Anatomy & Physiology 101-805
Unit 7
The Muscular
System
Paul Anderson 2012
Biceps brachii
Rectusabdominis
Tendons
Organs of the Muscular System
Martini &
Bartholomew fig
1-2c
The muscular system consists of all the skeletal muscle organs of the body together with their connections to bones (e.g. tendons).
The muscle tendon
• is continuous with other muscle connective tissue sheaths
• binds muscles to the periosteum of a bone
• transmits the force of muscle contraction to the bone causing movement.
tendon of biceps brachii
3
Origins & Insertions of Muscles
The muscle that contracts to cause a movement is called a prime mover muscle.
• The biceps brachii is a prime mover for flexion (bending) of elbow.
• When the biceps brachii contracts its distal tendon pulls on the radius causing flexion of elbow.
• The point of attachment of the prime mover muscle to its distal moveable bone is the insertion of the muscle.
• The opposite (proximal) end of a prime mover muscle is attached to a stationary bone at the origin of the muscle.
tendon at insertion of biceps brachiion radius bone (moveable bone)
tendon at origin of biceps brachiion scapula bone(stationary bone)
flexion of elbow
at origin of muscle
Tendon at insertion of muscle
proximal end of muscle
distal end of muscle
biceps brachii
Muscular System: Major Functions - 1
Energy conversion by muscles is used for several specific functions of the muscular system.To power adaptive (homeostatic) movements, both voluntary and reflex (“behaviour”), breathing movements and facial expressions.
• Movements involve muscle contraction and relaxation• Muscle contraction is the generation of a force by a muscle• Muscle relaxation is the reverse process i.e. loss of force in a muscle
Muscle contractions may be• Isotonic: muscle shortens as the force of contraction exceeds the
external resistance • Isometric muscle does not shorten as the force of contraction is equal to or less than the external resistance.
The major homeostatic functions of the muscular systemare to convert chemical energy to mechanical energy for -contraction and relaxation of muscles - generation of heat.
All movements involve both isotonic and isometric contraction
Muscular System: Major Functions - 2
Heat production: Muscles are a major source of body heat for body temperature control
Cold stimulusshivering
↑Muscle tone
heat
glucose
Muscle contraction
Isotonic contraction
Isometric contractionGlycogen
Fatty acids
CHEMICAL ENERGY
MUSCLE CONTRACTION
MECHANICAL ENERGY (25%) + HEAT (75%)
ATP ADP + Pi + ENERGY
Muscular System: Major Functions - 3
Posture and Balance:• Posture is proper position or alignment of body parts against gravity.• Maintaining an upright posture means positioning of body parts in
opposition to gravity and is normally a function of “anti - gravity muscles” (extensors of legs, back & neck maintain upright posture).
• For Balance anti - gravity muscles put the center of gravity over the base of the body so that the body is stable.
In walking, the center of gravity shifts first over one foot then over the other.
Muscular System: Major Functions - 4
Maintenance of muscle tone for:•Stabilization of Joints by (especially for knee and shoulder joints):
•Support and Shape, (e.g. abdominal wall muscles)•Protection of abdominal organs (via abdominal flexors, e.g. rectus abdominis).
Voluntary Control of entrances and exits of digestive and urinary tracts.
• mouth• esophagus• anus (external anal sphincter muscle)• urethra (external urethral sphincter muscle)
8
Muscle tissue is specialised for the following properties:
• ability to generate an impulse when stimulated (excitability orirritability)
• ability to conduct the impulse to all parts of the cell (conductivity)
• ability to generate a force for movement (contractility)Muscle contraction = generation of a forceMuscle tension = degree of force generated
• ability to stretch (extensibility)
• ability to return to original length after contracting or stretching (elasticity).
Tissues of Muscular System
The two major tissues in the muscular system are skeletal (striated or voluntary) muscle and various collagenous denseconnective tissues (e.g. tendons).
These are organised into muscle organs e.g. biceps brachii muscle.
9
Properties of Skeletal Muscle Tissue
Martini & BartholomewFigure 7-2a
• Cells are multinucleated, very long (stretching the length of a muscle organ), with obvious cross striations.
• Force of contraction is usually transmitted to bone and produces visible movements.
• Contraction always requires a nerve impulse so skeletal muscle is not autorhythmic.
• Controlled by the somatic branch of the peripheral nervous system and so is under voluntary control.
• Speed of contraction (<0.1sec.) is faster.
• Skeletal muscle contraction is subject to muscle fatigue.
Skeletal (striated or voluntary) muscle tissue differs from both smooth and cardiac muscle as follows:
Striated muscle x1000
nucleistriations
10
Structure of Skeletal Muscle Organs
Muscle organs are composed of various connective tissue sheaths which are of non - contractile, elastic, collagenous tissues.
These connective tissue sheaths have the following functions:
• carry nerve fibers, blood & lymph vessels to muscle cells
• Bind cells together
• transmit the contractile force of the muscle cells to bones
• give shape to muscle organs
• contribute to muscle’s extensibility & elasticity.
