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Excitation-Contraction Coupling Excitation-Contraction Coupling

 Once generated, the action potential:

 Is propagated along the sarcolemma  Myosin cross bridges alternately attach and detach

 Travels down the T tubules  Thin filaments move toward the center of the
 Triggers Ca2+ release from terminal cisternae
 Hydrolysis of ATP powers this cycling process
 Ca2+ binds to troponin and causes:
 Ca2+ is removed into the SR, tropomyosin blockage
 The blocking action of tropomyosin to cease is restored, and the muscle fiber relaxes
 Actin active binding sites to be exposed

Excitation-Contraction Coupling Role of Ionic Calcium (Ca2+) in the Contraction


 At low intracellular Ca2+

 Tropomyosin blocks the
binding sites on actin
 Myosin cross bridges
cannot attach to binding
sites on actin
 The relaxed state of the
muscle is enforced
Figure 9.9
Figure 9.10 (a)

Role of Ionic Calcium (Ca2+) in the Contraction Role of Ionic Calcium (Ca2+) in the Contraction
Mechanism Mechanism

 At higher intracellular Ca2+

 Calcium-activated
 Additional calcium binds troponin undergoes a
to troponin (inactive conformational change
troponin binds two Ca2+)
 This change moves
 Calcium-activated tropomyosin away from
troponin binds an actin’s binding sites
additional two Ca2+ at a
separate regulatory site
Figure 9.10 (b) Figure 9.10 (c)


Role of Ionic Calcium (Ca2+) in the Contraction Sequential Events of Contraction

 Cross bridge formation – myosin cross bridge
attaches to actin filament
 Myosin head can
now bind and cycle  Working (power) stroke – myosin head pivots and
pulls actin filament
 This permits
contraction (sliding  Cross bridge detachment – ATP attaches to myosin
of the thin filaments head and the cross bridge detaches
by the myosin cross
bridges) to begin  “Cocking” of the myosin head – energy from
hydrolysis of ATP cocks the myosin head into the
high-energy state
Figure 9.10 (d)

Sequential Events of Contraction Motor Unit: The Nerve-Muscle Functional Unit

Myosin head

1 Myosin cross bridge attaches to

the actin myofilament
Thin filament

Thick ADP and Pi (inorganic

filament phosphate) released

4 As ATP is split into ADP and Pi, 2 Working stroke—the myosin head pivots and
cocking of the myosin head occurs bends as it pulls on the actin filament, sliding it
toward the M line

Myosin head

3 As new ATP attaches to the myosin

head, the cross bridge detaches Figure 9.11 Figure 9.12 (a)

Motor Unit: The Nerve-Muscle Functional Unit Motor Unit: The Nerve-Muscle Functional Unit

 A motor unit is a motor neuron and all the muscle

fibers it supplies  Large weight-bearing muscles (thighs, hips) have
large motor units
 The number of muscle fibers per motor unit can vary
from four to several hundred  Muscle fibers from a motor unit are spread throughout
the muscle; therefore, contraction of a single motor
 Muscles that control fine movements (fingers, eyes) unit causes weak contraction of the entire muscle
have small motor units


Muscle Twitch Graded Muscle Responses

 A muscle twitch is the response of a muscle to a
single, brief threshold stimulus
 Graded muscle responses are:
 The three phases of a muscle twitch are:
 Variations in the degree of muscle contraction
 Latent period –
first few milli-  Required for proper control of skeletal movement
seconds after  Responses are graded by:
when excitation-  Changing the frequency of stimulation
coupling is  Changing the strength of the stimulus
taking place

Muscle Response to Varying Stimuli Muscle Response to Varying Stimuli

 A single stimulus results in a single contractile  More rapidly delivered stimuli result in incomplete
response – a muscle twitch tetanus
 Frequently delivered stimuli (muscle does not have  If stimuli are given quickly enough, complete
time to completely relax) increases contractile force tetanus results
– wave summation

Figure 9.14

Treppe: The Staircase Effect Muscle Fatigue

 Muscle fatigue – the muscle is in a state of physiological
inability to contract
 Staircase – increased contraction in response to  Muscle fatigue occurs when:
multiple stimuli of the same strength
 ATP production fails to keep pace with ATP use
 Contractions increase because:  There is a relative deficit of ATP, causing contractures
 There is increasing availability of Ca2+ in the  Lactic acid accumulates in the muscle
sarcoplasm  Ionic imbalances are present (extracellular potassium)
 Muscle enzyme systems become more efficient  Calcium deficiency
because heat is increased as muscle contracts  Neurotransmitter (ACH) rundown


Muscle Tone Muscle Metabolism: Energy for Contraction

 Is the constant, slightly contracted state of all

 ATP is the only source used directly for contractile
muscles, which does not produce active movements
 Keeps the muscles firm, healthy, and ready to
respond to stimulus  As soon as available stores of ATP are hydrolyzed
(4-6 seconds), they are regenerated by:
 Essential for maintaining posture (head upright)
 The interaction of ADP with creatine phosphate
 Essential for maintaining blood pressure (tone of (CP)
smooth muscles in walls of blood vessels)
 Anaerobic glycolysis
 Responding to activation of stretch receptors in
muscles and tendons  Aerobic respiration

Muscle Metabolism: Energy for Contraction Muscle Metabolism: Anaerobic Glycolysis

 When muscle contractile activity reaches 70% of

 Bulging muscles compress blood vessels
 Oxygen delivery is impaired
 Pyruvic acid is converted into lactic acid

Figure 9.18

Muscle Metabolism: Anaerobic Glycolysis Oxygen Debt

 Vigorous exercise causes dramatic changes in

muscle chemistry

 The lactic acid:  For a muscle to return to a resting state:

