General physiology lecture 3

Muscle PhysiologyLecture 3

Muscular Tissue• Skeletal Muscle

• Cardiac Muscle

• Smooth Muscle

Skeletal Muscle

• Long cylindrical cells• Many nuclei per cell• Striated• Voluntary• Rapid contractions

Cardiac Muscle• Branching cells

• One or two nuclei per cell

• Striated

• Involuntary

• Medium speed contractions

Smooth Muscle• Fusiform cells

• One nucleus per cell

• Nonstriated

• Involuntary

• Slow, wave-like

contractions

SKELETAL MUSCLE CELL

- “Striated”; striped appearance is because of the orderly arrangement of the thin and thick filaments that makeup the majority of the contractile proteins.

- The contractile proteins are made of 3 types of filaments;

1. THIN FILAMENT2. THICK FILAMENT3. ELASTIC FILAMENT

CONTRACTILE PROTEINS1. THIN FILAMENT- Has 3 parts;

i) ACTIN PROTEIN (i.e. the main molecule of this filament). FUNCTION: Binds to myosin head.

ii) TROPONIN FUNCTION: Regulatory function by binding to Ca 2+

iii) TROPOMYOSIN FUNCTION: Has a regulatory function by blocking/unblockingthe binding site of actin to the myosin head

Microanatomy of Skeletal Muscle

Each muscle cell is called a muscle fiber.Within each fiber are many myofibrils.

ARRANGEMENT OF CONTRACTILE PROTEINS IN SKELETAL MUSCLE

Z line Z line

A myosin is elongated with an enlarged head at the end.

CONTRACTILE PROTEINS2. THICK FILAMENT

– made of myosin protein- has 2 main parts i) MYOSIN HEAD - forms cross-bridge with actin.ii) MYOSIN TAIL – forms the shaft of thick bands.

Many myosin molecules form the thick myosin filament.It has many heads projecting away from the main molecule.

The thinner actin filament is composed of three parts: actin, tropomyosin and troponin.

H Band

This sarcomere illustrates the thin actin and the thick myosin filaments. The area of the sarcomere has only myosin is called the H bond

Sarcomere Relaxed

Here is another diagram of a sarcomere. Note the A band. It is formed by both myosin and actin filaments. The part of the sarcomere with only actin filaments is called the I band.This is a sarcomere that is relaxed.

Sarcomere Partially Contracted

This sarcomere is partially contracted. Notice that the I bands are getting shorter.

Sarcomere Completely Contracted

The sarcomere is completely contracted in this slide. The I and H bands have almost disappeared.

Which filament has moved as the sarcomere contracted? Note the thick myosin filaments have not changed, but the thin actin filaments have moved closer together.

SLIDING FILAMENT THEORY

SLIDING FILAMENT THEORY A better understanding of how muscle contracts can

be demonstrated by the interaction between the contractile proteins in muscle as demonstrated by the sliding filament mechanism model.

(STEP WISE)1. Myosin heads are activatedHOW? – Myosin head hydrolyses (breakdown) ATP to ADP + Pi

NB: Part of myosin head acts as ATPase.ATPase is an enzyme that splits ATP to ADP and Pi (free phosphate group) through hydrolysis reaction.

- Hydrolysis of ATP transfers energy from ATP to myosin head (so myosin head becomes activated).

- Activated myosin head binds to ADP and is ready for actin binding (= cross bridge)

SLIDING FILAMENT THEORY2. Activated myosin head binds rapidly to

myosin- binding sites on actin3. Myosin head still bonded to actin;

i) Changes its shapeii) Moves towards the center of sarcomere

NB. i) and ii) called power stroke4. Myosin head is still bonded to actin- ADP released from myosin head

SLIDING FILAMENT THEORY

5. ATP binds to the myosin in the myosin-actin complex

6. Myosin head detaches from actin

7. Myosin head hydrolyses ATP to ADP + Pi

8. Steps 2 – steps 8 is repeated

Contraction: The Sliding-Filament Theory

• Sarcomeres change length when muscle contracts or is stretched = correspond the change in muscle length

• A bands (corresponds to length of thick filaments) maintains constant length when muscle shortens vs.

