muscle types and physiology types and characteristics of muscle muscle function and types ...

Muscle Types and Physiology Types and Characteristics of Muscle

Muscle Function and Types

Microscopic Anatomy of Muscle

Muscular Stimulation

Muscular Contraction Mechanism

Muscular Response Based on Stimulus

Energy Sources for Muscular Contraction

Types of Muscular Contractions

Effects of Exercise on Muscles

Developmental Aspects

Muscular Dystrophy

Function of Muscles Produce movement

Maintain posture

Stabilize joints

Generate heat

Skeletal Muscle: Attachments Muscles attach:

• Directly—epimysium of muscle is fused to the periosteum of bone or perichondrium of cartilage

• Indirectly—connective tissue wrappings extend beyond the muscle as a ropelike tendon or sheetlike aponeurosis

The Muscular System Muscles are responsible for all types of body

movement

Three basic muscle types are found in the body

Characteristics of Muscles Muscle cells are elongated (muscle cell =

muscle fiber)

Contraction of muscles is due to the movement of microfilaments within fiber cells

All muscles share some terminology

• Prefix myo refers to muscle

• Prefix mys refers to muscle

• Prefix sarco refers to flesh

Table 9.3

Skeletal Muscle Characteristics Most are attached by tendons to bones

Cells are multinucleate

Striated – have visible banding

Voluntary – subject to conscious control

Cells are cylindrical

Cells are surrounded

and bundled by

connective tissue

Plasma/cell membrane called a sarcolemma

Glycosomes for glycogen storage, myoglobin for O2 storage

Also contain myofibrils, sarcoplasmic reticulum (modified ER), and T tubules

Smooth Muscle Characteristics Has no striations

Spindle-shaped cells

Single nucleus

Involuntary – no conscious control

Found mainly in the walls of hollow organs

Cardiac Muscle Characteristics Has striations

Usually has a single nucleus

Joined to another muscle cell at an intercalated disc

Involuntary

Found only in the heart











Muscular Dystrophy

Table 9.1

Figure 9.1

Bone

Perimysium

Endomysium(between individualmuscle fibers)

Muscle fiber

Fascicle(wrapped by perimysium)

Epimysium

Tendon

Epimysium

Muscle fiberin middle ofa fascicle

Blood vessel

Perimysium

Endomysium

Fascicle

(b)

• Each fascicle is composed of muscle fibers (cells), surrounded by a perimysium• Each muscle fiber is surrounded by endomysium ( & then the sarcolemma)• Muscle fibers (cells) contain several myofibrils

• Whole muscle is surrounded by an epimysium and is composed of wrapped fascicles

Nested Structures in a Muscle Fib-Endo-Fas-Per-Ep

NucleusLight I bandDark A band

Sarcolemma

Mitochondrion

(b) Diagram of part of a muscle fiber showing the myofibrils. Onemyofibril is extended afrom the cut end of the fiber.

Myofibril

Figure 9.5

Myofibril

Myofibrils

Triad:

Tubules ofthe SR

Sarcolemma (muscle fiber

plasma membrane)

Sarcolemma

Mitochondria

I band I bandA band

H zone Z discZ disc

Part of a skeletalmuscle fiber (cell)

• T tubule• Terminal

cisternaeof the SR (2)

M line

Sarcoplasmic Reticulum is Modified Endoplasmic Reticulum(Storage Depot for Calcium Ions)

T tubules are continuous with the sarcolemma

They penetrate the cell’s interior at each A band–I band junction

They’re associated with the paired terminal cisternae to form triads that encircle each sarcomere

T tubules conduct impulses deep into muscle fiber; contains gated channels that regulate Ca 2+ release

Figure 9.2c, d

I band I bandA bandSarcomere

Thick (myosin)filament

M line

Z disc Z discM line

Sarcomere

Thin (actin) filament

Thick (myosin) filament

Elastic (titin) filaments

H zoneThin (actin)filament Z disc Z disc

Patterns Visible in the Sarcomere (Smallest Contractile Unit of a Myofibril)

Microscopic Muscle Anatomy (online)

http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structure/su/m4/s11/sum4s11_9.htm




Figure 9.3

Flexible hinge region

Tail

Tropomyosin Troponin Actin

Myosin head

ATP-bindingsite

Heads Active sitesfor myosinattachment

Actinsubunits

Actin-binding sites

Thick filamentEach thick filament consists of manymyosin molecules whose heads protrude at opposite ends of the filament.

Thin filamentA thin filament consists of two strandsof actin subunits twisted into a helix plus two types of regulatory proteins(troponin and tropomyosin).