11
Structure of Skeletal Muscle Organs-2
• The epimysium covers the surface of a muscle and shapes the muscle.
• The perimysium covers the fasciculi (fascicles) -bundles of microscopic muscle fibers and also contains stretch receptors.
• The thin endomysium surrounds each muscle fiber or cell.
Martini & Bartholomew
Figure 7-1
Muscle Organs are divided internally into Fascicles
12
Structure of Skeletal Muscle Organs - 3
epimysium
perimysium
fascicles
perimysium
endomysium
Striated muscle fiber (cell)
Muscle organ
Fascicles are divided internally into Muscle Fibersor Muscle Cells
13
Structure of Skeletal Muscle Organs - 4
perimysium
endomysium
Striated muscle fiber (cell)
Myofibrils within muscle cell
bandsdark
light
nuclei
Striated muscle x1000
bandsdark
light
sarcolemma
Muscle Fibers are divided internally into Myofibrils
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Structure of Skeletal
Muscle Cells
Myofibrils within muscle cell
dArk band
lIght band
H zone in center of
A band
line in center of I bandI band
A band
H zone
with protein myosin
with protein actin
Z
Z
Myofibrils contain
Myofilaments
15
Structure of a Sarcomere
• The muscle fiber is tightly packed with parallel cylindrical units called myofibrils.
• The myofibril has the same striated (or striped) appearance as the muscle fiber with alternating light (I) bands and dark (A) bands (lIght-dArk).
• The striations are caused by cylindrical proteins in each myofibril called myofilaments; these interact to cause muscle contraction.
I band
myofibril
Thick filament
Thin filament
A band
myofilamentsMartini & Bartholomew
Figure 7-2b
16
Structure of a Sarcomere- 2
•The light (I) bands consist of thin myofilaments containing actin.
•In the center of the I band is a line called the Z line (or Z disk) containing another protein connecting the thin actin myofilamentstogether.
•The dark (A) bands consist of thick myofilaments containing the protein myosin together with overlapping thin (actin) myofilaments.
•In the center of the A band is a lighter zone (the H zone; this represents the region containing only thick myosin myofilaments (no actin myofilaments).
I band
myofibril
Thick myosin
filament
Thin actinfilament
A bandZ line
H zone Zone of overlap
Z line
Martini & Bartholomew
Figure 7-2b
17
Structure of a Sarcomere- 3
•In the center of the H zone is another line (the M line) containing proteins that bind the myosin myofilamentstogether.
•The region of a myofibril between successive Z lines is called a sarcomere and is the functional unit of a muscle cell.
I band
myofibril
Thick filament
Thin filament
A bandZ line
H zone Zone of overlap
M line
sarcomere
Z line
Martini & Bartholomew
Figure 7-2b
Structure of a Sarcomere - Summary
I band (thin
filaments only)
A band (thick &
thin filaments
Z line in center
of I band
H zone (thick
filaments
only)
sarcomere
Z line
Thin filament with
actin
Thick filament
with myosin
Z line
M line in
center of
H zone
19
Sliding Filament Theory of Muscle Contraction
• The sliding filament theory of muscle contractionstates that when a muscle contracts the myofilaments do not shorten but instead slide past each other.
• The thin actin filaments are pulled towards the H zone by the thick myosin filaments which therefore approach the Z line.
H zone
Thick filaments
now near Z line
H zoneZ line ZZZ
MUSCLE ANIMATION\MUSCLE.htm
20
Sliding Filament Theory of Muscle Contraction - 2
Relaxed
Sarcomere
ContractedSarcomere
H zone
ZZ
ZZ
H zone now smaller
The Sliding Filament Theory is borne out by the following observed changes when a muscle contracts:
• the H zone gets smaller and disappears, as the thin actinfilaments on each side approach each other
• the I band gets smaller and disappears as the thick myosin filaments approach the Z line
I band
I band now smaller
21
Sliding Filament Theory of Muscle Contraction - 3
• the A bands get closer together but do not change their length since this is equal in length to the thick myosin filaments
• the sarcomere gets shorter since adjacent Z lines are pulled together
Relaxed
Sarcomere
ContractedSarcomere
Sarcomere now smaller
Sarcomere
I band now smaller
I band
Z
Z
A band
A band same length
ZZ
Z Z
H
H
22
Function of Myosin in Muscle Cell Contraction
•The thick filaments contain many myosin molecules each with two globular heads oriented towards the Z line. •Therefore on either side of the H zone the myosin molecules are oriented in opposite directions. •In the presence of Ca+2 the myosin heads bind to the adjacent actin molecules of the thin filament forming cross bridges and pull these towards the center of the sarcomere (the H zone) by “flexing”. •This happens during muscle contraction.
In presence of Ca+2 myosin heads “flex” & pull thin actin filaments to center of A band
Martini & Bartholomew fig 7-2e
Z Z
H
23
Storage & Release of Calcium Ions in Muscle Cells
•The cell membrane (sarcolemma) of a muscle cell has invaginations that form tubules (T tubules) running around each myofibril at the junction of A & I bands.
