Muscles
Skeletal
Cardiac
Smooth
Appearance
Striated, multiple peripheral nuclei,
muscle fiber runs length of whole
muscle
Striated, one nuclei, branching, cell
doesn’t extend length of heart
No striations, single nuclei centrally
located
Organization
Whole muscle  bundle of fascicles
 bundles of muscle fibers 
myofibrils (repeating sarcomere units)
 thin and thick filaments
Functional syncytia b/c of intercalated
disks (gap junctions) b/w cardiac cells
Sheet or bundles of fusiform (spindle-like)
cells
Connective tissue holding cells together
help them act in unison
Deep fascia  epimysium 
perimysium  endomysium
- All continuous w/ each other
Voluntary
Involuntary
Involuntary
Contractions
Rapid and sustained, not as strong of
a force as smooth
Rhythmic and coordinated, can be
rapid
Sustained, Greater force but slower
contraction
Filaments
Thin
F-Actin
-Tropomyosin
-Troponin
- C = Ca2+ binding site
- I = inhibitory  block acting
binding to myosin
- T = troponin  bind troponin to
tropomyosin
Same as skeletal except:
Thin
- Caldesmon and calponin (no troponin)
- Decrease Ca2+ b/c block cross-bridge
formation
Control
Thick
Myosin
- Bipolar
Both thin and thick attach to Z discs
Isoforms of troponin
- Troponin I (cTnI)
- Troponin T (cTnT)
- Both released in acute
myocardial infarction
Thick
-Side polar (no bare-zone)
- allows greater shortening of contracted
through α-actin and titin, respectively
units = greater force but slower
contraction
No Z discs or sarcomeres
Filaments attach to α-actin dense bodies
 bind to dense plaques  link cells
together = even contraction
Contractile unit align w/ long axis of cell
Fiber Arrangement
Linear (predominant) or Circular
Cytoskeleton
Dystrophin  connect sarcomere to
sarcolemma, basal lamina, and ECM
Preload
(tension in muscle b4
contraction)
This ensures force throughout all
fascia
Optimized at resting length (halfstretch)
Branching
Linear or Circular (predominant)
Desmin and vimentin  connect dense
bodies to dense plaques
Optimized at relaxed state (fully
stretched)
Action Potential (AP)
Always results in maximal release of
Ca2+ from SR
Short absolute refractory period =
twitches can summate (tetanus)
Ca2+ released from SR is modified by
ANS b/c one L-type channel to one
Ca2+ release channel… how ANS
controls heart rate
Depolarization
Not at the same time unless in muscle
fibers are in the same motor unit
Absolute refractory period is long =
plateau of AP
- can’t summate AP
- allows ventricles to fully
empty
All cells depolarize at same time =
rhythmic heartbeat
Sarcoplasmic
Reticulum (SR)
Triad at A/I band junction
Diads at Z line
Terminal cisternae : T-tubule :
terminal cisternae
T-tubules encircle each sarcomere of
each myofibril
See Calcium
Caveolus… No t-tubules
Calcium
(diagrams under table)
Neural (excitation-contraction coupling)
AP  voltage gated L-type Ca2+
channels  increase cytosolic Ca2+
via L-type Ca2+ receptors (not used
for contraction)
AND
AP  voltage gated L-type Ca2+
channels  mechanical activation of
Ca2+ release channels in SR 
increase cytosolic Ca2+  contraction
Ca2+ release channels in SR can also
respond to membrane depolarization
Neural
AP  voltage gated L-type Ca2+
channels  increase cytosolic Ca2+
(but not enough to contract)  Ca2+
induced Ca2+ release channels in SR
 increase cytosolic Ca2+ 
contraction
Chemical
- use hormones to increase
contractility and heart rate
- epinephrine and
norephinephrin  β1
adrenergic receptors 
cAMP  PKA 
phosphorylates 2 things
1. L-type Ca2+ channel = stays
open
2. phospholamban  inactive so
doesn’t inhibit SERCA  quicker
resequesteration = quicker heart
rate
Neural (effect a bunch of cells)
AP  L-type Ca2+ channels  increase
cytosolic Ca2+  open Ca2+ in SR
Chemical (local, only a few cells)
ANS  varicosities (neurotransmitter
vesicles)  chemical synapse 
hormone  IP3  open Ca2+ in SR 
increase cytosolic Ca2+
Cross-bridge
Formation
Termination of
Contraction
Types
Thin filament regulated
- b/c myosin activity is intrinsic
Resequesteration of Ca2+ to SR by
SERCA pump
- Ca2+ bind to calreticulin and
calsequestrin once in SR to keep
concentration gradient
Thin filament regulated
Thick filament regulated
- b/c myosin ATPase is not intrinsic
Ca2+  calmodulin  MLCK 
phosphorylates regulatory light chain w/
one ATP on myosin  myosin binds to
actin  still need one more ATP for
powerstroke
Myosin phosphatase
- Decreased Ca2+ alone does NOT
stop contraction
- Works when calcium concentration
is decreased
Na+/ Ca2+ exchanger – move Ca2+ to
extracellular space (minor
mechanism)
SERCA Pump
Red (Type 1), White (Type 2b),
Intermediate (Type 2a)
Phasic
- Contracts in waves/phases
(autorhythmic)
Ca2+ store pump brings in extracellular
Ca2+ when cell has lost too much
See chart below
-
Single unit – multiple cells
innervated by one neuron through
gap junctions (electrical coupling)
Tonic
- Maintain steady contraction
- Can be summated
- Multiple unit – one cell innervated by
one neuron
- Latch state - Ca2+ decreases less
rapidly = sustained contractile force
b/c cross-bridge remains awhile
even after myosin phosphatase (no
ATP consumed to hold contraction)
Miscellaneous
Graded muscle responses
- Stimulation frequency –
summating in time, add AP’s
together b4 contraction happens
= tetanus/fused tetanus =
increased cytosolic Ca2+ =
stronger contraction b/c more
cross-bridges
- Stimulation intensity –
Internal Pacemaker
- spontaneously depolarizes
(makes own AP) to set heart
rate
- does not require external AP
Cardiac muscle cells can only repair
by fibrosis… if you have a heart
attack than heart become more
Can do hypertrophy or hyperplasia
Length adaptation – maintain maximal
tension at non-optimal tension
summating in space – more
axon processes per one motor
neuron = increase in Ca2+ =
stronger contraction
fibrotic (bad)
Satellite cells (unspecialized
myoblasts)
- muscle repair usually by fibrosis
- they divide then combine at site
of injury and join up w/ preexisting muscle fiber to close
injury
Muscle fatigue
- decreased glycogen
- loss of electrolytes
- CNR reduce output
Calcium Release
Skeletal:
Cardiac:
Smooth: