bio 238 copyright 2010, john wiley & sons, inc. muscular system
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BIO 238
Copyright 2010, John Wiley & Sons, Inc.
Muscular System
Overview of Muscular TissueTypes of Muscular Tissue
SkeletalCardiacSmooth
Functions of Muscular TissueProducing Body Movements
Walking and runningStabilizing Body Positions
PostureMoving Substances Within the Body
Heart muscle pumping bloodMoving substances in the digestive tract
Generating heatContracting muscle produces heatShivering increases heat production
Skeletal Muscle Tissue
Copyright 2010, John Wiley & Sons, Inc.
Skeletal Muscle TissueSo named because most skeletal muscles move bonesSkeletal muscle tissue is striated:
Alternating light and dark bands (striations) as seen when examined with a microscope
Skeletal muscle tissue works mainly in a voluntary manner Its activity can be consciously controlled
Most skeletal muscles also are controlled subconsciously to some extentEx: the diaphragm alternately contracts and relaxes
without conscious control
Skeletal Muscle Tissue
Skeletal Muscle TissueConnective Tissue Components
FasciaDense sheet or broad band of irregular connective
tissue that surrounds musclesEpimysium
The outermost layerSeparates 10–100 muscle fibers into bundles called
fasciclesPerimysium
Surrounds numerous bundles of fasciclesEndomysium
Separates individual muscle fibers from one anotherTendon
Cord that attach a muscle to a boneAponeurosis
Broad, flattened tendon
Skeletal Muscle TissueSarcolemma
The plasma membrane of a muscle cellTransverse (T) tubules
Connect the plasma membrane to the interior of the cellMuscle action potentials travel through the T tubulesEnsure that action potential excites all parts of the muscle
fiber at the same timeSarcoplasm, the cytoplasm of a muscle fiber
Sarcoplasm includes glycogen used for synthesis of ATP and a red-colored protein called myoglobin which binds oxygen molecules
Myoglobin releases oxygen when it is needed for ATP production
Skeletal Muscle TissueNerve and Blood Supply
Neurons that stimulate skeletal muscle to contract are somatic motor neurons
The axon of a somatic motor neuron typically branches many timesEach branch extending to a different skeletal
muscle fiberEach muscle fiber is in close contact with
one or more capillaries
Skeletal Muscle TissueMicroscopic Anatomy
The number of skeletal muscle fibers is set before you are bornMost of these cells last a lifetime
Muscle growth occurs by hypertrophyAn enlargement of existing muscle fibers
Testosterone and human growth hormone stimulate hypertrophy
Satellite cells retain the capacity to regenerate damaged muscle fibers
Skeletal Muscle TissueMyofibrils
Thread-like structures which have a contractile function
Sarcoplasmic reticulum (SR)Membranous sacs which encircles each myofibrilStores calcium ions (Ca2+)Release of Ca2+ triggers muscle contraction
SarcomeresCompartments of arranged filamentsBasic contractile unit of a myofibril
FilamentsFunction in the contractile processTwo types of filaments (Thick Myosin and Thin Actin)There are two thin filaments for every thick filament
Organization of Skeletal Muscle
Myofibril and Filaments
Contraction and Relaxation of Skeletal Muscle
The Sliding Filament MechanismMyosin heads attach to and “walk” along
the thin filaments at both ends of a sarcomere
Progressively pulls the thin filaments toward the center of the sarcomere
The sarcomere shortensLeads to shortening of the entire muscle
Contraction and Relaxation of Skeletal Muscle
Contraction and Relaxation of Skeletal Muscle The Neuromuscular Junction
Motor neurons have a threadlike axon that extends from the brain or spinal cord to a group of muscle fibers
Action potentials arise at the interface of the motor neuron and muscle fiber
SynapseWhere communication occurs between a somatic motor neuron
and a muscle fiber Synaptic cleft
Gap that separates the two cells Neurotransmitter
Chemical released by the initial cell communicating with the second cell
Synaptic vesiclesSacs suspended within the synaptic end bulb containing
molecules of the neurotransmitter acetylcholine (Ach) Motor end plate
The region of the muscle cell membrane opposite the synaptic end bulbs
Contains acetylcholine receptors
Contraction and Relaxation of Skeletal MuscleNerve impulses elicit a muscle action
potential in the following way(1) Release of acetylcholine
Nerve impulse arriving at the synaptic end bulbs causes many synaptic vesicles to release ACh into the synaptic cleft
(2) Activation of ACh receptorsBinding of ACh to the receptor on the motor end plate opens
an ion channelAllows flow of Na+ to the inside of the muscle cell
(3) Production of muscle action potentialThe inflow of Na+ makes the inside of the muscle fiber more
positively charged, triggering a muscle action potentialThe muscle action potential then propagates to the SR to
release its stored Ca2+
(4) Termination of ACh activityACh effects last only briefly because it is rapidly broken down
by acetylcholinesterase (AChE)
Neuromuscular JunctionsInteractions AnimationsNeuromuscular Junctions
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Contraction and Relaxation of Skeletal MuscleThe contraction cycle consists of 4 steps
ATP hydrolysisReorients and energizes the myosin head
Formation of cross-bridgesOnce myosin binds to the actin, active sites become
available. Myosin head attaches to active site on actinPower stroke
The myosin head pivots (power stroke) and causes the cross-bridge rotates, sliding the filaments towards the center of the sarcomere.