•The cytoplasm of a muscle cell (sarcoplasm) has an extensive SER (sarcoplasmicreticulum or SR) which stores Ca+2 in its lateral sacs.
•Each T tubule passes between two adjacent lateral sacs of the SR forming a triad.
•When an impulse from T tubules reaches the triad it causes release of Ca+2 from the lateral sacs of the SR. This triggers muscle contraction.
store Ca+2
Muscle cell(fiber)
T tubule + 2 lateral
sacs forms a TRIAD
Impulse in T tubule causes Ca+2
release here
24
Microscopic Anatomy of a Skeletal Muscle Fiber
lateral sac
of SR
Martini & Bartholomew fig 7 - 2a, Martini, fig 10-3
T tubuleTRIAD
lateral sac
of SR
TRIAD =T tubule
+ 2 lateral sacs
Each Myofibril in a muscle fiber is surrounded by
the SR.
25
Storage of Calcium in Resting Muscle Cell
•In the resting muscle cell Ca+2 is actively transported into the SR, the function of which is to store Ca+2
until needed.
•Therefore there is a low ICF [Ca+2] in the resting cell, insufficient to trigger contraction.
Calcium ions stored in lateral sacs of SR in resting muscle cell
sarcolemma
T tubule
Z
sarcomere
26
Calcium Release Triggers Muscle Cell Contraction
•Muscle cell contraction is triggered by the release of Ca+2 from the SR into the ICF. •Ca+2 release from the sacs of the SR is triggered by an impulse (action potential) which arrives at the triad from the sarcolemma via the T tubules. •The triggering of muscle contraction by an impulse is called excitation – contraction coupling.
Release of Calcium ions from lateral sacs of SR triggers muscle cell contraction
Impulse in sarcolemmaenters T tubules causing release of Ca+2 from lateral sacs of SR
ZZ
27
Removal of Calcium Causes Muscle Cell Relaxation
•In the absence of impulses Ca+2 is pumped back into the sacs of the SR.
•Removal of Ca +2 from the muscle cell ICF causes relaxation of muscle cells.
Calcium ions pumped back into lateral sacs of SR in relaxing muscle cell
ZZ
28
Three Roles of ATP in Muscle Contraction
ATP plays three roles when it powers muscle contraction.
1.Energy from ATP hydrolysis activates myosin moleculesso they can pull on actin molecules causing muscle contraction. Myosin heads have an enzyme (ATPase) to split ATP and release energy that activates the myosin heads.
2.When the energy from ATP hydrolysis is spent, a new ATP molecule binds to myosin. Binding of ATP to myosin causes the detachment of myosin from actin allowing a new contraction cycle to begin.
3.Energy from ATP hydrolysis is used to pump Ca+2 into the SR after contraction.
29
Two Proteins Block Contraction in a Resting Muscle
• In the resting muscle binding of activated myosin is prevented by two proteins in the thin filament (troponin and tropomyosin).
•These are attached to actin molecules and protect their binding sites.
•All myosin heads are in “extended” position.
•Ca+2 concentration is low.
TroponinADP
P
Myosin headspreviously activated by ATP hydrolysis
active sites of actin blocked byTropomyosin
Actin molecules in thin filament
thick filament with Myosin
Resting Sarcomere
ADPP
Martini & Bartholomew fig 7-5
30
Release of Ca+2 Unblocks Binding Sites on Actin
•Release of Ca+2 from the sacs of the SR causes a shape change in troponin.
•Troponin pulls tropomyosinaway from the actin binding site.
•This allows myosin to bind to actin and muscle contraction to occur.
ADPP
active sites of actinnow exposed
thick filament with Myosin
Active Site Exposure
ADPP
Ca+2
Ca+2
Ca+2 binds to troponin & unblocks active sites on actin
Tropomyosinmoves away
Martini & Bartholomew fig 7-5 STEP 1
31
Myosin Binds to Actin:Cross Bridge Formation
•If Ca+2 is present the activatedmyosin heads bind to actin forming cross bridges and flexing.
•Actin is pulled towards the center of the sarcomere (center of H zone).
•This releases ADP and Pi from myosin which allows another ATP to bind to myosin.
ADP
P
Myosin heads bind to actin & forms cross bridge
thick filament with Myosin
Cross Bridge Formation
ADPP
Ca+2
Ca+2
Martini & Bartholomew fig 7-5
STEP 2
Pivoting (“flexing”) of myosin heads
ADP
Ca+2
Ca+2
ADP P
Myosin head flexes & pulls actin toward H zone P
ADP & P released from myosin head
Martini & Bartholomew fig 7-5 STEP 3
32
ATP Causes Detachment of Myosin Heads
•ATP binds to myosin heads.
•The binding of ATPto the myosin headcauses it to detach from actin.
ATP
Detachment of myosin heads
Ca+2
Martini & Bartholomew fig 7-5 STEP 4
Ca+2
ATP
33
Myosin is Reactivated by ATP Hydrolysis
•ATP hydrolysis reactivates the myosin head.
