101-805 unit 7 the muscular system - john abbott...

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


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


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.


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

14

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


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


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


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


Cross Bridge Formation

ADPP

Ca+2

Ca+2


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


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


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


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]


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


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


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.

64

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

67

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

69

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

70

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

71

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

72

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.

73

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

75

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

80

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

81

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

82

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

84

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

101-805 unit 7 the muscular system - john abbott...

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