• I bands & H-zone (zones where actin & myosin do not overlap in the resting muscle) become shorter

• When muscle is stretched, A bands again maintain a constant length and I bands & H zone become longer

Contraction: The Sliding-Filament Theory con’t• Neither the myosin thick filaments nor the actin

thin filaments change in length when a sarcomere shorted/stretched but it is the extent of over-lap between actin & myosin filaments that changes = became the basis of the sliding-filament theory

• Sarcomeres shorten during muscle contraction as thin filaments actively slide along thick filaments i.e. thin filament are pulled closer to center of sarcomere & because they are firmly anchored in Z-disks, sarcomere shortens & vice versa = when muscle relaxes/stretched, the overlap between thin & thick filaments is reduced and sarcomeres elongate.

Binding Site Tropomyosin

Troponin

Myosin

The binding sites are now exposed and myosin headsare able to attach to form cross bridges.

Neuromuscular Junction

NEUROMUSCULAR JUNCTION

DEFINITION -Is the junction between the terminal of a motor neuron and a muscle fiber.

- The neuromuscular junction is also called the myoneural junction.

- It is a kind of chemical synapse. The terminals of motor axons contain thousands of vesicles filled with acetylcholine (ACh).

- The ACh are released when nerve impulses (action potentials) traveling down the motor neurons of the

sensory-somatic branch of the nervous system. The end

result is that it causes the skeletal muscle fibers at

which they terminate to contract.

Acethy

Acethylcholine is released from the motor neuron.

Acetylcholine Opens Na+ Channel

Excitation-Contraction Coupling

EXCITATION- CONTRACTION COUPLING

(SEQUENCE OF EVENTS)

EXCITATION- CONTRACTION COUPLING

EXCITATION- CONTRACTION COUPLING (cont’d)

EXCITATION- CONTRACTION COUPLING (cont’d)

Muscle Contraction Summary• Nerve impulse reaches myoneural junction

• Acetylcholine is released from motor neuron

• ACh binds with receptors in the muscle membrane to allow sodium to enter

• Sodium influx will generate an action potential in the sarcolemma

Muscle Contraction Continued

• Action potential travels down T tubule

• Sarcoplamic reticulum releases calcium

• Calcium binds with troponin to move the troponin, tropomyosin complex

• Binding sites in the actin filament are exposed

Muscle Contraction Continued

• Myosin head attach to binding sites and create a power stroke

• ATP detaches myosin heads and energizes them for another contraction

• When action potentials cease the muscle stop contracting

Motor UnitAll the muscle cells controlled by one

nerve cell

MOTOR UNIT

DEFINITION - Is a motor neuron plus all skeletal muscle fiber it stimulates

- So one skeletal muscle can have many motor units.

- We generally see 2 patterns;

1. MUSCLES CONTROLLING PRECISE MOVEMENTS

2. MUSCLES CONTROLLING POWERFUL GROSS MOVEMENTS

Motor Unit Ratios

• Back muscles– 1:100

• Finger muscles– 1:10

• Eye muscles– 1:1

Motor units come in different sizes.The ratio is about one nerve cellTo 100 muscle cells in the back.Finger muscles have a much smaller Ratio of 1:10.Eye muscles have 1:1 ratio becauseOf the precise control needed in vision.

ATPATP is the form ofenergy that muscles and all cells of the body use. The chemical bond bet the last 2 phosphates has just the right amount of energy to unhook myosin heads and energize them for another contraction.Pulling of the end phosphate from ATP will release the energy. ADP and a single phosphate will be left over. New ATP can be regenerated by reconnecting the phosphate with the ADP with energy from our food.

Creatine

• Molecule capable of storing ATP energy

Creatine + ATP Creatine phosphate + ADP

Creatine Phosphate

• Molecule with stored ATP energy

Creatine + ATPCreatine phosphate + ADP

Creatine phosphate is an important chemical to muscles.It is a molecule that is able to store ATP energy. It can combine with an ADP to produce creatine and ATP. This process occurs faster than the synthesis of ATP from food.

Muscle Fatigue

• Muscle fatigue is often due to lack of oxygen that causes ATP deficit

• Lactic acid builds up from anaerobic respiration in the absence of oxygen.

• Lactic acid fatigues the muscle.

