Muscles and Muscle Tissue: Part C: Prepared by Janice Meeking, Mount Royal College

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PowerPoint® Lecture Slides

prepared by
Janice Meeking,
Mount Royal College

CHAPTER 9
Muscles and
Muscle
Tissue: Part C

Copyright © 2010 Pearson Education, Inc.


Force of Muscle Contraction

• The force of contraction is affected by:


• Number of muscle fibers stimulated
(recruitment)
• Relative size of the fibers—hypertrophy of
cells increases strength

Copyright © 2010 Pearson Education, Inc.


Force of Muscle Contraction

• The force of contraction is affected by:


• Frequency of stimulation— frequency allows
time for more effective transfer of tension to
noncontractile components
• Length-tension relationship—muscles contract
most strongly when muscle fibers are 80–
120% of their normal resting length

Copyright © 2010 Pearson Education, Inc.


Large Muscle and
number of sarcomere
muscle Large High stretched to
fibers muscle frequency of slightly over 100%
activated fibers stimulation of resting length

Contractile force

Copyright © 2010 Pearson Education, Inc. Figure 9.21


Sarcomeres Sarcomeres at Sarcomeres excessively
greatly resting length stretched
shortened

75% 100% 170%

Optimal sarcomere
operating length
(80%–120% of
resting length)

Copyright © 2010 Pearson Education, Inc. Figure 9.22


Velocity and Duration of Contraction

Influenced by:
1. Muscle fiber type
2. Load
3. Recruitment

Copyright © 2010 Pearson Education, Inc.


Muscle Fiber Type

Classified according to two characteristics:


1. Speed of contraction: slow or fast,
according to:
• Speed at which myosin ATPases split ATP
• Pattern of electrical activity of the motor
neurons

Copyright © 2010 Pearson Education, Inc.


Muscle Fiber Type

2. Metabolic pathways for ATP synthesis:


• Oxidative fibers—use aerobic pathways
• Glycolytic fibers—use anaerobic glycolysis

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Muscle Fiber Type

Three types:
• Slow oxidative fibers
• Fast oxidative fibers
• Fast glycolytic fibers

Copyright © 2010 Pearson Education, Inc.


Copyright © 2010 Pearson Education, Inc. Table 9.2
Predominance Small load Predominance
of fast glycolytic of slow oxidative
(fatigable) fibers (fatigue-resistant)
fibers

Contractile Contractile
velocity duration

Copyright © 2010 Pearson Education, Inc. Figure 9.23


FO

SO

FG

Copyright © 2010 Pearson Education, Inc. Figure 9.24


Effects of Exercise

Aerobic (endurance) exercise:


• Leads to increased:
• Muscle capillaries
• Number of mitochondria
• Myoglobin synthesis
• Results in greater endurance, strength, and
resistance to fatigue
• May convert fast glycolytic fibers into fast oxidative
fibers

Copyright © 2010 Pearson Education, Inc.


Effects of Resistance Exercise

• Resistance exercise (typically anaerobic)


results in:
• Muscle hypertrophy (due to increase in fiber
size)
• Increased mitochondria, myofilaments,
glycogen stores, and connective tissue

Copyright © 2010 Pearson Education, Inc.


The Overload Principle

• Forcing a muscle to work hard promotes


increased muscle strength and endurance
• Muscles adapt to increased demands
• Muscles must be overloaded to produce
further gains

Copyright © 2010 Pearson Education, Inc.


Smooth Muscle

• Found in walls of most hollow organs


(except heart)
• Usually in two layers (longitudinal and
circular)

Copyright © 2010 Pearson Education, Inc.


Longitudinal layer
of smooth muscle
(shows smooth
muscle fibers in
cross section)

Small
intestine Mucosa

(a) (b) Cross section of the Circular layer of


intestine showing the smooth muscle
smooth muscle layers (shows longitudinal
(one circular and the views of smooth
other longitudinal) muscle fibers)
running at right
angles to each other.

Copyright © 2010 Pearson Education, Inc. Figure 9.26


Peristalsis

• Alternating contractions and relaxations of


smooth muscle layers that mix and squeeze
substances through the lumen of hollow
organs
• Longitudinal layer contracts; organ dilates and
shortens
• Circular layer contracts; organ constricts and
elongates

Copyright © 2010 Pearson Education, Inc.


