Cellular Movement and

Muscles

Chapter 5; Part2 06.10.2010

CONTRACTION-RELAXATION CYCLE
AP arrives at NM junction
ACh release
postsynaptic depolarization above threshold
muscle action potential
depolarization of sarcolemma and T tubules
conformational change in dihydropyridine receptors
movement of ryanodine
SR Ca2+ channels open briefly
increase in sarcoplasmic [Ca2+]
Ca2+ binding to troponin C
conformational change in troponin
movement of tropomyosin
exposure of binding sites of actin
myosin heads attach
cross-bridge cycling in presence of Ca2+ and ATP
filament sliding
sarcomere shortening
Ca2+ uptake and sequestration in SR
sarcoplasmic [Ca2+]
inhibition of binding site; muscle relaxes

MOTOR UNIT
One motor neuron
Muscle fibers innervated by that neuron
1 AP in motor neuron
twitch in all muscle fibres in that
motor unit
all muscle fibres in a motor unit
are same metabolic type
GRADATION IN STRENGTH OF
MUSCULAR CONTRACTION
BY RECRUITMENT
increase in number of active motor
units

BY SUMMATION
increase in frequency of AP in motor unit
twitches summate to tetanus

Excitation of Vertebrate Striated Muscle

Skeletal muscle and cardiac muscle differ in
mechanism of excitation and EC coupling
Differences include
Initial cause of depolarization
Time course of the change in membrane potential
(action potential)
Propagation of the action potential along the
sarcolemma
Cellular origins of Ca2+

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Action Potentials
APs along sarcolemma signal contraction
Na+ enters cell when Na+ channels open
Depolarization

Voltage-gated Ca2+ channel open

Increase in cytoplasmic [Ca2+]

Na+ channels close

K+ leave cell when K+ channels open
Repolarization

Reestablishment of ion gradients by Na+/K+ ATPase

and Ca2+ ATPase

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Initial Cause of Depolarization

Myogenic (beginning in the muscle)
Spontaneous
For example, vertebrate heart

Pacemaker cells
Cells that depolarize fastest
Unstable resting membrane potential

Neurogenic (beginning in the nerve)

Excited by neurotransmitters from motor nerves
For example, vertebrate skeletal muscle

Can have multiple (tonic) or single (twitch)

innervation sites
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Neurogenic Muscle
Twitch muscles:
Motor neurons innervate individual
myofibers, making contacts at
regions on the myofiber called motor
end plates. Twitch muscles possess
myofibers that are innervated by
single motor neuron.
In these muscles the AP spreads
rapidly along the sarcolemma,
causing a uniform contraction along
the length of the myofiber.

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Figure 5.25

Uniform depolarization of sarcolemma

Because of their electrical nature, APs move rapidly, but in
many muscles passive conductance from the motor end
plate is inadequate to ensure that the signal reaches the
entire muscle essentially simultaneously.

There are two main ways that muscles are able to ensure
the entire sarcolemma is depolarized uniformly in space
and time: through multiple innervations (tonic muscle) and
through invaginations of the sarcolemma (T-tubules) that
penetrate deep into the myofiber to speed the spread of the
AP.

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Figure 5.25

Tonic Muscle
Tonic muscles are vertebrate striated muscles with multiple
innervations.
When motor neurons are stimulated, neurotransmitter
release occures at many sites along the tonic muscle fiber.
Tonic muscles contract slowly, but maintain tension for
long periods.
In contrast to twitch muscles, tonic muscles are not all-ornone. The level of depolarization of the sarcolemma
depends on the number and frequency of stimulatory
signals from the motor neuron.

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Figure 5.25

T-Tubules and Sarcoplasmic Reticulum

Transverse tubules (T-tubules)
Invaginations of sarcolemma
(cell membrane of a muscle
fiber)
Enhance penetration of
action potential into
myocyte
More developed in larger,
faster twitching muscles
Less developed in cardiac
muscle
Sarcoplasmic reticulum (SR)
Stores Ca2+ bound to protein
sequestrin
Terminal cisternae increase
storage
T-tubules and terminal cisternae
are adjacent to one another
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Figure 5.28

Fig. 5.28

CALCIUM CHANNELS IN SR

CALCIUM CHANNELS IN SR
In skeletal muscle,
conformational change in DHP receptor
in T tubule
mechanical interaction with ryanodine
receptor in SR
opening of Ca2+ channels in
sarcoplasmic reticulum
SR main source of Ca2+
In cardiac muscle,
conformational change in DHP receptor
in T tubule
Ca2+ enters from ECF
[Ca2+] activates ryanodine receptors
opening of Ca2+ channels in
sarcoplasmic reticulum
ECF and SR sources of Ca2+