 Diffuses into the bloodstream  Oxygen reserves must be replenished

 Is picked up and used as fuel by the liver, kidneys,  Lactic acid must be converted to pyruvic acid
and heart  Glycogen stores must be replaced
 Is converted back into pyruvic acid by the liver  ATP and CP reserves must be resynthesized
 Oxygen debt – the extra amount of O2 needed for
the above restorative processes


Heat Production During Muscle Activity Force of Muscle Contraction

 The force of contraction is affected by:

 The number of muscle fibers contracting – the
 Only 40% of the energy released in muscle activity more motor fibers in a muscle, the stronger the
is useful as work contraction
 The remaining 60% is given off as heat  The relative size of the muscle – the bulkier the
 Dangerous heat levels are prevented by radiation of muscle, the greater its strength
heat from the skin and sweating  Degree of muscle stretch – muscles contract
strongest when muscle fibers are 80-120% of their
normal resting length

Isotonic Contractions Isometric Contractions

Figure 9.17 (b)

Muscle Fiber Type: Functional Characteristics Muscle Fiber Type: Speed of Contraction

 Speed of contraction – determined by speed in

which ATPases split ATP
 Slow oxidative fibers contract slowly, have slow
 The two types of fibers are slow and fast acting myosin ATPases, and are fatigue resistant
 ATP-forming pathways  Fast oxidative fibers contract quickly, have fast
 Oxidative fibers – use aerobic pathways myosin ATPases, and have moderate resistance to
 Glycolytic fibers – use anaerobic glycolysis
 Fast glycolytic fibers contract quickly, have fast
 These two criteria define three categories – slow myosin ATPases, and are easily fatigued
oxidative fibers, fast oxidative fibers, and fast
glycolytic fibers


Smooth Muscle Smooth Muscle

 Composed of spindle-shaped fibers with a diameter

of 2-10 m and lengths of several hundred m
 Lack the coarse connective tissue sheaths of skeletal
muscle, but have fine endomysium
 Organized into two layers (longitudinal and
circular) of closely apposed fibers
 Found in walls of hollow organs (except the heart)
 Have essentially the same contractile mechanisms
as skeletal muscle
Figure 9.24

Peristalsis Innervation of Smooth Muscle

 When the longitudinal layer contracts, the organ

dilates and contracts  Smooth muscle lacks neuromuscular junctions
 When the circular layer contracts, the organ  Innervating nerves have bulbous swellings called
elongates varicosities
 Peristalsis – alternating contractions and relaxations  Varicosities release neurotransmitters into wide
of smooth muscles that mix and squeeze substances synaptic clefts called diffuse junctions
through the lumen of hollow organs

Innervation of Smooth Muscle Microscopic Anatomy of Smooth Muscle

 SR is less developed than in skeletal muscle and lacks

a specific pattern
 T tubules are absent
 Ca2+ is sequestered in the extracellular space, allowing
rapid influx when channels are opened
 There are no visible striations and no sarcomeres
 Thin and thick filaments are present

Figure 9.25


Proportion and Organization of Myofilaments in Proportion and Organization of Myofilaments in

Smooth Muscle Smooth Muscle
 Ratio of thick to thin filaments is much lower than in
skeletal muscle
 Thick filaments have heads along their entire length
 There is no troponin complex
 Thick and thin filaments are arranged diagonally,
causing smooth muscle to contract in a corkscrew

Figure 9.26

Contraction of Smooth Muscle Contraction Mechanism

 Whole sheets of smooth muscle exhibit slow,
synchronized contraction  Actin and myosin interact according to the sliding
 They contract in unison, reflecting their electrical filament mechanism
coupling with gap junctions
 The final trigger for contractions is a rise in
 Action potentials are transmitted from cell to cell intracellular Ca2+
 Some smooth muscle cells:  Ca2+ is released from the SR and from the
extracellular space
 Act as pacemakers and set the contractile pace for
whole sheets of muscle  Ca2+ interacts with calmodulin and myosin light
 Are self-excitatory and depolarize without external chain kinase to activate myosin

Role of Calcium Ion Special Features of Smooth Muscle Contraction

 Ca2+ binds to calmodulin and activates it

 Activated calmodulin activates the kinase enzyme  Unique characteristics of smooth muscle include:

 Activated kinase transfers phosphate from ATP to  Smooth muscle tone

myosin cross bridges
 Slow, prolonged contractile activity
 Phosphorylated cross bridges interact with actin to
 Low energy requirements
produce shortening
 Response to stretch
 Smooth muscle relaxes when intracellular Ca2+
levels drop


Hyperplasia Developmental Aspects: Regeneration

 Certain smooth muscles can divide and increase  Cardiac and skeletal muscle become amitotic, but
their numbers by undergoing hyperplasia can lengthen and thicken
 This is shown by estrogen’s effect on the uterus  Smooth muscle has good regenerative ability
 At puberty, estrogen stimulates the synthesis of
more smooth muscle, causing the uterus to grow to
adult size
 During pregnancy, estrogen stimulates uterine
growth to accommodate the increasing size of the
growing fetus

Developmental Aspects: Male and Female Developmental Aspects: Age Related

 With age, connective tissue increases and muscle fibers decrease

 There is a biological basis for greater strength in
men than in women  Muscles become stringier and more sinewy
 By age 80, 50% of muscle mass is lost (sarcopenia)
 Women’s skeletal muscle makes up 36% of their
 Regular exercise can dramatically slow sarcopenia
body mass
 Aging of the cardiovascular system affects every organ in the body
 Men’s skeletal muscle makes up 42% of their body