Download Chapter 8a

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
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 sarcomeressliding-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 filaments
Ideal resting length:
generate maximum
force.
Overlap to small: few
cross-bridges can attach.
No overlap: no crossbridges can attach to
actin.
3 pairs of molecules:
1. myosin heavy chains
2. essential light chains
3. regulatory light chains
Actin - thin filaments
1. comprised of protein dimers linked in "chains"
2. each actin monomer has a myosin binding site
3. thin filaments are anchored at one end to "Z-line"
proteins
4. thin filaments are free at other end
5. "sarcomere" is the name for unit between "Z-lines"
G-actin
polymerize
F-actin (filamentous)
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
Cross-bridge chemistry
1. Attachable
2. Revisable
Transduction of chemical to mechanical energy
in muscle causes the filaments to slide:
Partial rotation of the actin-bound myosin head.
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++ regulation
a. neural activation >> muscle is electrically excited >> AP
AP ionic currents reach SR, open voltage sensitive Ca++
channels
Ca++ 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.
• Troponintropomyosin
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 ATPbinding 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.
++
Ca in
Role of
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%)