Detachment of myosin from actinAs the next ATP binds to the myosin head, the myosin
head detaches from actinThe contraction cycle repeats as long as ATP is available
and the Ca2+ level is sufficiently highContinuing cycles apply the force that shortens the
sarcomere
Copyright 2010, John Wiley & Sons, Inc.
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptor
Muscle action potential
Nerveimpulse
1
ACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptor
Muscle action potential
Nerveimpulse
1
2 ACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron.
Muscle action potential
Nerveimpulse
1
2
3
ACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+
Muscle action potential
Nerveimpulse
SR
Muscle AP travelling alongtransverse tubule opens Ca2+
release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.
1
2
3
4
Transverse tubuleACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+
Muscle action potential
Nerveimpulse
SR
Ca2+ binds to troponin onthe thin filament, exposingthe binding sites for myosin.
Muscle AP travelling alongtransverse tubule opens Ca2+
release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.
1
2
3
4
5
Transverse tubuleACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+
Muscle action potential
Nerveimpulse
SR
Contraction: power strokesuse ATP; myosin heads bindto actin, swivel, and release;thin filaments are pulled towardcenter of sarcomere.
Ca2+ binds to troponin onthe thin filament, exposingthe binding sites for myosin.
Muscle AP travelling alongtransverse tubule opens Ca2+
release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.
Elevated Ca2+
1
2
3
4
5
6
Transverse tubuleACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+
Muscle action potential
Nerveimpulse
SR
Contraction: power strokesuse ATP; myosin heads bindto actin, swivel, and release;thin filaments are pulled towardcenter of sarcomere.
Ca2+ activetransport pumps
Ca2+ release channels inSR close and Ca2+ activetransport pumps use ATPto restore low level of Ca2+ in sarcoplasm.
Ca2+ binds to troponin onthe thin filament, exposingthe binding sites for myosin.
Muscle AP travelling alongtransverse tubule opens Ca2+
release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.
Elevated Ca2+
1
2
3
4
5
67
Transverse tubuleACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+
Muscle action potential
Nerveimpulse
SR
Contraction: power strokesuse ATP; myosin heads bindto actin, swivel, and release;thin filaments are pulled towardcenter of sarcomere.
Troponin–tropomyosincomplex slides back into position where it blocks the myosinbinding sites on actin.
Ca2+ activetransport pumps
Ca2+ release channels inSR close and Ca2+ activetransport pumps use ATPto restore low level of Ca2+ in sarcoplasm.
Ca2+ binds to troponin onthe thin filament, exposingthe binding sites for myosin.
Muscle AP travelling alongtransverse tubule opens Ca2+
release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.
Elevated Ca2+
1
2
3
4
5
67
8
Transverse tubuleACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).
Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).
Synaptic vesiclefilled with ACh
ACh receptorAcetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+
Muscle action potential
Nerveimpulse
SR
Contraction: power strokesuse ATP; myosin heads bindto actin, swivel, and release;thin filaments are pulled towardcenter of sarcomere.
Troponin–tropomyosincomplex slides back into position where it blocks the myosinbinding sites on actin.
Muscle relaxes.
Ca2+ activetransport pumps
Ca2+ release channels inSR close and Ca2+ activetransport pumps use ATPto restore low level of Ca2+ in sarcoplasm.
Ca2+ binds to troponin onthe thin filament, exposingthe binding sites for myosin.
Muscle AP travelling alongtransverse tubule opens Ca2+
release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.
