November 24, 2023 Flashcards
Questions from beginning of lecture:
- Pg. 146: EF problem
- Use words to explain to yourself everything that is going on with EDV and ESV during the transition from rest to max exercise
why does EDV not increase in a linear function as exercise intensity increases
because despite an increase in VR, there is an proportional decreases in diastolic time (time for heart to fill with blood).
page 147 graph for visual representation
what is the Frank-Starling Mechanism:
↑ VR →
↑ stretch of fibers to optimal length →
↑ force
Detailed explanation:
When you stretch cardiac cell to a longer length, there is a more optimal actin and myosin interaction which generates more force → higher SV
page 147 graph for visual representation
why does ESV decrease as exercise intensity increases
↑ contractility (hormonal effect)
↑ stretch → ↑ force
Detailed explanation:
ESV decreases due to increase in contractility due to hormones (catecholamines which have a positive inotropic effect); also increase in
stretch and force
page 147 graph for visual representation
how does a trained person have a higher SV at any given exercise intensity (even at rest), than an Untrained person
training:
↑ ventricular volume → ↑ EDV
↑ sensitivity of the myofibrils to calcium →
↑ force for given level of calcium
page 147 graph for visual representation
review of cardiac ventricular “E-C coupling”
- Current spreads through the gap junctions to contractile cell
- Action potentials travel along plasma membrane and t-tubules
- L-type Ca channels open in plasma membrane
- Ca induces Ca release from SR (CICR)
- Ca binds to troponin, exposing myosin-binding sites
- Crossbridge cycle begins and fibre contracts (systole)
- Ca is actively transported back into the SR and ECF; K+ efflux restores the RMP
- Ca removal allows for muscle fibre relaxation (diastole)
Sodium-calcium exchange doesn’t exist in skeletal muscle, only cardiac muscle. True or false
True
Sodium-calcium exchange doesn’t exist in skeletal muscle, only cardiac muscle. How does exercise change this through the use of hormones?
What are the results?
- Activation of AC by binding of NE or Epi →
- production of cAMP →
- Activation of Protein kinase A →
- phosphorylates L-type calcium channel →
- ↑ calcium to come in and release more calcium into the cytoplasm
Results:
cardiac twitch to occur faster and to a higher level because this is more force generated
Relaxation phase is also faster; phosphorylation also allows the reuptake of Ca into the SR to occur faster (through Ca-ATPase); bond breaks
page 150
are Catecholamines negative or positive inotropic agents
Catecholamines are positive inotropic agents; positively impacting the force output
Kinases job is to __________
phosphorylate
Beta-adrenergic agonists act on:
act on the receptor like NE or EPI, but have a longer
half-life in the circulation (positive inotropic); isoproterenol, dobutamine
Beta adrenergic antagonists act on:
act on the receptor to block the action of EPI or NE;
beta blockers; propranolol
Calcium channel blockers (verapamil);
inhibits the L-type Ca entry channels and reduce the force of contraction (for use post-MI)
Digitalis (or digoxin):
directly inhibits the Na-K ATPase, preventing the removal of Na from the cytoplasm.
This increase in Na reduces the gradient for Na entry
via the action of the Na-Ca exchanger (NCX), so more Ca stays inside the cytoplasm
Result:
more internal Ca, greater force of contraction (for use in congestive heart failure) (indirectly inhibits Na-Ca exchanger)
10^7-10^5 =
Page 151 graph on bottom
depolarization → Ca entry → SR Ca release → contraction
