muscles and muscle tissue: part c
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9. Muscles and Muscle Tissue: Part C. 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. Force of Muscle Contraction. - PowerPoint PPT PresentationTRANSCRIPT
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PowerPoint® Lecture Slides prepared by Janice Meeking, Mount Royal College
C H A P T E R
Copyright © 2010 Pearson Education, Inc.
9Muscles and Muscle Tissue: Part C
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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
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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
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Copyright © 2010 Pearson Education, Inc. Figure 9.21
Largenumber of
musclefibers
activated
Contractile force
Highfrequency ofstimulation
Largemusclefibers
Muscle andsarcomere
stretched to slightly over 100%of resting length
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Copyright © 2010 Pearson Education, Inc. Figure 9.22
Sarcomeresgreatly
shortened
Sarcomeres atresting length
Sarcomeres excessivelystretched
170%
Optimal sarcomereoperating length(80%–120% ofresting length)
100%75%
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Velocity and Duration of Contraction
Influenced by:
1. Muscle fiber type
2. Load
3. Recruitment
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Muscle Fiber Type – 2 characteristics
Classified according to two characteristics:
I. Speed of contraction: slow or fast, according to:
1) Speed at which myosin ATPases split ATP
2) Pattern of electrical activity of the motor neurons (i.e. changes in stimulus frequency and stimulus strength)
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Muscle Fiber Type – 2 characteristics
II. Metabolic pathways for ATP synthesis:
1) Oxidative fibers — use aerobic pathways
2) Glycolytic fibers — use anaerobic glycolysis
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Muscle Fiber Type – combining the 2
Results in 3 types:
1. Slow oxidative fibers
2. Fast oxidative fibers
3. Fast glycolytic fibers
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Copyright © 2010 Pearson Education, Inc. Table 9.2
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Copyright © 2010 Pearson Education, Inc. Figure 9.23
Predominanceof fast glycolytic(fatigable) fibers
Predominanceof slow oxidative(fatigue-resistant)
fibers
Small load
Contractilevelocity
Contractileduration
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Influence of Recruitment
Recruitment faster contraction and duration of contraction
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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
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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
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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
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Smooth Muscle
• Found in walls of most hollow organs(except heart)
• Usually in two layers (longitudinal and circular)
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Copyright © 2010 Pearson Education, Inc. Figure 9.26
Smallintestine
(a) (b) Cross section of theintestine showing thesmooth muscle layers(one circular and theother longitudinal)running at rightangles to each other.
Mucosa
Longitudinal layerof smooth muscle (shows smooth muscle fibers in cross section)
Circular layer ofsmooth muscle (shows longitudinalviews of smooth muscle fibers)
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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
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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
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Copyright © 2010 Pearson Education, Inc. Table 9.3
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Copyright © 2010 Pearson Education, Inc. Table 9.3
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Innervation of Smooth Muscle
• Autonomic nerve fibers innervate smooth muscle at diffuse junctions
• Varicosities (bulbous swellings) of nerve fibers store and release neurotransmitters
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Copyright © 2010 Pearson Education, Inc. Figure 9.27
Smoothmusclecell
Varicosities releasetheir neurotransmittersinto a wide synaptic cleft (a diffuse junction).
Synapticvesicles
Mitochondrion
Autonomicnerve fibersinnervatemost smoothmuscle fibers.
Varicosities
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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+
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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
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Copyright © 2010 Pearson Education, Inc. Figure 9.28a
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Copyright © 2010 Pearson Education, Inc. Figure 9.28b
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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
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Copyright © 2010 Pearson Education, Inc. Table 9.3
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Copyright © 2010 Pearson Education, Inc. Table 9.3
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Copyright © 2010 Pearson Education, Inc. Figure 9.29
Calcium ions (Ca2+)enter the cytosol fromthe ECF via voltage-dependent or voltage-independent Ca2+
channels, or fromthe scant SR.
ATP
Pi
Pi
Extracellular fluid (ECF)
ADP
Ca2+
Ca2+
Ca2+
Plasma membrane
Sarcoplasmicreticulum
Inactive calmodulin
Inactive kinase
Inactivemyosin molecule
Activated (phosphorylated)myosin molecule
Activated kinase
Activated calmodulin
Cytoplasm
Ca2+ binds to andactivates calmodulin.
Activated calmodulinactivates the myosinlight chain kinaseenzymes.
The activated kinase enzymescatalyze transfer of phosphateto myosin, activating the myosinATPases.
Activated myosin forms crossbridges with actin of the thinfilaments and shortening begins.
Thinfilament
Thickfilament
1
2
3
4
5
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Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 1
Calcium ions (Ca2+)enter the cytosol fromthe ECF via voltage-dependent or voltage-independent Ca2+
channels, or fromthe scant SR.
Extracellular fluid (ECF)Ca2+
Ca2+
Plasma membrane
Sarcoplasmicreticulum
Cytoplasm
1
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Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 2
Ca2+
Inactive calmodulin Activated calmodulin
Ca2+ binds to andactivates calmodulin.
2
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Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 3
Inactive kinase Activated kinase
Activated calmodulinactivates the myosinlight chain kinaseenzymes.
3
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Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 4
ATP
Pi
Pi
ADP
Inactivemyosin molecule
Activated (phosphorylated)myosin molecule
The activated kinase enzymescatalyze transfer of phosphateto myosin, activating the myosinATPases.
4
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Copyright © 2010 Pearson Education, Inc. Figure 9.29, step 5
Activated myosin forms crossbridges with actin of the thinfilaments and shortening begins.
Thinfilament
Thickfilament
5
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Copyright © 2010 Pearson Education, Inc. Figure 9.29
Calcium ions (Ca2+)enter the cytosol fromthe ECF via voltage-dependent or voltage-independent Ca2+
channels, or fromthe scant SR.
ATP
Pi
Pi
Extracellular fluid (ECF)
ADP
Ca2+
Ca2+
Ca2+
Plasma membrane
Sarcoplasmicreticulum
Inactive calmodulin
Inactive kinase
Inactivemyosin molecule
Activated (phosphorylated)myosin molecule
Activated kinase
Activated calmodulin
Cytoplasm
Ca2+ binds to andactivates calmodulin.
Activated calmodulinactivates the myosinlight chain kinaseenzymes.
The activated kinase enzymescatalyze transfer of phosphateto myosin, activating the myosinATPases.
Activated myosin forms crossbridges with actin of the thinfilaments and shortening begins.
Thinfilament
Thickfilament
1
2
3
4
5
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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
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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
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Regulation of Contraction
Hormones and local chemicals:
• May bind to G protein–linked receptors
• May either enhance or inhibit Ca2+ entry
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Special Features of Smooth Muscle ContractionStress-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
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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
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Copyright © 2010 Pearson Education, Inc. Table 9.3
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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
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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
• All muscle tissues develop from embryonic myoblasts• Multinucleated skeletal muscle cells form
by fusion • Growth factor agrin stimulates clustering
of ACh receptors at neuromuscular junctions• Cardiac and smooth muscle myoblasts
develop gap junctions
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Developmental Aspects
• Cardiac and skeletal muscle become amitotic, but can lengthen and thicken• Myoblast-like skeletal muscle satellite cells
have limited regenerative ability• Injured heart muscle is mostly replaced by
connective tissue• Smooth muscle regenerates throughout
life