Function depends on structure

Muscle classification

1. Striated muscle

A. Skeletal Muscle - voluntary muscles that allow for movement

B. Cardiac Muscle - heart - specialized, involuntary

2. Non-striated muscle

Smooth Muscle such as blood vessels, digestive tract, internal organs, involuntary

Muscle functions

Muscle perform four import functions:

1. Produce movement

2. Maintaining posture

3. Stabilizing joints

4. Generating heat

Functional characteristics of muscles

Excitability (irritability): the ability to receive and respond to a stimulus

Contractility: the ability to shorten forcibly when adequately stimulated

Extensibility: the ability to be stretched or extended

Elasticity: the ability of a muscle fiber to resume its resting length after being stretched.

Sarcomere: the contractile unit of a myofibril

contains actin thin filament and myosin thick filament

I band A band I band

Cross bridge

Thick filament Thin filament

Fig. 8-4, p.317

Contraction of sarcomeres-sliding-filament theory

muscle contraction- sarcomeres shorten, actin and myosin move past each other and increase overlap between actin and myosin.

muscle stretched- Sarcomeres elongate. Reduce overlap between actin and myosin.

Note: Length of thick (myosin) and thin (actin) filaments remains constant.

Length-tension relation

Total tension is proportional to the total number of cross-bridges (overlap) between actin and myosin filamentsIdeal resting length: generate maximum force.Overlap to small: few cross-bridges can attach.No overlap: no cross-bridges can attach to actin.

3 pairs of molecules:

1. myosin heavy chains

2. essential light chains

3. regulatory light chains

G-actin polymerize F-actin (filamentous)

Actin - thin filaments1. comprised of protein dimers linked in "chains"2. each actin monomer has a myosin binding site3. thin filaments are anchored at one end to "Z-line" proteins4. thin filaments are free at other end5. "sarcomere" is the name for unit between "Z-lines"

Troponin is a complex of 3 protein subunits:

Troponin C binds Ca 2+

Troponin T binds tropomyosin

Troponin I binds both actin & tropomyosin

Troponin C binds Ca 2+

Troponin T binds tropomyosin

Troponin I binds both actin & tropomyosin

Transduction of chemical to mechanical energy in muscle causes the filaments to slide:

Partial rotation of the actin-bound myosin head.

Cross-bridge chemistry

1. Attachable

2. Revisable

neuromuscular junctions Each muscle cell is directly innervated by the terminal branch of a motor neuron. The contact between nerve and muscle occurs at a small specialized spot termed the neuromuscular junction (NMJ).

Transverse tube (T tube not Z disk): transmit excitation into muscle fibers

Frog Crab

Sarcoplasmic reticulum (SR): Ca2+ is stored and released as free Ca2+ during excitation-contraction

Calsequestirin: Ca2+ binding protein in SR

Ca2+/Ma2+ pump (ATPase): proteins in SR actively transport Ca2+ ions (requires ATP).

Ca++ regulationa. neural activation >> muscle is electrically excited >> AP

AP ionic currents reach SR, open voltage sensitive Ca++ channelsCa++ rushes out of SR, binds to troponin C, actin-myosin permitted to interact >> contraction

b. AP stops, voltage sensitive Ca++ channels close, Ca++ rapidly pumped into SR, tropomyosin returns, actin-myosin interactions blocked >> relaxation

c. Ca++ is sequestered (pumped and stored) in Sarcoplasmic Reticulum (SR)

- SR is the endoplasmic reticulum of muscle cells- SR is intracellular Ca++ store

d. Ca++ is actively pumped into SR from muscle cytoplasm

Ryanodine receptor: located on SR membrane

Dihydropyridine receptor: located on T tubule membrane, no or little Ca2+ passes through in skeletal muscle.

Releasing Ca2+ from SR into the myoplasm depends

1. interaction of activated dihydropyridine receptor and ryanodine receptor-plunger model

2. Calcium-induced calcium release

Mechanisms of Contraction• AP travels down the motor neuron to bouton.• VG Ca++ channels open, Ca++ diffuses into the

bouton.• Ca++ binds to vesicles of NT.• ACh released into neuromuscular junction.• ACh binds onto receptor.• Chemical gated channel for Na+ and K+open.

Mechanisms of Contraction• Na+ diffuses into and

K+ out of the membrane.

• End-plate potential occurs (depolarization).

• + ions are attracted to negative membrane.

• If depolarization sufficient, threshold occurs, producing AP.

Mechanisms of Contraction

• AP travels down sarcolema and T tubules.

• Terminal cisternae release Ca++.

Mechanisms of Contraction

• Ca++binds to troponin.

• Troponin-tropomyosin complex moves.

• Active binding site on actin disclosed.

Sliding Filament Theory• Sliding of filaments is produced by

the actions of cross bridges.• Cross bridges are part of the myosin

proteins that form arms that terminate in heads.

• Each myosin head contains an ATP-binding site.

• The myosin head functions as a myosin ATPase.

Contraction• Myosin binding site splits ATP to ADP and

Pi.• ADP and Pi remain bound to myosin until

myosin heads attach to actin.• Pi is released, causing the power stroke to

occur.

Contraction

• Power stroke pulls actin toward the center of the A band.

• ADP is released, when myosin binds to a fresh ATP at the end of the power stroke.

• Release of ADP upon binding to another ATP, causes the cross bridge bond to break.

• Cross bridges detach, ready to bind again.

Contraction• ACh-esterase degrades ACh.• Ca++ pumped back into SR.• Choline recycled to make more ACh.• Only about 50% if cross bridges are

attached at any given time.– Asynchronous action.

Contraction

• A bands:– Move closer together.– Do not shorten.

• I band: – Distance between A bands of successive sarcomeres.– Decrease in length.

• Occurs because of sliding of thin filaments over and between thick filaments.

• H band shortens.– Contains only thick filaments.

Regulation of Contraction

• Regulation of cross-bridge attachment to actin due to:

– Tropomyosin.

– Troponin.

Role of Ca++

• Relaxation:– [Ca++ ] in sarcoplasm low when

tropomyosin block attachment.

– Ca++ is pumped back into the SR in the terminal cisternae.

– Muscle relaxes.

Role of Ca++ in Muscle Contraction

• Stimulated:• Ca++ is released from

SR.• Ca++ attaches to

troponin• Tropomyosin-troponin

configuration change

Two major processes require ATP in muscle contraction:

1. Hydrolysis ATP by myosin (70-80%)

2. Pumping of Ca2+ back into SR (20-30%)