•If Ca+2 is reabsorbed into the SR the contraction cycle ends here.
•If Ca+2 is not reabsorbed into the SR the contraction sequence repeats.
ADP
Myosin Reactivation
Ca+2
Martini & Bartholomew fig 7-5
STEP 5
Ca+2
ADP
P
P
ATP
ATP
34
Arrival of Impulse at Neuromuscular Junction
•A nerve impulse (action potential) arrives at the axon terminals of a motor neuron to a skeletal muscle.•The junction of the two cells is called a neuromuscular junction.
myofibril
Martini Figure 10.10a,
35
Excitation of Muscle Cell at the Motor End Plate
Martini & Bartholomew Fig 7-4b: Martini Figure 10.10a,
•The axon terminal ends in a swelling which fits into a depression in the sarcolemma called the motor end plate.
•Release of neurotransmitter acetylcholine from thesynaptic terminal causes excitation of the motor end plate
impulse
motor end plate
motor end plate
Release of Acetylcholine at the Neuromuscular Junction
Martini & Bartholomew Fig 7-4c STEP 2: Martini Figure 10.10c,
•The motor impulse causes release of the neurotransmitter acetylcholine (Ach) by exocytosis.
•Ach activates membrane receptors in the motor end platetriggering an impulse in the sarcolemma of the muscle cell.
An enzyme acetylcholinesterase(AchE) in the synaptic cleft later destroys Ach by hydrolysis
SARCOLEMMA OF MOTOR END PLATE
SYNAPTICCLEFT
Acetylcholine (Ach) in synaptic vesicles
is released by exocytosis into the
synaptic cleft
SYNAPTICVESICLES
MOTOR MPULSE
Ach MEMBRANE RECEPTOR
37
Excitation of Muscle Cell
Martini & Bartholomew Fig 7-4c STEP 3: Martini Figure 10.10c,
•The binding of ACh to the membrane receptors at the motor end plate increases the membrane permeability to Na+.
•Na+ rapidly flows into the sarcoplasm from the ECF by net diffusion.
•Na+ inflow depolarises the motor end plate, triggering an impulse in the sarcolemma.
Na+
Na+
Na+
Na+ enters sarcoplasm, depolarising muscle cell & causing an impulse in the sarcolemma of muscle cell.
Ach binds to
membrane receptor
IMPULSE IN
MUSCLE CELL
38
Excitation of Muscle Cell
Martini & Bartholomew Fig 7c STEP 4: Martini Figure 10.10c
•The impulse spreads over the surface of the muscle cell and enters the T tubules where it is conducted to the triad.
•Arrival of the impulse causes Ca+2 release from the lateral sacs of the SR.
•Ca+2 release triggers muscle cell contraction.
AchE breaks down Ach in the
synaptic cleft
Impulse causes Ca+2 release from lateral sacs of SR, triggering muscle cell contraction
IMPULSE ENTERS
MUSCLE CELL
39
Summary of Contraction Steps in a Muscle
Martini & Bartholomew Table 7-1
ImpulseNo
Impulse
40
Contraction Cycle of a
Muscle Cell
Martini, Figure 10.12
Contraction
Relaxation
Impulse
No Impulse
41
RIGOR MORTIS
In the complete absence of ATP (following cellular death):
•Ca+2 cannot be actively transported into the SR.
•Therefore ICF Ca+2 levels will be high so actinsites are exposed and myosin can bind to actin.
•Myosin molecules are unable to detach from actin since this requires ATP.
•Therefore the muscle remains stiffly contracted, a condition called rigor mortis.
42
Contraction and Relaxation of Muscle Organs
•MUSCLE CONTRACTION is the process of generating a force in a muscle organ.
•The net force produced by a muscle organ is called muscle tension.
•MUSCLE RELAXATION is loss of force in a muscle and so is the opposite of muscle contraction.
Muscle contractions may be
•Isotonic: muscle usually shortens as the force of contraction exceeds the external resistance
•Isometric muscle does not shorten as the force of contraction is equal to or less than the external resistance.
43
Isotonic Muscle Contraction
•ISOTONIC CONTRACTION occurs whenever a muscle changes its length (usually shortening) while contracting.
•Part of the energy of contraction performs
•mechanical work (= resistance x distance moved).
•Resistance is the load or force opposing the action
•Any movement involves Isotonic Contraction.
Muscle contracts
In Isotonic ContractionMuscle changes its length
In Concentric Contraction
Muscle shortens
Resistance here is load due to gravity
Martini Fig 10.18
2 kg2 kg
44
Concentric Muscle Contraction
• CONCENTRIC CONTRACTION occurs whenever a muscle shortens while contracting isotonically.
• Here the tension generated by the muscle exceeds the load (resistance, or force opposing the muscle).
There are two types of Isotonic Contraction•Concentric •Eccentric
2 kg
45
Eccentric Muscle Contraction
•Sometimes an antagonistic muscle lengthens while contracting isotonically e.g. the quadriceps femoris (knee extensors) while sitting down, or the biceps brachii (elbow flexor) while lowering a weight in the hand).
