FORM & FUNCTION (Cardiac Muscle) Flashcards by Danielle Groenendijk

Cardiac muscle function:

-generates waves of contraction responsible for squeezing the heart to pump blood throughout the body

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Cardiac muscle connected to:

-pulmonary circulation (lungs)
-systemic circulation (rest of the body)

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Four chambers:

-right atrium (RA), right ventricle (RV) to the lungs
-left atrium (LA), left ventricle (LV) to systemic organs
*left: oxygenated (red)
*right: deoxygenated (left)

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Cardiac muscle fibers:

-contractile fibers (striated and like skeletal fiber)
-conduction fibers (ex. pacemakers)

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Contractile fibers:

-cardiomyocytes form complex junctions between extended processes
-only 1-2 centrally located nuclei
-dark-staining lines
-junctions at intercalated discs: desmosomes and fascia adherents
-gap junctions

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Desmosomes:

-joins the intermediate filaments in one cell to the neighbouring (lateral side)
-mechanical strength

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Adherents:

-join an actin bundle in one cell to a similar bundle in a neighbouring cell (lateral side)
-mechanical strength

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Dark-staining lines (contractile fibers):

-intercalated discs
>interface between cells
*need to contract together!

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Gap junctions: (contractile fibers)

-between cells longitudinally
=electrical synapses
-allow Aps to pass in wave from one cell to the next cardiac cells
-all cells contract as a single unit
*functional syncytium

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Functional syncytium:

-simultaneous contraction of all cardiac muscle fibers

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Conducting fibers: specialized cells

-nodes (SA and AV node)
-bundles of His
-bundle branches
-Purkinje fibers

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Nodes: conducting fibers

-generate and relay electrical impulses
-SA node cells: primary pacemakers of the heart

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Bundle of His, Bundle branches and Purkinje fibers: conducting fibers

-transmit impulses to the ventricular myocardium

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Conducting fibers: structural characteristics:

-few myofibrils: optimized for rapid conduction
-highly branched: allow for quick signal propagation

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How does the duration of cardiac muscle AP compare to that of skeletal muscle?

-last longer and has a plateau
*lasts as long as the contraction

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Sequential propagation of the AP:

Initiation in SA (SinoAtrial node)
Propagates through the atria
Through the AV (AtrioVentricular) node
Through the Purkinje fibers
Through the ventricles

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AP phases in cardiomyocytes:

Phase 0: rapid depolarization
Phase 1: initial repolarization
Phase 2: plateau phase
Phase 3: rapid repolarization
Phase 4: resting membrane potential

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Phase 0:

-rapid depolarization
-triggered by the opening of voltage-gated Na+ channels
-rapid influx of Na+ ions

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Phase 1:

-initial repolarization
-closure of Na+ channels and opening of K+ channels
-outward flow of K+ ions

Phase 2:

-plateau phase
-sustained depolarization
-opening of slow L-type calcium channels (voltage gated) allowing Ca2+ influx
*unique to cardiomyocytes

Phase 3:

-rapid repolarization
-closure of Ca2+ channels
-rapid outflow of K+ ions

Phase 4:

-Na/K pump and a Na/Ca exchanger to re-establish ion balance

Regulation of L-type Ca channel:

Sympathetic: E binds to beta-adrenergic receptor (GPCR) leading to activation of adenylyl cyclase=increased cAMP
Parasympathetic: ACh binds to muscarinic cholinergic receptor leading to inactivation of adenylyl cyclase=decreased cAMP
*cAMP activates PKA that phosphorylates L-type Ca2+ channels

Phosphorylated L-type Ca2+ channel:

-more likely to open

T-tubules and SR in cardiac muscle:

-larger T-tubules and less developed SR=’dyads’ rather than ‘triad’ -DHPR does NOT mechanically affect RyR opening -rise in intracellular Ca2+ comes form extracellular space through DHPR from the t-tubules >more Ca2+ released by Ca-induced Ca release mechanism through RyRs *cross-bridge cycling is the same as skeletal muscle

Contrast between skeletal and cardiac muscle AP:

-AP of cardiac has a plateau phase and a long refractory period: overlaps the time scale of force generation *prolonged refractory period until the end of contraction means no summation occurs in cardiac muscle

Length-tension relationship: skeletal vs. cardiac muscle

-skeletal: wider range of length over which tension is near optimum -cardiac myocyte: narrower and steeper curve

Skeletal and cardiac muscle at 75% sarcomere length

-skeletal: 84% force -cardiac: 0% force

Cardiac myocyte length-tension: increase from 75 to 90% sarcomere length

-increases tension from 0-70% of the maximum -tension that develops during contraction increases with increased length: Frank Starling Relationship

Frank Starling Relationship

*when change of cardiac muscle it will produce more force -more blood volume=stretch cardiac muscle more=need more force to pump it around the body

Force-velocity relationship: skeletal vs. cardiac muscle

-skeletal: Vmax=0 force (different for different fiber types) -cardiac muscle: if increase preload or contractibility you get more force and increased Vmax

Increase preload: cardiac muscle:

-stretching of cardiac cells before contraction *increases force

Increased contractility:

-heart’s inherent capacity to contract

Preload:

-volume of blood in the ventricle prior to contraction

Inotrophy:

-contractility refers to how powerful the heart can contract

Energy sources for cardiac muscles:

*oxidative phosphorylation -60% of ATP from FFA -30% of ATP from glucose and other CHO -glycogen granules and lipid droplets are abundant -lactate, ketone bodies and AA can be used for energy -ATP creatine phosphate system

ATP Creatine phosphate system:

-creatine kinase-MB (isoforms in heart muscle) is a biomarker for myocardial infraction (heart attack >now clinicians use troponin

Oxygen demand for cardiac muscles:

*required -almost entirely aerobic -depends heavily on oxygen supply -relies on myoglobin to store and release oxygen within cells -limited capacity to use glycolysis

Fatigue of cardiac muscles:

-high resistance due to constant demand for ATP and rich blood supply >lots of mitochondria to make sure they don’t fatigue

Mitochondrial density of cardiac muscles:

-make up 25-30% of cell volume (skeletal: only 2% of cell volume)

Cardiac muscle: innervation receptors

-ACh receptors: muscarinic cholinergic (slow GPCR) -E/NE receptors: beta-adrenergic receptor

Cardiac muscle innervation divisions:

-autonomic system -sympathetic and parasympathetic stimulation

Sympathetic stimulation:

-NT: NE -increases heart rate and contractility -beta-adrenergic receptor activates the cAMP second-messenger system

Parasympathetic stimulation:

-NT: ACh -decreases heart rate -muscarinic receptors

Cardiac muscle adaptation:

-hypertrophy -hyperplasia: NOT >if myocardial fibers die, they are replaced by fibrous noncontractile scar tissues