MUSCLE FATIGUEDEFINE: Is when muscle is unable to

maintain its strength of contraction or tension

WHAT HAPPENS AT CELL LEVEL?- Muscle can not produce enough ATP

to meet its needsFACTORS CONTRIBUTING TO MUSCLE

FATIGUEi) Insufficient oxygenii) Depleted glycogeniii) Build-up of lactic acidiv) Failure for action potential in motor

neuron to release enough ATP

Muscle Atrophy

• Weakening and shrinking of a muscle

• May be caused– Immobilization– Loss of neural stimulation

MUSCLE ATROPHYDEFINITION – Is wasting away of musclesDESCRIBE – Individual muscle fibers within muscle

size caused by progressive loss of myofibrils.

Muscle Hypertrophy

• Enlargement of a muscle• More capillaries• More mitochondria• Caused by

– Strenuous exercise– Steroid hormones such as testosterone stimulate muscle growth and

hypertrophy

MUSCLE MUSCLEHYPERTROPHY ATROPHY

Muscle Tonus

• Also called muscle tone

• It refers to the tightness of a muscle

• In a muscle, some fibers always contracted to add tension or tone to the muscle.

Tetany

• Sustained contraction of a muscle

• Result of a rapid succession of nerve impulses

What is a muscle twitch?

• The brief contractile response of skeletal muscle to a single maximal volley of impulses in the motor neuron supplying it is called a twitch.

• It is the fundamental unit of recordable muscle activity.

• The duration of a twitch is between 1/5 and 1/200 second, depending of the type of muscle

PHASES OF A MUSCLE TWITCH

What are the three phases of a muscle twitch?

• Latent phase- indicates the period between the time the stimulus is applied and the beginning of the contractile response (0.01 sec)

• Contraction phase – follows the latent phase when the muscle responds to the stimulus by shortening (0.04 sec)

• Relaxation phase – is the period when the muscle returns to its original length(0.05 sec)

Tetanus

This slide illustrates how a muscle can go into a sustained contraction by rapid neural stimulation.In number 4, the muscle is in a complete sustained contraction or tetanus.

Refractory Period

• Brief period of time in which muscle cells will not respond to a stimulus

Refractory Period

The area to the left of the red line is the refractory period for themuscle contraction. If the muscle is stimulated at any time to theleft of the line, it will not respond. However, stimulating the muscle to the right of the red line will produce a second contraction on top of the first contraction. Repeated stimulations can result to tetany.

Skeletal Muscle Cardiac Muscle

Refractory Periods

Cardiac muscle tissue has a longer refractory period than skeletal muscle. This prevents the heart from going into tetany.

Isometric Contraction

• Produces no movement

• They are used in standing, sitting and maintaining our posture.

• For example when you are standing, muscles in your back and abdomen pull against each other to keep you upright. They do not produce movement, but enable you to stand.

Isotonic Contraction

• Isotonic contractions are the types that produce movement.

• Used in– Walking– Moving any

part of the body

Fast and Slow twitch muscles1. Slow twitch muscles are Type I or slow oxidative fibers or red muscles – are designed to sustain slow but long-lived muscular contractions and are able to function for long periods on aerobic activity.

2. Fast twitch muscles are white fibers or Type II – have larger diameter, more extensive sarcoplasmic reticulum, more folds in their neuromuscular junctions, more glycolytic enzymes, less myoglobin, and fewer mitochondria.

Subtypes of Fast Twitch Muscles

• Type IIa or intermediate fast twitch muscles- or fast oxidative glycolytic fibers (FOG)- because of their ability to display, when exposed to the relevant training stimuli; has the high capacity to contract under conditions of aerobic energy production.

• Type IIb fibers are the “turbo chargers” in our muscles and are also called fast glycogenolytic (FG) fibers since they rely almost exclusively on the short-term alactic/glycolytic energy system to fire them up.

MYSTHENIA GRAVIS

MYSTHENIA GRAVIS- A characteristic symptom is fatigability, which means that a

muscle that is used repeatedly starts to become weak.  - The symptoms usually start in the face and spread to the

other parts of the body as the disease progresses.  - Patients initially complain of drooping eye lids that gets

worst as the day goes on; they develop double vision, difficulty talking, and difficulty chewing. 

- All of these symptoms are worst with repeated use and improve with rest. 

- As the disease progresses the shoulders and the thighs become week and the weakness could eventually spread tothe muscles that are used to breath; the patient coulddevelop shortness of breath and stop breathing if nottreated properly.

Next meetingQuiz on Muscle Physiology