Microscopic Structure

• Spindle-shaped fibers: thin and short


compared with skeletal muscle fibers
• Connective tissue: endomysium only
• SR: less developed than in skeletal muscle
• Pouchlike infoldings (caveolae) of
sarcolemma sequester Ca2+
• No sarcomeres, myofibrils, or T tubules

Copyright © 2010 Pearson Education, Inc.


Copyright © 2010 Pearson Education, Inc. Table 9.3
Innervation of Smooth Muscle

• Autonomic nerve fibers innervate smooth


muscle at diffuse junctions
• Varicosities (bulbous swellings) of nerve fibers
store and release neurotransmitters

Copyright © 2010 Pearson Education, Inc.


Varicosities

Autonomic Smooth
nerve fibers muscle
innervate cell
most smooth
muscle fibers.

Synaptic Mitochondrion Varicosities release


vesicles their neurotransmitters
into a wide synaptic
cleft (a diffuse junction).
Copyright © 2010 Pearson Education, Inc. Figure 9.27
Myofilaments in Smooth Muscle

• Ratio of thick to thin filaments (1:13) is much


lower than in skeletal muscle (1:2)
• Thick filaments have heads along their entire
length
• No troponin complex; protein calmodulin binds
Ca2+

Copyright © 2010 Pearson Education, Inc.


Myofilaments in Smooth Muscle

• Myofilaments are spirally arranged, causing


smooth muscle to contract in a corkscrew
manner
• Dense bodies: proteins that anchor
noncontractile intermediate filaments to
sarcolemma at regular intervals

Copyright © 2010 Pearson Education, Inc.


Copyright © 2010 Pearson Education, Inc. Figure 9.28a
Copyright © 2010 Pearson Education, Inc. Figure 9.28b
Contraction of Smooth Muscle

• Slow, synchronized contractions


• Cells are electrically coupled by gap junctions
• Some cells are self-excitatory (depolarize
without external stimuli); act as pacemakers
for sheets of muscle
• Rate and intensity of contraction may be
modified by neural and chemical stimuli

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Contraction of Smooth Muscle

• Sliding filament mechanism


• Final trigger is  intracellular Ca2+
• Ca2+ is obtained from the SR and extracellular
space

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Role of Calcium Ions

• Ca2+ binds to and activates calmodulin


• Activated calmodulin activates myosin (light
chain) kinase
• Activated kinase phosphorylates and activates
myosin
• Cross bridges interact with actin

Copyright © 2010 Pearson Education, Inc.


Copyright © 2010 Pearson Education, Inc. Table 9.3
Copyright © 2010 Pearson Education, Inc. Table 9.3
Extracellular fluid (ECF)
Ca2+
Plasma membrane

Cytoplasm

1 Calcium ions (Ca2+)


enter the cytosol from
the ECF via voltage-
dependent or voltage- Ca2+
independent Ca2+
channels, or from
the scant SR.

2 Ca2+ binds to and Sarcoplasmic


activates calmodulin. reticulum

Ca2+

Inactive calmodulin Activated calmodulin

3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase Activated kinase

4 The activated kinase enzymes ATP


catalyze transfer of phosphate
to myosin, activating the myosin ADP
ATPases.

Pi
Pi

Inactive Activated (phosphorylated)


myosin molecule myosin molecule

5 Activated myosin forms cross


bridges with actin of the thin
filaments and shortening begins.

Thin
filament

Thick
filament

Copyright © 2010 Pearson Education, Inc. Figure 9.29


Extracellular fluid (ECF)
Ca2+
Plasma membrane

Cytoplasm

1 Calcium ions (Ca2+)


enter the cytosol from
the ECF via voltage-
dependent or voltage-
Ca2+
independent Ca2+
channels, or from
the scant SR.

Sarcoplasmic
reticulum

Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 1


2 Ca2+ binds to and
activates calmodulin.

Ca2+

Inactive calmodulin Activated calmodulin

Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 2


3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase Activated kinase

Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 3


4 The activated kinase enzymes ATP
catalyze transfer of phosphate
to myosin, activating the myosin ADP
ATPases.

Pi
Pi

Inactive Activated (phosphorylated)


myosin molecule myosin molecule

Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 4


5 Activated myosin forms cross
bridges with actin of the thin
filaments and shortening begins.

Thin
filament

Thick
filament

Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 5


Extracellular fluid (ECF)
Ca2+
Plasma membrane

Cytoplasm

1 Calcium ions (Ca2+)


enter the cytosol from
the ECF via voltage-
dependent or voltage- Ca2+
independent Ca2+
channels, or from
the scant SR.