•Here the load exceeds the tension. This is referred to as ECCENTRIC CONTRACTION (or paradoxical action) and the muscle performs negative work.
•The function of the contracting muscle in this case is to slow the rate of descent of the body part to protect the body from injury.
•Note that in eccentric contraction the prime mover for the movement may be relaxed as gravity is causing the movement.•Here the triceps muscle, (elbow extensor) is relaxed while lowering a weight
Biceps muscle contracts eccentrically when lowering a weight
2 kg
46
Isometric Muscle Contraction
Martini Fig 10.18
•ISOMETRIC CONTRACTION occurs when the tension exerted by a muscle does not exceed the load (resistance) opposing the muscle and the muscle organ does not change its length.
•Here all the energy escapes as heat and no mechanical work is done.
•Examples: standing still (extensors of leg), pushing against a closed door (extensors of arm), holding a weight in a stationary position.
Isometric ContractionMuscle does not change length
2 kg
Biceps muscle contracts isometrically while holding a weight
No movement
47
All Movements Involve Isotonic and Isometric Phases
• In walking and running isometric contractions keep the legs stiff when the feet touch the ground.
• All movements begin with a brief isometric phase when the tension is increasing but is still less than the load.
Muscle contraction
2 kg
Isotonic contraction
Isometric contraction
Concentric contraction
Eccentric contraction
Movement
No Movement
Normal functioning of the skeleto-muscular system depends on a combination of isotonic and isometric contractions.
F > R muscle shortens
F < R muscle lengthens
F < or = R muscle length unchanged
Force (F)Resistance (R)
48
Muscle Twitch vs Graded Responses of Muscle Organs
•A single impulse to a muscle produces a single brief all- or -none contraction and relaxation response called a muscle twitch.
• However, muscle responses are normally smooth and vary in intensity according to needs.
Such GRADED RESPONSES of muscles depend on temporal andspatial summation of individual contractions (twitches).
temporal
spatial
Summation of twitches
↑↑↑↑smoothness
↑↑↑↑intensity
Muscle Twitch
Martini & Bartholomew Fig 7-6
Martini Fig 10.15
49
Temporal (Wave) Summation
• A TEMPORAL (OR WAVE) SUMMATION occurs when motor impulses arrive in such rapid succession (i.e. at a high frequency) that each contraction adds onto the previous one.
• Eventually a fusion of twitches occurs, forming a smooth sustained stronger contraction, called tetanus.
• Most normal movements involve tetanus.
Complete tetanus
Incomplete Tetanus
Temporal summation of muscle twitches
Martini & Bartholomew Fig 7-7 Martini Fig 10.16
stimulus
incomplete fusion of twitches
time
tensio
n
Stronger
contraction
Higher frequency stronger
smoother contraction
Maximum frequency
strongest smooth
contraction
complete fusion of twitches
50
Causes of Temporal (Wave) Summation
TEMPORAL (OR WAVE) SUMMATION is caused by
• Increased availability of Ca+2 .Each impulse releases more Ca+2
• Sustained stretching of non- contractile tissues (“serieselastic elements”) such as tendons in the muscle (i.e. these are not allowed to recoil as in a twitch).
Greater Increase in [Ca+2]
Repeated impulses cause Increased [Ca+2]
Maximum increase in [Ca+2]
Martini & Bartholomew Fig 7-7 Martini Fig 10.16
51
Spatial Summation of Muscle Twitches (Recruitment of Motor Units)
• A motor unit consists of all the muscle cells controlled by a single motor neuron.
• A motor unit is the smallest unit of contraction for a muscle, i.e. represents the minimum response of a muscle.
• Each muscle cell contracts as part of a motor unit. Both muscle cells and motor units obey the all – or – none law.
• Spatial summation (by multiple motor unit summation orrecruitment) is therefore largely responsible for increasing the force of contraction of the muscle.
• Recruitment occurs when the brain activates more axons in each motor nerve to a muscle.
SPATIAL SUMMATION refers to the RECRUITMENT of increasing numbers of motor units in a muscle.
52
Recruitment of Motor Units
Martini & Bartholomew Fig 7-8 Martini Fig 10.17
Motor Unit•Muscle cells controlled by one axon•minimum response unit of muscle •obeys all or none law
Fascicle: does not obey all or none law
Constant tension in
muscle due to:
• Rotation of motor units
• Asynchronous motor
unit summation
53
Innervation Ratio of a Muscle
•The Innervation Ratio is the ratio between the number of axons in a motor nerve to a muscle and the number of muscle cells in the muscle. It is used to calculate the average motor unit size for a muscle.
•Muscles controlling precision movements requiring many fine gradations of movement have small motor units- flexors of the fingers, 1 axon: 10 muscle fibers- extrinsic eye muscles, 1: 3.
•Muscles controlling gross movements requiring little variation have large motor units, e.g. extensors of the thighs 1: 150.
