kuliah muscle contraction 2010

7/30/2019 Kuliah Muscle Contraction 2010

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MUSCLECONTRACTION

DODY TARUNA,dr, M.KesDEPT. OF PHYSIOLOGY

HANG TUAH MEDICAL FACULTY

SURABAYA


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Muscle Types

Cardiac heart

Smooth internal organs

Skeletal

"voluntary"Attach to bone

Move appendages

Support body

Antagonistic pairs

Flexors

Extensors


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Muscle Types


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Describe the structural and physiological

differences between cardiac muscle and

skeletal muscle;

Describe the structural and physiological

differences between smooth muscle and

skeletal muscle; and

Relate the unique properties of smooth

muscle to its locations and functions.


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About 40% body mass

Muscle fibers cells

Fascicle

bundleMotor unit

Muscle

sheath

Attach to tendons (which attach to bone)

Skeletal Muscle Anatomy


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Skeletal Muscle Anatomy


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Multiple nuclei

Sarcolemma

T-tubules

Sarcoplasmic reticulum

Sarcoplasm

Mitochondria Glycogen & ions

Myofibrils

Muscle Fiber Structure


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Muscle Fiber Structure

Figure 12-3b: ANATOMY SUMMARY: Skeletal Muscle


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Actin "thin fibers"

Tropomysin

Troponin

Myosin "thick fibers"

Tinin

elastic anchorNebulin non-elastic

Myofibrils: Site of Contraction


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Myofibrils: Site of Contraction

Figure 12-3c-f: ANATOMY SUMMARY: Skeletal Muscle


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Sarcomere length

Problem


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Muscular

Contraction

The sliding filamentmodel Movement of the

actin filament overthe myosin filament

Formation of cross-bridges betweenactin and myosinfilaments

Reduction in thedistance between Z-discs of thesarcomere Actin

Myosin

Actinin (z-disc)


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MUSCLE CONTRACTION

The process of muscle contraction and

relaxation can be viewed as occurring in

four major phases:

(1)excitation.

(2)excitation-contraction coupling.

(3)contraction.(4)relaxation.


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MUSCLE CONTRACTION

1.Excitation

Excitation is the process in which actionpotentials in the nerve fiber lead to action

potentials in the muscle fiber.


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EXCITATION

1.1.A nerve signal the synaptic knob

stimulates voltage-gated calcium channels

OPEN Calcium ions enter the synaptic knob.

1.2.Calcium ions stimulate exocytosis of thesynaptic vesicles release acetylcholine (ACh)

into the synaptic cleft.

One action potential causes exocytosis of about

60 synaptic vesicles, and each vesicle releases

about 10,000 molecules of ACh.


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EXCITATION

1.3.ACh diffuses across the synaptic cleft

binds to receptor proteins (LIGAND GATEDion channels) on the sarcolemma.

1.4.ACh (the ligand) binds to receptor rec.change shape open an ion channel

through the middle of the rec. proteinNadiffuse quickly into the cell and K diffuseoutward the sarcolemma reversespolarityits voltage quickly jumps fromRMP(resting membrane potential) of -90 mVto a peak of +75mV as Na enters, and thenfalls back to a level mV as Na close to theRMP as K diffuses out called the end-platepotential (EPP).


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EXCITATION

1.5.Areas of sarcolemma next to the end

plate have voltage-gated ion channels

open in response to the EPP. Some of the

voltage-gated channels are and admit it tothe cell, while specific for Na others are

specific for K and allow it to leave.

These ion movements create an actionpotential.The muscle fiber is now excited


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MUSCLE CONTRACTION

2.Excitation-Contraction Coupling

Link the action potentials on thesarcolemma activation of the

myofilaments, Preparing them to

contract


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Excitation-Contraction Coupling

2.1.A wave of action potentials spreads from

the end plate in all directions, like ripples

on a pond. When this wave of excitation

reaches the T tubules, it continues downthem into the sarcoplasm.


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2.2.Action potentials open voltage-regulated

ion gates in the T tubules. These are

physically linked to calcium channels in

the terminal cisternae of the sarcoplasmicreticulum (SR), so gates in the SR open as

well and calcium ions diffuse out of the

SR, down their concentration gradient andinto the cytosol.