2 Ca2+ binds to and Sarcoplasmic


activates calmodulin. reticulum

Ca2+

Inactive calmodulin Activated calmodulin

3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase Activated kinase

4 The activated kinase enzymes ATP


catalyze transfer of phosphate
to myosin, activating the myosin ADP
ATPases.

Pi
Pi

Inactive Activated (phosphorylated)


myosin molecule myosin molecule

5 Activated myosin forms cross


bridges with actin of the thin
filaments and shortening begins.

Thin
filament

Thick
filament

Copyright © 2010 Pearson Education, Inc. Figure 9.29


Contraction of Smooth Muscle

• Very energy efficient (slow ATPases)


• Myofilaments may maintain a latch state for
prolonged contractions
Relaxation requires:
• Ca2+ detachment from calmodulin
• Active transport of Ca2+ into SR and ECF
• Dephosphorylation of myosin to reduce
myosin ATPase activity

Copyright © 2010 Pearson Education, Inc.


Regulation of Contraction

Neural regulation:
• Neurotransmitter binding   [Ca2+] in
sarcoplasm; either graded (local) potential or
action potential
• Response depends on neurotransmitter
released and type of receptor molecules

Copyright © 2010 Pearson Education, Inc.


Regulation of Contraction

Hormones and local chemicals:


• May bind to G protein–linked receptors
• May either enhance or inhibit Ca2+ entry

Copyright © 2010 Pearson Education, Inc.


Special Features of Smooth Muscle
Contraction
Stress-relaxation response:
• Responds to stretch only briefly, then adapts
to new length
• Retains ability to contract on demand
• Enables organs such as the stomach and
bladder to temporarily store contents
Length and tension changes:
• Can contract when between half and twice its
resting length

Copyright © 2010 Pearson Education, Inc.


Special Features of Smooth Muscle
Contraction
Hyperplasia:
• Smooth muscle cells can divide and increase
their numbers
• Example:
• estrogen effects on uterus at puberty and
during pregnancy

Copyright © 2010 Pearson Education, Inc.


Copyright © 2010 Pearson Education, Inc. Table 9.3
Types of Smooth Muscle

Single-unit (visceral) smooth muscle:


• Sheets contract rhythmically as a unit (gap
junctions)
• Often exhibit spontaneous action potentials
• Arranged in opposing sheets and exhibit
stress-relaxation response

Copyright © 2010 Pearson Education, Inc.


Types of Smooth Muscle: Multiunit

Multiunit smooth muscle:


• Located in large airways, large arteries,
arrector pili muscles, and iris of eye
• Gap junctions are rare
• Arranged in motor units
• Graded contractions occur in response to
neural stimuli

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Developmental Aspects

• Muscular development reflects neuromuscular


coordination
• Development occurs head to toe, and
proximal to distal
• Peak natural neural control occurs by
midadolescence
• Athletics and training can improve
neuromuscular control

Copyright © 2010 Pearson Education, Inc.


Developmental Aspects

• Female skeletal muscle makes up 36% of


body mass
• Male skeletal muscle makes up 42% of body
mass, primarily due to testosterone
• Body strength per unit muscle mass is the
same in both sexes

Copyright © 2010 Pearson Education, Inc.


Developmental Aspects

• With age, connective tissue increases and


muscle fibers decrease
• By age 30, loss of muscle mass (sarcopenia)
begins
• Regular exercise reverses sarcopenia
• Atherosclerosis may block distal arteries,
leading to intermittent claudication and severe
pain in leg muscles

Copyright © 2010 Pearson Education, Inc.


Muscular Dystrophy

• Group of inherited muscle-destroying


diseases
• Muscles enlarge due to fat and connective
tissue deposits
• Muscle fibers atrophy

Copyright © 2010 Pearson Education, Inc.


Muscular Dystrophy

Duchenne muscular dystrophy (DMD):


• Most common and severe type
• Inherited, sex-linked, carried by females and
expressed in males (1/3500) as lack of dystrophin
• Victims become clumsy and fall frequently; usually die
of respiratory failure in their 20s
• No cure, but viral gene therapy or infusion of stem
cells with correct dystrophin genes show promise

Copyright © 2010 Pearson Education, Inc.

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