Excitation contraction coupling

Transmission of action potential along transverse tubules (T tubules)

T tubules action potentials caused release of Ca ions inside the muscle fiber.

Ca ions caused contraction Overall process called Excitation

Contraction Coupling

Axon Terminal

Opening of Voltage gated Calcium channels

Entry of Calcium ions from Extracellular fluid

Opening of vesicles & release of Ach

Synaptic cleft

Binding of Ach with Receptor and formation of Ach-Receptor complex

Opening of the ligand gated sodium channels

& entry of sodium ions from ECF

Development of end plate potential

Passage of Ach

Postsynaptic membrane

Muscle Fiber

Generation of Action Potential

Excitation contracting coupling

Muscular contraction

Neuromuscular transmission

The function of neuromuscular junction is to transmit the impulses from the nerve to the muscle.

When the impulses are transmitted from nerve to the muscle, a series of events occur in the neuromuscular junction:

1. Release of acetylcholine 2. Action of acetylcholine 3. Binding with receptors 4. Miniature end plate potential 5. Destruction of acetylcholine

Action Potential through motor nerve fiber

Exciting Contraction Coupling

Neuromuscular Transmission

1. Nerve impulse reaches end of axon2. Ca channels open3. Release of Ach into synaptic cleft4. Diffusion of Ach across the cleft5. Attachment of Ach to ach receptors on sarcolemma6. Opening of Na channels which initiates

depolarization of sarcolemma 7. Development of end plate potential8. Generation of action potential9. The action potential causes the release of Ca ion

from the terminal cisternae10. Muscular contraction

Generation of Action potential Resting sarcolemma is polarizedOutside the cell is positive

(predominant extracellular ion is Na)

Inside the cell is negative (predominant intracellular ion is K)

Stimulation Ach binding to Ach receptors on sarcolemma

Ion gates open (Na rushes into cell and K rushes out of cell

Cells interior becomes less negative Depolarization

Generation of Action potential

DepolarizationLoss of state of polarityLoss of negative membrane potentials Nerve stimulus is strong enoughAction potential is generated from

neuromuscular junction across the sarcolemma in all directions

Action potential separates over cell surface

Generation of Action potential

Generation of Action Potential

Generation of Action Potential

Sliding Filament

Explains the relationship between thick and thin filaments as contraction proceeds

1. The influx of Ca ion, triggering the exposure of binding sites on actin

The Action potential brings about the release of Ca ion from the terminal cisternae

Ca ion binds to the troponin, causing change in conformation of the troponin tropomyosin complex

This conformation changes exposes the binding site on actin

Sliding Filament

2. The binding of myosin to actin Myosin head bind to actin site and

forming cross bridge3. Movement of thin filament Release of ADP and Pi The myosin cross bridge pulls the

thin filament inward toward the centre of sarcomere

Sliding Filament

4. Disconnecting Myocin head from Actin ATP binds to the myosin head disconnecting from

actin5. Repositioning of the myosin head The release of myosin head trigger the hydrolysis

of ATP molecule into ADP and Pi Energy is transferred from ATP to the myosin head 6. Removal of Ca ion Ca ion transported back into the sarcoplasmic

reticulum Troponin - tropomyosin complex covers the

binding sites on Actin

Sliding-Filament Mechanism

Sliding-Filament Mechanism

CONTRACTION

ISOTONIC CONTRACTIONS CAUSES THE MUSCLE LENGTH TO CHANGE

AND THE LOAD TO MOVEUSED IN

WALKING MOVING ANY PART OF THE BODY

CONTRACTIONS

CONTRACTIONS

ISOMETRIC CONTRACTIONSTENSION BUILDS TO THE MUSCLE’SCAPACITY, BUT THE MUSCLENEITHER SHORTENS OR LENGTHENS. USED IN

STANDING SITTING

CONTRACTIONS

MUSCLE TWITCH

A single rapid contraction in response of muscle to a stimulus

Muscle fiber contracts and then relaxes

Strong twitch Weak Twitch Depends on the number of motor

units activated

MUSCLE CONTRACTION

THERE ARE THREE PHASES:

1. LATENT PERIOD

2. PERIOD OF CONTRACTION

3. PERIOD OF RELAXATION

LATENT PERIOD

First few seconds following stimulation

Increase in muscle tension Ca release Cross bridge No shortening of muscles

PERIOD OF CONTRACTION

Cross bridges are active Sarcomere shorten

PERIOD OF RELAXATION

Re entry of Ca to Sarcoplasmic Reticulum

Muscle tension decreases to zero Cross bridge ends Muscle returns to original length

GRADED MUSCLE RESPONSES

Variations in the degree of muscle contraction

Three ways muscle contraction are graded

1. Degree of muscle stretch2. By changing the strength of the stimulus3. By changing the frequency (speed) of

stimulation Summation Tetanus

Degree of muscle stretch (The Effect of Sarcomere Length on Tension)

Amount of tension (force) generated by the muscle depends on length of muscle before it was stimulated

Unstretched (Overly contracted , results weak contraction) Overlapping of thin filaments

Overstretched (Too stretched, weak contraction results) Thin filaments are pulled to the end of thick filaments

Moderately stretched (Optimum resting length produces greatest force when muscle contracts Moderate overlapping produces maximum contraction

developed when optimum overlap of thick and thin filaments

Degree of muscle stretch (The Effect of Sarcomere Length on Tension)