54
Innervation Ratio of a Muscle
Martini & Bartholomew Fig 7-8 Martini Fig 10.17
Innervation Ratio•Average motor unit size•3 axons: 20 muscle cells•= 1 axon: 7 muscle cells•This is a precision muscle with small IR
3
20
55
Muscle Tone and the Stretch Reflex
•Tone is most important for "anti- gravity" muscles.
•The STRETCH REFLEX is initiated by stretching of a muscle: in response the same muscle shortens.
Quadriceps femorisanti - gravity knee extensors contract via stretch reflexwhen gravity causes knees to buckle
Stretching of extensor muscles of the trunk and legs ("anti - gravity" muscles) by gravity causes a reflex contraction of the same muscles which therefore stiffen and oppose gravity.
MUSCLE TONE is the continual partial contraction of a resting muscle and is maintained by the stretch reflex.
Martini &
Bartholomew
fig 1-2c
56
The Stretch Reflex
The nerve pathway mediating the stretch reflex involves muscle receptors called muscle spindles, a sensory nerve fiber, a motor nerve fiber and a synapse in the spinal cord.
“anti -gravity”extensor muscle
gravity causes
synapse
Stretching of muscle tendonstimulates muscle spindles
Stretch
Contraction
Muscle spindle(stretch receptor)
REFLEXARC
Spinalcord
Activation of motorneuron produces reflexmuscle contraction
Example of Stretch Reflex:
The Knee Jerk
Martini & Bartholomew Figure 8-29
58
Importance of Muscle Tone for Health
•Muscle tone is present during waking hours and is dependent on
- the stretch reflex and on
- descending motor pathways from the brain.
•Tone is reduced during sleep and in flaccid paralysis.
Muscle tone is important for muscle health, rapidity of response, for stabilizing joints and for posture.
59
Muscle Paralysis
Muscle Paralysis means loss of voluntary control over muscles.
•Spastic paralysis is characterised by hypertonia(spasticity) and exaggerated reflexes.
•Spasticity is caused by the stretch reflex which is overactive. The usual cause is a stroke (cerebrovascularaccident) which damages upper motor neurons.
•Flaccid paralysis is characterised by hypotonia(flaccidity) and the absence of reflexes.
•Flaccidity is caused by muscle denervation , i.e. damage to lower motor neurons (e. g. with poliomyelitis).
60
Damage to Motor Neurons Causes Paralysis
Inhibitory
synapse
+
•Upper motor neuron (UMN) in brain damaged by stroke (CVA)
•“lower”motor neuron (LMN) to muscle damaged e.g. by polio
•Loss of inhibitory control over LMNs
•Loss of voluntary control
•LMNs overactive (exaggerated reflexes)
•Spastic paralysis
•Loss of voluntary & reflex control
•LMNsinactive
•Flaccid paralysis
+
Excitatory
synapses
-
X
61
Muscle Atrophy & Hypertrophy
• Flaccid paralysis causes muscle atrophy or shrinking of the muscle caused by shrinking of cells and/or reduction in cell number.
• Types of Muscle Atrophy.
There are two types of muscle atrophy depending on the cause:
• Atrophy of Denervation is caused by the cutting of the nerve supply (innervation) to the muscle i.e. denervation (e.g. in poliomyelitis); unless the muscle is renervated (or electrically stimulated) within four months the atrophy is irreversible.
• Atrophy of Disuse occurs when a muscle is not used for an extended period (e.g. limb in a cast, bedridden person; since the muscle is not stretched muscle tone is reduced (hypotonia). This type of atrophy is reversible if the muscle is reused.
• Muscle Hypertrophy refers to an increase in size of the muscle by an increase in the size of individual cells (more myofibrils)without increase in cell number.
• This is caused by increased use of muscles with or without the use of anabolic steroids.
62
Roles of Muscles in Movements
• During any movement muscles may function as
• Prime Movers (or agonists) which directly cause a movement by their contraction e.g. biceps brachii is a prime mover for flexion of the elbow.
• Antagonists which oppose a given movement when they contract e.g. the triceps brachii is an antagonist for flexion of the elbow.
• Synergists which are muscles which also contract during a movement but do not directly cause the movement but help the prime mover to work efficiently.
• Fixators are synergists which steady the movement by stabilising (or “fixing”) a joint e.g. the pectoralismajor and deltoid muscles steady the humerus bone during flexion of the elbow and so are fixators.
63
Reciprocal Inhibition of Antagonists during Movements
• Muscles in the body are grouped into antagonistic pairs.
• The two members of the antagonistic pair are prime movers for opposing movements and occur on opposite sides of the limb or trunk (e.g. biceps brachii and triceps brachii are on opposite sides of the upper arm.
• During any movement the antagonist must relax while the prime mover contracts.
• Relaxation of the antagonist during a movement involves inhibiting the motor nerve fibers going to the muscle, thus preventing the stretch reflex (which would otherwise cause contraction of the antagonist).
• The reflex inhibition of motor fibers to an antagonistduring a movement with the simultaneous excitation of motor fibers to the prime mover is called reciprocal inhibition.