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2.3.The calcium ions bind to the troponin of

the thin filaments.

2.4.The troponin-tropomyosin complex

changes shape and shifts to a new

position. This exposes the active sites on

the actin filaments and makes them

available for binding to myosin heads.


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MUSCLE CONTRACTION

3. Contraction

In 1954, two researchers at theMassachusetts Institute of Technology, Jean

Hanson and Hugh Huxley, found evidence fora model now called the sliding filamenttheory.

This theory holds that the thin filaments slide

over the thick ones and pull the Z discsbehind them, causing the cell as a whole toshorten


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CONTRACTION

3.1.The myosin head must have an ATPmolecule bound to it to initiate thecontraction process. Myosin ATPase, anenzyme in the head, hydrolyzes this ATP.The energy released by this processactivates the head, which cocks into anextended, high-energy position. The headtemporarily keeps the ADP and phosphate

group bound to it.3.2.The cocked myosin binds to an activesite on the thin filament.


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CONTRACTION

3.3.Myosin releases the ADP andphosphate and flexes into a bent, low-energy position, tugging the thin

filament along with it. This is called thepower stroke. The head remains boundto actin until it binds a new ATP.

3.4.Upon binding more ATP, myosinreleases the actin. It is now prepared torepeat the whole Process.


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CONTRACTION

A fiber, however, may shorten by as much

as 40% of its resting length, so obviously

the cycle of power and recovery must be

repeated many times by each myosinhead. Each head carries out about five

strokes per second, and each stroke

consumes one molecule of ATP.


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MUSCLE CONTRACTION

4.Relaxation

When its work is done, a muscle fiberrelaxes and returns to its resting length.


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Relaxation

4.1.Nerve signals stop arriving at the neuromuscularjunction, so the synaptic knob stops releasing ACh.

4.2.As ACh dissociates (separates) from its receptor,acetylcholinesterase breaks it down into fragments that

cannot stimulate the muscle. The synaptic knobreabsorbs these fragments for recycling. All of thishappens continually while the muscle is beingstimulated, too; but when nerve signals stop, no new

ACh is released to replace that which is broken down.

Therefore, stimulation of the muscle fiber by AChceases.


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Relaxation4.3.Active transport pumps in the

sarcoplasmic reticulum (SR) pumpCa from the cytosol back into thecisternae. Ca binds toCalsequestrinstored until fiber

stimulated again. ATP is needed formuscle relaxation as well as for musclecontraction

4.4.As calcium ions dissociate fromtroponin, they are pumped into the SRand are not Replaced.


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Relaxation

4.5.Tropomyosin moves back into the

position where it blocks the active sites of

the actin filament. Myosin can no longer

bind to actin, and the muscle fiber ceasesto produce or maintain tension.


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Relaxation

A muscle returns to its resting length with the aid

of two forces:

(1)like a recoiling rubber band, the series-elastic

components stretch it; and(2)since muscles often occur in antagonistic pairs,

the contraction of an antagonist lengthens the

relaxed muscle. Contraction of the triceps

brachii, for example, extends the elbow and

lengthens the biceps brachii.


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Energy for Contraction: ATP &

Phosphocreatine

Aerobic Respiration Oxygen

Glucose

Fatty acids

30-32 ATPs

Anaerobic Respiration Fast but

2 ATP/glucose

PhosphocreatineATPs


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Energy for Contraction: ATP &

Phosphocreatine

Figure : Phosphocreatine


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Central "Feeling"

Lactic acid

Peripheral Glycogen depletion

Ca2+ interference

High Pi

levels

ECF high K+

ACh depletion

Muscle Fatigue: Causes not well known

Figure : Locations and possible causes of muscle fatigue

Fiber Contraction Speed: Fast


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Rate 2-3 times faster

SR uptake of Ca2+

ATP splitting

Anaerobic/Fatigue easily

Power lifting

Fast/delicate

Sprint


Twitch



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Twitch

Figure : Fast-twitch glycolytic and slow-twitch muscle fibers

Fiber Contraction Speed: Oxidative


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Oxidative Fast Twitch Intermediate speed