Ca2+ Channels and Transporters Involved in EC Coupling

Channels allow Ca2+
to enter cytoplasm
Ca2+ channels in
cell membrane
Dihydropyri
dine
receptor
(DHPR)
Ca2+ channels in
the SR
membrane
Ryanodine
receptor
(RyR)

Transporters remove Ca2+ from cytoplasm

Ca2+ transporters in cell membrane
Ca2+ ATPase
Na+/Ca2+ exchanger (NaCaX)
Ca2+ transporters in SR membrane
Ca2+ ATPase (SERCA)

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Figure 5.27

Induction of Ca2+ Release From SR

AP along sarcolemma conducted down T-tubules
Depolarization opens DHPR
Ca2+ enters cell from extracellular fluid
In heart, [Ca2+] causes RyR to open, allowing release of
Ca2+ from SR
Ca2+ induced Ca2+ release
In skeletal muscle, change in DHPR shape causes RyR to
open, allowing release of Ca2+ from SR
Depolarization induced Ca2+ release

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Ca2+ Induced Ca2+ Release

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Figure 5.29

Depolarization Induced Ca2+ Release

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Figure 5.30

Relaxation
Repolarization of sarcolemma
Remove Ca2+ from cytoplasm
Ca2+ ATPase in sarcolemma and SR
Na+/Ca2+ exchanger (NaCaX) in sarcolemma
Parvalbumin
Cytosolic Ca2+ binding protein buffers Ca2+

Ca2+ dissociates from troponin

Tropomyosin blocks myosin binding sites
Myosin can no longer bind to actin

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SOURCES OF ENERGY FOR MUSCLE CONTRACTION

ATP
required for :
detachment of myosin head
during cross-bridge cycling
pumping Ca2+ into SR

Factors Determining Muscle-Fibre Properties

membrane properties
ATPase activity
x-bridge cycling rate
slow vs fast contraction rate
SR Ca2+ - pumping rate
short vs long duration of elevated [Ca2+] in ICF
[mitochondria]
[myoglobin]
blood supply
resistance to fatigue (low vs high)

FATIGUE
cellular ACh depletion
ATP depletion (affects excitation contraction coupling)
lactic acid, pH Ca2+ pumping
Ca2+ enters ECF
fast motor units fatigue first

Time Course of Depolarization

While the contraction
profiles are similar, the
action potential in cardiac
muscle is prolonged. This
is attributed to Ca2+
channels remaining open.

Cardiac muscle
extended repolarization
plateau phase
long refractory period
tetanus can not occur

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Figure 5.24

1 MAP 1 twitch
all-or-none responses
many MAPs tetanus

Summation of contraction
with repeated rapid stimulation:
Ca 2+ released from SR into sarcoplasm faster than Ca2+ pumps remove Ca2+ from
sarcoplasm
prolonged availability of binding sites for myosin heads maximum contraction

Twitch

minimum all-or-none muscular

contraction due to single MAP in
response to single AP in motor neuron

Tetanus
sustained muscular contraction due to
(electrophysio.) summation of twitches resulting from high-frequency of
APs from motor neuron
Tetanus (medical)

tetanic contraction of muscles due to

tetanus toxin produced by Clostridium tetani
Blocks release of glycine from inhibitory
neurons synapsing on cell body of motor
neuron in CNS
AP
rigid paralysis

N.B. botulinum toxin produced by Clostridium botulinum

Blocks release of ACh at NM junction
no stimulation of skeletal muscle
flacid paralysis

Cardiac action potentials

synchronization of APs in different parts of the heart
role of gap junctions
long duration of cardiac AP
long refractory period
twitch, but no tetanus
muscle cells relax between each
heart beat

Fig. 8.26

EXCITATION OF THE HEART

Fig. 8.27

VERTEBRATE HEART IS MYOGENIC

i.e. self-excitable rhythmic instrinsic contractility
all cardiac cells are electrically coupled
cardiac cells with fastest intrinsic activity set pace
Normal pacemaker is the SINOATRIAL NODE
Heart beat: begins at SA node
spreads through atria
delayed at AV node
spreads through ventricles

Cardiac muscle - myogenic

pacemaker potential
gCa2+ gK+ (SA NODE )
gNa+ gK+ (ventricular pacemaker)

Fig. 8.24 The effects of norepinephrine on heart rate

Fig. 8.25 The effects of acetylcholine on heart rate

Summary of Striated Muscles

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Table 5.5