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Reciprocal Inhibition of Antagonists during Movements
• The withdrawal reflexinvolves reflex inhibition of nerve fibers to ipsilateral(same side) limb extensors.
• In the crossed -extensor reflexflexion of one limb is accompanied by reflex inhibition of flexors of the opposite (contralateral) limb so that this limb can extend and support the body’s weight.
Painful
stimulus to left foot
Withdrawal reflex of left leg
Crossed extensor reflex of right leg
Left Leg
• Excitation
of flexors
• Inhibition
of
extensors
+
+
-
+
+
-
Right Leg
• Excitation of extensors
• Inhibition of flexors Right Leg extends Left Leg flexes
65
Flexor & Crossed Extensor Reflexes
Martini Figure 13.22
• Painful stimulus to right foot
• withdrawal reflex of right leg
• Painful stimulus to right foot • withdrawal reflex of right leg• Crossed extensor reflex of left leg
Martini & Bartholomew Figure 8-30
66
Muscles provide Force for Levers
The skeleto - muscular system is a system of levers(devices for performing work).
A Lever is a rigid bar (in the body, a bone) that turns about an axis of rotation or a fulcrum (in the body, a joint)
• the insertion point of a muscle is the power point (P) of the lever
• the fulcrum (F) of the lever is the moveable joint at which movement occur
• the resistance (R) is the weight of the part being moved
P
R
F
Power point (P) = Insertion of muscleResistance (R)
= Weight of body part moved
Fulcrum(F) = Joint
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The Action of the Biceps Brachii in Elbow Flexion
The most common type of lever in the body is type III (R - P - F) as in biceps brachii flexing the elbow.
P
R
F
Power point (P) = Insertion of muscle on radial tuberosity
Resistance (R) = Weight of lower arm
Fulcrum( F) = elbow Joint
Type III leverBiceps brachiimuscle
animation
68
Mechanical Advantage of Levers
• A lever may offer a mechanical advantage (less muscle power required to move a given weight).
• The PF/RF ratio determines the mechanical advantage of a lever.
• If the PF/RF ratio of a lever is >1 the lever works at a mechanical advantage i.e. the power used can be less than the load (resistance).
• If the PF/RF ratio of a lever is <1 the lever works at a mechanical disadvantage, i.e. the power used must be much greater than the load (resistance).
P
R
FRF
PFTherefore Type 3 levers always have a mechanical
disadvantage
PF/RF ratio <1
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Mechanical Advantage vs Mobility of Levers
•For the biceps brachii PF/RF may equal 1/6 or 0.17, a mechanical disadvantage.
•Thus to lift a 10kg wt. the biceps must generate a force of 10/0.17 = 60 kg (or 6 x10kg).
•However, the speed of hand movement is increased by an equivalent factor of 6 giving increased mobility of the hand.
•If the biceps moves 1cm in 1 sec the hand moves 6cm.
R
P
F
6cm
1cm
Many levers in the body sacrifice mechanical advantage (i.e. power) for increased speed and range of movement by having a smaller PF/RF ratio.
1
6
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How the Insertion of a Muscle Affects Mobility & Power
•The MOBILITY (degree of movement), SPEED & Power of a muscle depends partly on the INSERTION POINT of the muscle tendon on the bone.
- The closer the insertion point is to the fulcrum of the lever the greater is the muscle’s mobility. This is because a small degree of movement near the fulcrum causes a large degree of moment of the other end of the bone.
- The further the insertion point is from the fulcrum of the lever the greater is the mechanical advantage and so the greater the muscle’s power.
•Short insertion•Greater hand mobility
•Reduced muscle power
•Long insertion
•reduced hand mobility
•Greater muscle power
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How the Tendon -Fiber Angle of a Muscle Affects Mobility
•The smaller the tendon - fiber angle the greater the mobility and speed.
•Maximum mobility and speed occurs when the tendon -fiber angle is zero (i.e. they are parallel) where the muscle fibers are pulling the tendon in the direction of the movement.
•This also means that fewer fasciculi are possible so the muscle power is relatively weak e.g. rectus abdominis, sartorius, sternohyoid, superior rectus, gracilis muscles.
•Muscle with parallel tendons & muscle fibers•Great mobility•Fewer fasciculi so often weaker muscles
Biceps brachii achieves power by its
fusiform shape- bulky in center
Parallel muscle
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How the Number of Fasciculi of a Muscle Affects Power
•The STRENGTH (POWER) of a muscle depends partly on theNUMBER OF FASCICULI (bundles of fibers).
•The greater the number of fasciculi the stronger the muscle. •This is achieved by having the muscle fibers pulling at an angle to the tendon.
•By increasing the tendon - muscle fiber angle more fasciculi can be packed into the same muscle diameter which increases power but reduces mobility.
•Unipennate muscle have muscle fibers pulling the tendon on one side only•Bipennate muscle (with even more fasciculi) have fibers on two sides of the tendon•The more fasciculi the stronger the muscle.
Unipennate Vastus muscle
Bipennate Rectus femoris muscle
muscle fibers pull at an angle to the tendon.