Elevated Ca2+
1
2
3
4
9
5
67
8
Transverse tubule
Muscle MetabolismMuscle Fatigue
Inability of muscle to maintain force of contraction after prolonged activity
Factors that contribute to muscle fatigueInadequate release of calcium ions from the SRDepletion of creatine phosphate (storage form of ATP)Insufficient oxygenDepletion of glycogen and other nutrientsBuildup of lactic acid and ADPFailure of the motor neuron to release enough
acetylcholine
Muscle MetabolismOxygen Consumption After ExerciseAfter exercise, heavy breathing
continues and oxygen consumption remains above the resting level
Oxygen debtThe added oxygen that is taken into the body
after exerciseThis added oxygen is used to restore muscle
cells to the resting level in three waysConverts lactic acid into glycogenSynthesizes creatine phosphate and ATPReplaces the oxygen removed from myoglobin
Motor UnitsConsist of a motor neuron and the muscle
fibers it stimulatesThe axon of a motor neuron branches out
forming neuromuscular junctions with different muscle fibers
A motor neuron makes contact with about 150 muscle fibers
Control of precise movements consists of many small motor units
The total strength of a contraction depends on the size of the motor units and the number that are activated
Types of Skeletal Muscle Fibers
Muscle fibers contract at different speeds, and vary in how quickly they fatigue
Muscle fibers are classified into three main typesSlow oxidative fibers (Type I)Fast oxidative-glycolytic fibers (Type IIA)Fast glycolytic fibers (Type IIB)
Slow Oxidative Fibers (SO fibers)
Least powerful type of muscle fibersAppear dark red (more myoglobin)Generate ATP mainly by aerobic cellular
respirationRich blood supply and many mitochondria
Have a slow speed of contractionVery resistant to fatigueCapable of prolonged, sustained contractions for
many hoursAdapted for maintaining posture and for
aerobic, endurance-type activities such as running a marathon
Fast Oxidative–Glycolytic Fibers (FOG fibers)
Generate considerable ATP by aerobic cellular respiration (still has decent blood supply, large amount of myglobin, and many mitochondria)
Resistance to fatigue is intermediateGenerate some ATP by anaerobic glycolysisSpeed of contraction fasterContribute to activities such as walking and
sprinting
Fast Glycolytic Fibers (FG fibers)
Generate the most powerful contractionsHave low myoglobin contentRelatively few blood capillariesFew mitochondriaAppear white in colorGenerate ATP mainly by glycolysisFibers contract strongly and quicklyFatigue quicklyAdapted for intense anaerobic movements of
short durationWeight lifting or throwing a ball
Types of Skeletal Muscle FibersDistribution and Recruitment of
Different Types of FibersMost muscles are a mixture of all three types of
muscle fibersProportions vary, depending on the action of the
muscle, the person’s training regimen, and genetic factorsPostural muscles of the neck, back, and legs have a
high proportion of SO fibersMuscles of the shoulders and arms have a high
proportion of FG fibersLeg muscles have large numbers of both SO and FOG
fibers
Types of Contractions
Isotonic contractionThe tension developed remains constant while
the muscle changes its lengthUsed for body movements and for moving
objectslike picking a book up off a table
Isometric contractionThe tension generated is not enough for the
object to be moved and the muscle does not change its length
Holding a book steady using an outstretched arm
Isotonic and Isometric Contractions
Aging and Muscular TissueAging
Brings a progressive loss of skeletal muscle mass
A decrease in maximal strengthA slowing of muscle reflexesA loss of flexibility
With aging, the relative number of slow oxidative fibers appears to increase
Aerobic activities and strength training can slow the decline in muscular performance
Muscle DisordersCramps
Involuntary, painful, sustained tetanic contractions
Possible causesChemical changes in the musclePhysical blow to the muscle
FibrosisAbnormal increase of fibrous connective
tissue in muscleOccurs from connective tissue replacing dead
muscle fibers after injury
FibrositisInflammation of connective tissue in a
muscleProduces muscular rheumatism
Muscular dystrophyInherited muscular disorders characterized
by progressive degeneration of musclesMuscles weaken and atrophy, producing
progressive crippling
MyositisInflammation of muscle tissueSymptoms similar to fibrositis
Strains or “pulled muscles”Due to excessive muscle stretching
Mild strains damage only a few muscle fibers
Severe strains tear both connective and muscle tissuesSevere impairment of muscle function
Copyright 2010, John Wiley & Sons, Inc.
HypertrophyIncrease in muscle size due repeated activity
or hormonesAtrophy
Decrease in muscle size due to lack of useContractures
Shortened, contracted muscles or muscle groups in with the muscle atrophies and shrinks while the connective tissue thickens
Seen in people that have been immobile for while
Copyright 2010, John Wiley & Sons, Inc.
TendonitisInflammation of the tendons
FibromyalgiaCharacterized by pain, fatigue, and stiffness
in the connective tissues of the muscles, tendons, and ligaments.
Neurological Disorders Affecting MusclesBotulism
Poisoning caused by neurotoxin from bacterium Clostridium botulinum
Prevents release of acetylcholineDeath can result due to paralysis of
breathing musclesCaused by eating contaminated, improperly
canned vegetables and meat
Myasthenia gravisExtreme muscular weakness
Improper functioning of the neuromuscular junctionAutoimmune disease
Blocks the stimulatory effect of acetylcholine by reducing or blocking ACh receptors
PoliomyelitisViral disease of motor neurons in spinal cordDestruction of motor neurons leads to
paralysisPolio vaccination is available
SpasmsSudden, involuntary contractions of a muscle
or group of musclesCauses
Irritation of motor neuronsEmotional stressNeurological disorders
Muscle Spasms Effect Blood Flow
TetanusCaused by neurotoxin of anaerobic bacterium
Clostridium tetani Usually caused by puncture woundsNeurotoxin affects motor neurons
Causes continuous stimulation and tetanic contractions of certain muscles
Mortality is high without treatmentVaccination is available