Anaerobic & aerobic

Slow Twitch: Aerobic, less fatigue More mitochondria

More capillaries

Myoglobin

Endurance activities

Postural muscles

Fiber Contraction Speed: Oxidative

Fast & Slow


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Coordinating the Fibers: Force of Contraction

Figure : Length-tension relationships in contracting skeletal muscle

Excitation and Twitch

LengthTension: more crossbridges: more

tension

M t U it Fib I t d


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Motor Unit: Fibers Innervated

from 1 neuron"All or none"Fine touch

1:1 nerve to fiber

Finger tips

Big muscles

1: 2000

Leg muscles

PLAYAnimation: Muscular System:

Contraction of Motor Units

Figure 12-18: Motor units

Recruitment of Fibers: Produce
http://localhost/var/www/apps/conversion/tmp/Animations/systems/motounit.htmlhttp://localhost/var/www/apps/conversion/tmp/Animations/systems/motounit.html


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Weak stimulus

Lowest threshold fibers

Slow twitch typically

Moderate: adds Fast

OxidativeHigh stimulus: all fibers

Asynchronous:

Units take turns

Prevents fatigue

Recruitment of Fibers: Produce

Graduated Force

Figure 12-18: Motor units

Mechanics of Body Movement:


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Tendons: muscle to bone

Ligaments: bone to boneMuscles: contraction force

Isotonic: movement

Isometric: no movement


Joints



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Joints

Figure 12-19: Isotonic and isometric contractions

Coordinating the Fibers: Summation to


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Coordinating the Fibers: Summation to

Tetanus

Figure : Summation of contractions

Hi t h i l St i i f Fib


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Histochemical Staining of Fiber

Type

Type IIa

TypeIIb

Type I


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Preferential recruitment of

fibres by exercise type


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Higher % of

type 1 fibers

elevates

VO2max

True of both

athletes and

non-athletes


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Muscle: origin near body, insertion distal

Levers: bones, Fulcrum: joints

Physics of Joint Movement:

Figure : The arm is a lever and fulcrum system


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Establishes smooth

voluntary muscle

contractions and tone

Alpha/gamma co-

activation

Gamma activation leads

alpha activation in

voluntary movement

The Gamma system

Vestibular Apparatus and


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Vestibular Apparatus and

Equilibrium

Located in the innerear

Responsible formaintaining generalequilibrium andbalance

Sensitive tochanges in linearand angularacceleration


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Motor Control Functions of the Brain

Brain stem

Cerebrum

Cerebral cortex

Organization of complex movement

Storage of learned experiencesReception of sensory information

Motor cortex M1 (Area 4 and 6)

Most concerned with voluntary

movement

Cerebellum

Monitoring complex movement


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Smooth Muscles: Contrasted to


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Homeostatic role

Control fluid

Sphincters

Tonic contractions

Support tubes

Move products

Slow contractions

Little fatigue

Low O2 use


Skeletal Muscle

Figure : Duration of muscle contraction in

three types of muscle



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Skeletal Muscle

Figure : Types of smooth muscle

S th M l Ch t i ti


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Stimulation

Electrically coupled

Hormones

Paracrines

Various receptors

Single Unit

Multiple unit

Single tapered cells

Longer actin & myosin

Smooth Muscles: Characteristics

S th M l Ch t i ti


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Smooth Muscles: Characteristics

Figure : Anatomy of smooth muscle

Smooth Muscle Contraction:


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Smooth Muscle Contraction:

Mechanism

Figure : Smooth muscle contraction

Smooth Muscle Relaxation:


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Smooth Muscle Relaxation:

Mechanism

Figure : Relaxation in smooth muscle

Cardiac Muscle: Contrasted to


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SkeletalShort branched fibers

Single nucleus

Intercalated discs

Gap junctions

Stimulation

Pacemaker

Autonomic

Hormonal



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Skeletal

Figure : ANATOMY SUMMARY: The Heart

Summary: Comparison of Three


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Su a y Co pa so o ee

Muscle Types

Table : Comparison of Three Muscle Types


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kuliah muscle contraction 2010

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