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Physiology
Dr. Dominguez
Cardiac Muscle Contraction

ria
Extracellular cycle
Extracellular Ca

Cardiac muscle
- Striated
- Intercalated discs - contain Gap
junctions facilitates propagation
of stimulus
- Desmosomes anchor between
cardiac cells
- Predominance of Mitochondria
supply energy needed
Contractile Apparatus
o Sarcomere contractile units
(both cardiac and skeletal
muscles)
o Z lines attachment for
filaments
o Actin thin filament
o Myosin attached to z line (titin
holds myosin tightly)
- thick filament
o Tropomyosin hides myosin
binding sites in relax state
Toponin Complex
Troponin C, I, T binding site of Ca,
specifically C

Increase Ca Ca bind to
troponin C, tropomyosin moves
away from binding site -exposing the binding site

Cardiac muscle fiber thin filament

regulated because of tropomyosintroponin complex (essential for
cross bridge)
T tubules facilitate entry of Ca
Parameter Cardiac
Skeletal
muscle
muscle
Contractile Sarccomer Sarcomer
unit
e
e
Striated
Yes
Yes
Connectiv More
Less
e tissue
Mitochond More
Less

Enters the muscle thru L

type Ca channels

Stimulate the release of Ca

from sarcoplasmic
reticulum (Ca triggered/
release)

Release of Intracellular Ca

Muscle contraction

Main bulk of Ca is from

intracellular cycle (sarcoplasmic
reticulum)

Decrease Ca

Ca detaches to Troponin C

Ca goes back to
sarcoplasmic reticulum Ca
channel (SERCA)

Actin and myosin separates

Muscle relaxation

REGULATORS OF Ca:
1. SERCA
2. Na Ca exchanger
3. Plasma membrane pump serve
to lower intracellular Ca levels

Parameter
Muscle
activity
Contractio
n

Intracellul
ar Ca after
action
potential
Relaxation

Cardiac
muscle
Involuntary

Skeletal
muscle
Voluntary

Synchronous

Independe
nt/
grouped
Chemical

Electrochem
ical coupling
Regulated

SERCA, NaCa
exchanger,
plasma
membrane
pump

Noerepinephrine binds to
1 receptor

Increase formation of cAMP

High

Increase cAMP

L type Ca channels open

SERCA

Extracellular Ca

Stimulate RYR (Ryanodine

Receptor)

Electrical action potential (Ca

trigger/ release)
Mechanical causes voltage
gated ion potential

Facilitate Ca exit from

sarcoplasmic reticulum

Continuous increase Ca levels

causes faster contraction
Skeletal immediate (Ca should
always be increased)

Contraction
1. Intracellular Ca direct
relationship
- increase Ca = stronger
contraction
2. ANS sympha/parasympathetic
stimulation
- catecholamine
- adrenergic
- cholinergic

Ca bind to Actin

Systole (cardiac
contraction)

1 agonist (bronchodilator)
Salbutamol, Albuterol
- side effect: tachycardia
Ca channel act in LTCC
Verapamil and Diltiazem- block
L-type Ca-channel thus
inhibiting Ca-triggered Ca
release

Frank Starling Law

- between length (pressure inside
the ventricles) and stretch (force of
contraction)
1. Stretched muscle more sensitive
to Ca leads to greater force of
heart contraction
2. Greater proximity for
interdigitation of actin and myosin
(when stretched) = greater force of
contaction

3. Increase blood

Heart failure causes ventricles

to enlarge (it pumps weaker)
Parameter Cardiac
Skeletal
muscle
muscle
Length
Stretched Maximal
resistance
tension
Passive
Greater
Greater
resistance
ECF Ca for Required
Not
contractio
required
n
Metabolis
ATP from
lipolysis
glycolysis,
m
creatinine
phosphate

Glycolysis aerobic
Creatine phosphate - anaerobic