Thin filamentThick filament

In the center of the sarcomere, the thickfilaments lack myosin heads. Myosin heads are present only in areas of myosin-actin overlap.

Longitudinal section of filamentswithin one sarcomere of a myofibril

Portion of a thick filamentPortion of a thin filament

Myosin molecule Actin subunits

Tropomyosin and troponin: regulatory proteins bound to actin

Thin and Thick Filament Composition

Figure 9.6

I

Fully relaxed sarcomere of a muscle fiber

Fully contracted sarcomere of a muscle fiber

IA

Z ZH

I IA

Z Z

1

2











Muscular Dystrophy

Nucleus

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal ofneuromuscular junction

Sarcolemma ofthe muscle fiber

Ca2+Ca2+

Axon terminalof motor neuron

Synaptic vesiclecontaining ACh

MitochondrionSynapticcleft

Fusing synaptic vesicles

1 Action potential arrives ataxon terminal of motor neuron.

2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.

Figure 9.8

Skeletal muscles are stimulated by the axon termini of somatic motor neuronsAssociation of one axon to a particular group of fibers = 1 motor unit

How Muscle Contracts: 1) Events at the Neuromuscular Junction

Figure 9.8

Nucleus

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal ofneuromuscular junction

Sarcolemma ofthe muscle fiber

Ca2+Ca2+


Synaptic vesiclecontaining AChMitochondrionSynapticcleft

Junctionalfolds ofsarcolemma

Fusing synaptic vesicles

ACh

Sarcoplasm ofmuscle fiber

Postsynaptic membraneion channel opens;ions pass.

Na+ K+

Ach–

Na+

K+

Degraded ACh

Acetyl-cholinesterase

Postsynaptic membraneion channel closed;ions cannot pass.

1 Action potential arrives ataxon terminal of motor neuron.

2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.

3 Ca2+ entry causes some synaptic vesicles to release their contents (acetylcholine)by exocytosis.

4 Acetylcholine, aneurotransmitter, diffuses across the synaptic cleft and binds to receptors in the sarcolemma.

5 ACh binding opens ionchannels that allow simultaneous passage of Na+ into the musclefiber and K+ out of the muscle fiber.

6 ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase.

How Muscle Contracts: 1) Events at the Neuromuscular Junction

Events at neuro-muscular junction movie

Nerve impulse causes muscular contraction: excitation-contraction (E-C) coupling

Figure 9.9

Na+

Na+

Open Na+

Channel

Closed Na+Channel

Closed K+

Channel

Open K+ Channel

Action potential++++++

+++++

+

Axon terminal

Synapticcleft

ACh

ACh

Sarcoplasm of muscle fiber

K+

2 Generation and propagation ofthe action potential (AP)

3 Repolarization

1 Local depolarization: generation of the end plate potential on the sarcolemma

K+

K+Na+

K+Na+

Wave ofde

po

lari

zatio

n

How Muscle Contracts: 2) Initiation of an Action Potential

Figure 9.10

Na+ channelsclose, K+ channelsopen

K+ channelsclose

Repolarizationdue to K+ exit

Threshold

Na+

channelsopen

Depolarizationdue to Na+ entry

How Muscle Contracts: 3) How the Sarcolemma Resets











Muscular Dystrophy


Muscle fiberTriad

One sarcomere

Synaptic cleft

Sarcolemma

Action potentialis generated

Terminal cisterna of SR ACh

Ca2+

How Muscle Contracts: 4) Action Potential Causes Ca++ Release

Figure 9.11, step 1

Figure 9.11, step 4

Steps inE-C Coupling:

Terminal cisterna of SR

Voltage-sensitivetubule protein

T tubule

Ca2+

releasechannel

Ca2+

Sarcolemma

Action potential ispropagated along thesarcolemma and downthe T tubules.

Calciumions arereleased.

1

2

How Muscle Contracts: 4) Action Potential Causes Ca++ Release

Figure 9.11, step 5

Troponin Tropomyosinblocking active sitesMyosin

Actin

Ca2+

The aftermath

How Muscle Contracts: 5) Ca++ Binds to Troponin

Figure 9.11, step 6


Actin

Active sites exposed and ready for myosin binding

Ca2+

Calcium binds totroponin and removesthe blocking action oftropomyosin.

The aftermath

3

How Muscle Contracts: 5) Ca++ Binds to Troponin

Figure 9.11, step 7


Actin

Active sites exposed and ready for myosin binding

Ca2+

Myosincross bridge

Calcium binds totroponin and removesthe blocking action oftropomyosin.

