firing lower → HR lower

Question 20

Length tension relationship

Answer 20

affect of preload on developed tension (initial muscle length)
preload up → tension up
duration contraction stays the same

Question 21

Exercise induced troponin

Answer 21

prolonged exercises
sarcolemmal permeability up → TN released

creatin peptide myoglobin is a long term heart effect of exercise