FORM & FUNCTION (Cardiac Muscle) Flashcards
Cardiac muscle function:
-generates waves of contraction responsible for squeezing the heart to pump blood throughout the body
Cardiac muscle connected to:
-pulmonary circulation (lungs)
-systemic circulation (rest of the body)
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)
Cardiac muscle fibers:
-contractile fibers (striated and like skeletal fiber)
-conduction fibers (ex. pacemakers)
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
Desmosomes:
-joins the intermediate filaments in one cell to the neighbouring (lateral side)
-mechanical strength
Adherents:
-join an actin bundle in one cell to a similar bundle in a neighbouring cell (lateral side)
-mechanical strength
Dark-staining lines (contractile fibers):
-intercalated discs
>interface between cells
*need to contract together!
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
Functional syncytium:
-simultaneous contraction of all cardiac muscle fibers
Conducting fibers: specialized cells
-nodes (SA and AV node)
-bundles of His
-bundle branches
-Purkinje fibers
Nodes: conducting fibers
-generate and relay electrical impulses
-SA node cells: primary pacemakers of the heart
Bundle of His, Bundle branches and Purkinje fibers: conducting fibers
-transmit impulses to the ventricular myocardium
Conducting fibers: structural characteristics:
-few myofibrils: optimized for rapid conduction
-highly branched: allow for quick signal propagation
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
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
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
Phase 0:
-rapid depolarization
-triggered by the opening of voltage-gated Na+ channels
-rapid influx of Na+ ions
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