Contraction begins

The aftermath

3

4

How Muscle Contracts: 6) Troponin Slides Tropomyosin Off Myosin Binding Sites

Calcium is sequestered again by the SR, lowering Ca++ levels, and causing muscle to relax as tropomyo. covers binding sites

Figure 9.12

1

Actin

Cross bridge formation.

Cocking of myosin head. The power (working) stroke.

Cross bridge detachment.

Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

ATPhydrolysis

ATP

ATP

24

3

ADP

Pi

ADPPi

Four Step Power Cycle or “Cross Bridge Cycle”

Figure 9.12, step 1

Actin


Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

1

Step One of the Cross Bridge Cycle

Figure 9.12, step 3

The power (working) stroke.

ADP

Pi

2

Step Two of the Cross Bridge Cycle

Figure 9.12, step 4


ATP

3

Step Three of the Cross Bridge Cycle

Figure 9.12, step 5

Cocking of myosin head.

ATPhydrolysis

ADPPi

4

Step Four of the Cross Bridge Cycle

Figure 9.12

1

Actin


Cocking of myosin head. The power (working) stroke.


Ca2+

Myosincross bridge

Thick filament

Thin filament

ADP

Myosin

Pi

ATPhydrolysis

ATP

ATP

24

3

ADP

Pi

ADPPi

Sliding Filament Theory

Summary of the Cross Bridge Cycle




The Power CycleA. Masking protein complex (tropomyosin) binds Ca++ released from the

SR moves aside to expose head-binding sitesB. Steps of the Power Cycle

1. "Cocked" myosin head binds to actin myofilament site 2. Head bends towards the M line (sarcomere center-line), pulling

thin filament along and releasing ADP and P (broken ATP) for the power stroke

3. ATP binds to the myosin head, causing it to detach4. Myosin head “recocks” as ATP broken down to ADP and P











Muscular Dystrophy

2. Contraction produces tension, the force exerted on the load or object to be moved

Principles of Muscle Mechanics

3. Contraction does not always shorten a muscle:

• Isometric contraction: no shortening; muscle tension increases but does not exceed the load

• Isotonic contraction: muscle shortens because muscle tension exceeds the load

4. Force and duration of contraction vary in response to stimuli of different frequencies and intensities

1. The same principles apply to contraction of a single fiber and a whole muscle

Muscle Twitch Response of a muscle to a single, brief threshold

stimulus

Simplest contraction observable in the lab (recorded as a myogram)

Three phases of a twitch:

• Latent period: events of excitation-contraction coupling

• Period of contraction: cross bridge formation; tension increases

• Period of relaxation: Ca2+ reentry into the SR; tension declines to zero

Figure 9.14a

Latentperiod

Singlestimulus

Period ofcontraction

Period ofrelaxation

(a) Myogram showing the three phases of an isometric twitch

Excitation-contraction coupling

Cross bridge formation; tension

increases

Ca2+ reentry into the SR; tension declines to zero

Graded Muscle ResponsesVariations in the degree of muscle contraction

Required for proper control of skeletal movement

Responses are graded by:

1. Changing the frequency of stimulation

2. Changing the strength of the stimulus

Response to Change in Stimulus Frequency

A single stimulus results in a single contractile response—a muscle twitch

Contraction

Relaxation

Stimulus

Single stimulus single twitch

A single stimulus is delivered. The muscle contracts and relaxes

Response to Change in Stimulus Frequency Increases frequency of stimulus (muscle does not have time to

completely relax between stimuli). Distinct peaks are still seen in the myogram.

Figure 9.15b

Stimuli

Partial relaxation

Low stimulation frequency -->unfused (incomplete) tetanus

(b) If another stimulus is applied before the muscle relaxes completely, then more tension results. This is temporal (or wave) summation and results in unfused (or incomplete) tetanus.

Response to Change in Stimulus Frequency Ca2+ release stimulates further contraction temporal (wave) summation

Further increase in stimulus frequency unfused (incomplete) tetanus If stimuli are given quickly enough, fused (complete) tetany results

Figure 9.15c

Stimuli

High stimulation frequency fused (complete) tetanus

(c) At higher stimulus frequencies, there is no relaxation at all between stimuli. This is fused (complete) tetanus.