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Strongest Muscles have Greatest Numbers of Fasciculi
The following muscles have fibers pulling on several sides of the tendon, have the greatest numbers of fasciculiand so are the strongest muscles.- Multipennate muscles (e.g. deltoid)- Convergent muscles (e.g. pectoralis major) and - Circumpennate muscles (e.g. tibialis anterior)
Circumpennatetibialis anterior
Convergent pectoralis major
Mutiipennate deltoid
Martini Figure 11-1
Muscle Activity & Muscle Strength
The STRENGTH (POWER) of a muscle depends on three factors:
•NUMBER OF FASCICULI
•INSERTION POINT of the muscle
•DEGREE OF ACTIVITY OF THE MUSCLE.
-If a muscle is used forcefully (especially isometrically) on a regular (daily) basis there will be an increase in muscle cell diameter, number of contractile units and strength of connective tissue components.
-The muscle will therefore show hypertrophy and increased strength.
Fixed by muscle anatomy
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Sources of Energy for Muscle Contraction
•Muscle contraction depends directly on energy from ATPhydrolysis. •ATP is replenished in exercising muscle cells from two sources, - hydrolysis of creatine phosphate (CP)- cell respiration of glucose and other organic molecules.
Aerobic cell respiration
energy energyenergyenergy
Muscle glycogen
Blood sugar
76
Hydrolysis & Synthesis of ATP
Muscle contraction
“high energy”bond stores energy in ATP
77
Creatine Phosphate Transfers Energy to ATP for Muscle Contraction
•Creatine phosphate (CP) is a second high energy molecule in muscle cells. •During rest CP is formed from ATP•During exercise as ATP is being depleted CP is the most direct and so is the first source for regenerating ATP.
CreatinePhosphate
“high energy” bond stores energy in CP
Creatine + ATP CP + ADPrest
exercise
78
During Rest Creatine Phosphate & Glycogen Reserves are built up using ATP
Fatty acids are major source of energy for ATP in resting muscles
During rest Energy from ATP hydrolysis is used to make CP & Glycogen from glucose
Glycogen
energy
energy
By using fatty acids during rest glucose in muscle cells is available to form glycogen.
79
Metabolism of Resting Muscle Cell
Martini & BartholomewFigure 7-9(a)
During rest Energy from ATP hydrolysis is used to make CP & Glycogen from glucose
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Anaerobic Respiration in Muscle Cells supplies little ATP & forms Lactic Acid
During intense exercise blood supply cannot keep up with oxygen demands of muscles and muscles respire anaerobically.
Anaerobic respiration (anaerobic glycolysis) oxidises glucose incompletely
to lactic acid and forms only 2 ATP per glucose.
Anaerobically muscles therefore fatigue easily due to
-a shortage of ATP
- buildup of lactic acid (which lowers the pH of muscle cells).
After anaerobic exercise an “oxygen debt” must be paid to reoxidiseexcess lactic acid to CO2 and H2O and to replenish ATP and CPreserves from aerobic respiration: therefore hyperventilation occurs.
C6H12O6
INTENSE EXERCISE
+ ENERGY
2ATP 2ADP + 2Pi
2 lactic acid
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Anaerobic Metabolism of Contracting
Muscle Cell
Martini & BartholomewFigure 7-9(c)
Absence of
oxygen
LIVER
GLUCOSE
Lactic Acid Cycle: Liver converts lactic acid to glucose for use by muscles
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Aerobic Respiration in Muscle Cells forms Maximum ATP
During moderate exercise ATP is replenished by aerobic respiration of glucose or fatty acids.
Glucose is first obtained from glycogen reserves and then from the blood sugar.
Aerobic respiration of glucose forms 36 – 38 ATP per glucosemolecule and completely oxidises glucose to CO2 and H2O.
Muscle fatigue occurs more slowly since more ATP is available and lactic acid is not formed.
Provides energy for Muscle contraction
C6H12O6 + 6O2
AEROBIC RESPIRATION
+ ENERGY
38 ATP
6CO2 + 6H2O
38ADP + 38Pi
83
Summary of Respiration in Muscle Cells
Some is converted
to glucose by liver
& sent back to
musclesMain source of ATP when oxygen
available
Occurs in mitochondrion
Occurs in cytosolProvides some ATP anaerobically
ATP
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Aerobic Metabolism of Contracting Muscle Cell
Martini & BartholomewFigure 7-9(b)
Oxidative (Red) Muscle Fibers vs Glycolytic (White) Muscle fibers
Muscle cells which specialize for aerobic respiration are called oxidative fibers or “slow fibers”.
•Slow fibers have many mitochondria and contain muchmyoglobin for O2 storage so are also called “red fibers”.
Muscle cells which specialize for anaerobic respiration(anaerobic glycolysis) are called glycolytic fibers or“fast fibers”.
•Fast fibers have few mitochondria and little myoglobinso are also called “white fibers”.
•Fast fibers are adapted for rapid bursts of intense exercise and fatigue easily