Smooth Muscle
Muscle Contraction Differences:
Much slower (and variable) velocity of
contraction
Slower onset of contraction and relaxation
Force of contraction per cross sectional area
equal to or greater than SKM
Shortens to much greater % of its rest length
(80-90%)
Shows stress relaxation and reverse stress
relaxation (can change to better
accommodate diameter of the organ
Only small change in velocity with increasing
force
Length-Tension Curves Similar for both
Contraction time much longer; prolonged
tonic contraction due to “Latch State”
Slow cycling of cross bridges -10-15% the
rate of SKM
Other differences:
Integrator of many excitatory and inhibitory
inputs: processes to produce final reaction
EC coupling dependent on sarcolemmal
control, sarcoplasmic reticulum (small
amount), modulation of contractile force.
SR less extensive, Ca stores not significant
No T-tubules
Requires much less energy to maintain force
(1/10-1/300 less)
Tone affected by : neural; humoral/paracrine;
metabolic; and physical influences
Autonomic n. fibers form diffuse junctions
and terminal axons forming varicosities in
the tissue
Thin filaments do not include troponin
Actin filaments attach to dense bodies
Myosin Light chains very important
(regulatory role)
No striations or sarcomeres
Contains intermediate filaments: desmin
and vimentin
Thin:Thick Filament ratio 15-18:1
Caldesmon and Calponin inhibit ATPase
activity
Less ATPase activity (slower degradation of
ATP leads to slower cross bridge cycling)
Thick filament regulation (myosin) of
contraction
Calcium essential for contraction
Calcium influx generates ATP, Na+
insignificant,…therefore not affected by
tetrodotoxin (puffer fish)
Resting potential -40 (b/c lower conductance
Skeletal Muscle
Faster velocity of contraction
Faster onset of contraction
Equal or less than (force of contraction/area)
Shortens less % (30%)
As force increases, velocity decreases
Length-Tension Curves Similar for both
Short contraction time
Rapid cycling of cross bridges “twitch”
On or off response to APonly (all or none)
Depends on changes in membrane potential
and internal membrane systems; relies on
sarcoplasmic reticulum
Large SR, Stores most Ca
Contains T-tubules for dispersing AP
Requires more energy to maintain force;
major source of metabolic heat
Tone only affected by nerve impulse. Causes
contraction and nothing more. On or off.
Neuromuscular junctions
Thin filaments include actin, troponin and
tropomyosin
No dense bodies
Myosin Light chains not very important
Striations and sarcomeres
None
Thin:Thick 2:1
More ATPase activity
Thin filament regulation (actin, troponin,
tropomyosin) of contraction
Calcium also essential for contraction
Na+ influx generates AP, Calcium less
significant in AP generation (tetrodotoxin can
affect)
Resting potential -60 (higher conductance of
of K+ out of cell) K+ out of cell)
Calcium levels crucial determinant of All or None (must reach a certain potential
contractile force mainly through Na+ activity)
SR releases calcium through IP3 SR releases calcium due to AP

Cardiac Muscle Skeletal Muscle

Duration of contraction of atrial and Shorter duration of contraction
ventricular mm is much longer than SKM
Excitatory/Conductive m contracts very Stronger contraction when compared to
“feebly” Excitatory m
Striation; myofibrils with actin and myosin; Same, but no latticework
latticework arrangement of muscle fibers
Intercalated discs separate cell membranes Individual cells, less connection (?)
of individual cardiac muscle cells- many cells
connected in series an in parallel
Permeable, communicating “gap” junctions No syncytium or gap junctions
at the intercalated discs = free diffusion of
ions = syncytium of hrt muscle cells allows
for easy spread of AP
Ventricular contraction lasts 15 times as long Shorter contraction period
as in SKM
AP average is 105 mV (from -85 to +20) on No plateau in AP; no delay
average

0.2 sec plateau visible before repolarization

AP caused by both fast Na+ channels and AP caused by sudden influx of Na+ (thru fast
slow Ca channels (Ca/Na channels); Ca sodium channels) Open only briefly before
channels slower to open and remain open abruptly closing
longer lengthening the AP and causing the
plateau
After onset of AP, membrane permeability for Permeability of K+ does not decrease; rapid
K+ decreases 5fold; decreases ouflux of + loss
charges, prolonging AP (rapid loss of K+
does occur when Ca/Na channels close)
Conduction of AP in atrial and ventricular m Faster conduction of AP
is 1/250 the velocity in large n fibers and
1/10 the velocity in SKM
Conduction in Purkinje fibers is 4m/sec…fast!
Has normal and relative refractory periods same
during AP
AP spreads through T-tubules to interior Same
AP then acts on SR to release Calcium ions Same
Extra Ca ions also diffuse into SR from T- No extra source of Ca, just from SR
tubules; increases strength of contraction b/c
SR not as extensive as in SKM
Strength of contraction varies depending on Not affected y extracellular fluid Ca
extracellular Ca content concentrations