Response to Change in Stimulus Strength

Threshold stimulus: stimulus strength at which the first observable muscle contraction occurs

Muscle contracts more vigorously as stimulus strength is increased above threshold

Contraction force is precisely controlled by recruitment (multiple motor unit summation), which brings more and more muscle fibers into action

Figure 9.16

Stimulus strength

Proportion of motor units excited

Strength of muscle contraction

Maximal contraction

Maximalstimulus

Thresholdstimulus

Response to Change in Stimulus Strength

Response to Change in Stimulus Strength Size principle: motor units with larger and larger fibers are

recruited as stimulus intensity increases

Figure 9.17

Motorunit 1Recruited(smallfibers)

Motorunit 2recruited(mediumfibers)

Motorunit 3recruited(largefibers)











Muscular Dystrophy

Energy for Muscle Contraction

Figure 9.20

Short-duration exerciseProlonged-durationexercise

ATP stored inmuscles isused first.

ATP is formedfrom creatinePhosphateand ADP.

Glycogen stored in muscles is brokendown to glucose, which is oxidized togenerate ATP.

ATP is generated bybreakdown of severalnutrient energy fuels byaerobic pathway. Thispathway uses oxygenreleased from myoglobinor delivered in the bloodby hemoglobin. When itends, the oxygen deficit ispaid back.











Muscular Dystrophy

Isotonic Contractions Muscle changes in length

and moves the load

Isotonic contractions are either concentric or eccentric:

• Concentric contractions—the muscle shortens and does work

• Eccentric contractions—the muscle contracts as it lengthens

Isometric Contractions The load is greater

than the tension the muscle is able to develop

Tension increases to the muscle’s capacity, but the muscle neither shortens nor lengthens

Figure 9.21

Largenumber of

musclefibers

activated

Contractile force

Highfrequency ofstimulation

Largemusclefibers

Muscle andsarcomere

stretched to slightly over 100%of resting length

Summary of Factors Increasing Contractile Force











Muscular Dystrophy

Effects of Exercise on Muscle

Results of increased muscle use

• Increase in muscle size

• Increase in muscle strength

• Increase in muscle efficiency

• Muscle becomes more fatigue resistant










Muscle Fiber Types


Muscular Dystrophy

Muscle Fiber TypeFibers classified according to two characteristics:

1. Speed of contraction: slow or fast, according to:

• Speed at which myosin ATPases split ATP

• Pattern of electrical activity of the motor neurons

2. Metabolic pathways for ATP synthesis:

• Slow and fast oxidative fibers—use aerobic pathways (fast oxidative fibers = red meat in birds)

• Glycolytic fibers—use anaerobic glycolysis (these fibers are “fast twitch” white meat in birds)

Figure 9.23

Predominanceof fast glycolytic(fatigable) fibers:“fast twitch” or“white meat”

Predominanceof slow oxidative(fatigue-resistant)

fibers: “slow twitch” ordark meat

Small load

Contractilevelocity

Contractileduration











Muscular Dystrophy

Developmental Aspects Cardiac and skeletal muscle become amitotic, but can

lengthen and thicken

Injured heart muscle is mostly replaced by connective tissue

Smooth muscle regenerates throughout life

Myoblast-like skeletal muscle satellite cells have limited regenerative ability; are responsible for generating more fibers and in muscle repair

Muscular development reflects neuromuscular coordination

• Development occurs head to toe, and proximal to distal

• Peak natural neural control occurs by midadolescence

• Athletics and training can improve neuromuscular control

Diseases and Medical Conditions (Myopathies) of the Muscular System

• Myasthenia gravis (autoimmumity; destruction of ACh receptors so neuromuscular junctions don’t work)

• Poliomyelitis (viral infection of muscle nerves)

• Muscle strains cause myalgia (pain) and sometimes myositis (inflammation). Inflamed tendons are fibromyositis.

• Fibromyalgia- (muscle pain) causes widespread pain in the muscles accompanied by fatigue and sleep disorders. Thought to be neurologically, blood flow, based.

• Cramps (muscle spasms)

• Contusion (muscle bruise)

• Crush injury (severe trauma releasing myoglobin)

• Muscular dystrophy (e.g. Duchenne's; degeneration & atrophy of muscles)

Muscular Dystrophy Group of inherited muscle-destroying diseases

Muscles enlarge due to fat and connective tissue deposits

Muscle fibers atrophy

Duchenne muscular dystrophy (DMD):

• Most common and severe type

• Inherited, sex-linked, carried by females and expressed in males (1/3500) as a lack of dystrophin, a protein that links muscle fibers together

• Victims become clumsy and fall frequently; usually die of respiratory failure in their 20s

• No cure, but viral gene therapy or infusion of stem cells with correct dystrophin genes show promise











Muscular Dystrophy

muscle types and physiology types and characteristics of muscle muscle function and types ...

Documents

directlyepimysium of

basic muscle types

cardiac muscle characteristics

smooth muscle characteristics

sarcolemma muscle fibers

muscle prefix sarco

muscle prefix mys

elongated muscle cell