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Types of Muscles
- 1. Striated (skeletal + cardiac)
- 2. Smooth
highly organized into sarcomere structures giving a “striated” appearance under the microscope
performs mechanical work via the skeleton under voluntary neural control
performs mech work in the heart under its own pacing control modulated by ANS
contractile apparatus is loosely organized without a defined banding pattern
performs mechanical work in many target organ systems and is modulated by NT's, metabolic, local and hormonal factors.
Features of skeletal muscles
1. Cells are multinucleated, striated and organized in parallel bundles
- 2. Diameters-->10 mm - 100 mm
- lengths --> 1 mm - 20 cm
- 3. Activated by motor neurons from CNS
- (spinal cord) at neuromuscular junctions leading to muscle action potentials and
- voluntary contraction
Features of Smooth Muscles
1. no attachments to a skeleton which limit movement
- 2.cells are much smaller and attached (physically & electrically) to each
- other via Gap Junctions.
3.spindle shaped mono-nucleated cells w/ short lengths of 50 – 400 μm and diameters of 2 – 10 µm
4.found in a wide variety of organ systems
features of cardiac muscles
1. cells aka "myocytes"
2. diameter: 25 mm; length: 150 mm
3. 2 nuclei
4. myocytes are striated.
5. organized in layers/"syncytium"
6. connected by intercalated discs with gap junctions.
7. Myocytes are not individually innervated, but regions innervated by neurons from ANS.
8.Mechanical activity is rhythmical paced SA node of the right atrium (modulated by NT)
Structure of skeletal muscle from largest to smallest
muscle > myofiber > myofibril
Structure of cardiac muscles
- - has a "field" structure
- - formed from a syncytium of cells, not from distinct fibers.
components of ECM & Cytoskeleton
- 1. Collagen Matrix
- 2. Dystroglycan Complex (Dystrophin)
- - surrounds entire muscle fibers
- - collagen laid down by fibroblasts
Dystroglycan Complex (Dystrophin)
- protein complex that helps w/ membrane stability of muscles
- lack of dystrophin leads to Muscular Dystrophy
- what is it?
- present in what type of muscles
- basic repeating contractile units in striated muscle
- present in skeletal and cardiac
- A band = dark = thick filament = whole length of myosin superimposed by actin
- I band = light = thin filament = actin only
- H zone = region of myosin only
2 other components of sarcomeres
1. Alpha-actinin: interacts w/ thin filaments @ Z line
2. Titin filament: runs for M line to Z line and tethers both the thin and thick filament together (keeps sarcomere in line)
organization of skeletal vs cardiac muscle
Skeletal: organized into large fibers to form whole muscles
Cardiac: organized into “syncytial field” structure of individual myocytes
which bands/zone changes during sarcomere contraction?
I band and H zone SHORTENS
A band remains the SAME
The Sliding Filament hypothesis
the basis of striated muscle force generation and shortening
What components is the molecular motor that generates force and movement in muscle?
Components of Myosin molecule
- Each thick filament contains hundreds of myosin molecules which contain:
- 1. S1 region
- 2. S2 region
- 3. Light Chains (ELC + RLC)
- - business end of the mysosin molecule
- - regions that binds to the actin
- - contains ATP pocket (myosin is an ATPase)
- - "rope" part of the myosin
- - has a swivel that allows it to stick out
- - springy elastic protein
- (1) ELC
- (2) RLC = regulatory light chain
Force is Generated by?
- - Hydrolysis of ATP
- - This is CHEMOMECHANICAL TRANSDUCTION
Why are there 2 S1 heads on myosin?
- double head arrangement increases the probability of actomyosin binding and cycling via cooperativity
- angles at which the crossbridges stick out of the thick filament do not line up w/ each thin filament
- - double heads improve likelihood of alignment and increase contractile
- heads are otherwise independent force generators.
- Start: "energized crossbridge" = ADP + Pi bound to myosin head
- 1. Crossbridge binds to actin
- - due to rise in [Ca++]
- 2. Crossbridge moves/bound more tightly
- - due to release of ADP + Pi
- 3. Crossbridge detaches
- - due to ATP binding to myosin
- 4. Energize Crossbridge
- - due to hydrolysis of ATP to ADP
Do the crossbridges actually generate force and move the filaments?
Which protein component generates the force in this actomyosin complex?
S1 Head conformational change.
Where is the actual conformational change to generate movement?
Between the head region and the light chains of myosin
How much force does it generate and how far might it move/ATP?
For Myosin II (striated &smooth muscle) molecular motor can generate up to 10 pN with a stroke in the 5-10 nm/CB cycle range
Other Motor proteins
There are 17 Families & ~140 Distinct Motor Proteins
Myosin II is only a small portion of motor proteins
what regulates muscle contraction?
what is it released by?
Ca++. Released by sarcoplasmic reticulum under the control of electrical stimulation via action potentials
Ca++ interact with what to regulate muscle contraction?
troponin and tropomyosin.
how to troponin and tropomyosin help with regulation?
regulate the crossbridge cycle by covering and uncovering myosin binding site on actin depending upon [Ca++]
Tropomyosin = rope-like (covers up myosin crossbridge binding site on actin)
Troponin = physically binds with Ca++
Molecular characteristics of Troponin
- consists of 3 sub-units.
1. Troponin T (TnT) binds tropomyosin @ every 7 actin molecules
2. Troponin I (TnI) physically inhibits binding of myosin to actin when no Ca++ is present.
3. Troponin C (TnC) binds Ca++.
When Ca2+ is bound, what happens to TnI?
the conformation changes moving TnI off the myosin binding site on actin permitting crossbridge cycling
Features of TnC?
Diff btwn TnC in skeletal and cardiac?
There are 4 Ca2+ binding sites on TnC: 2 are always filled by Mg2+ and the other 2 can bind Ca2+
- cardiac: One of the two Ca2+ binding sites
- on cardiac troponin is not functional
therefore, it only takes 1 Ca++ ion to activate whole system for cardiac. Skeletal requires binding of 2 Ca++
How does cardiac muscle initiate the
contraction/ relaxation cycle necessary for the heart to beat?
Excitation Contraction Coupling
Excitation Contraction Coupling
- EC coupling is the sequence of events that link the depolarization of the surface membrane with tension development by the
- contractile machinery
EC coupling in cardiac muscles are initiated by?
the propagation of an action potential along the sarcolemma
Are Cardiac Myocytes individually innervated?
No! They also have no direct CNS input
Rate and magnitude of cardiac contractions are modulated by?
How is Ca++ released in cardiac muscles?
Calcium is released from SR like in skeletal muscle, but it also directly enters the cell from the outside via calcium channels.
how is cardiac muscle AP diff from other muscles?
compared to nerve or skeletal muscle, cardiac muscle has a much longer action potential duration due to the Ca2+ conductance.
Cardiac EC Coupling Sequence [Contraction]
- 1. depol of plasma membrane
- 2. opening of voltage-gated Ca++ channels in T-tubules
- 3. influx of Ca++ in cytosol
- 4. Ca++ binds to Ca++ receptors on SR
- 5. more influx of Ca++ in cytosol
- 6. increase cytosolic [Ca++] --> contraction
How much of Ca++ comes from SR vs outside?
- In humans and large mammals,
- 70% of the Ca++ comes from the SR
- 30% from the outside
Cardiac EC Coupling Sequence [Relaxation]
Ca++ must be proportionally pumped back to both reservoir sources for relaxation to occur
Ways to re-sequester Ca++ in cardiac muscle relaxation
- 1. SR Ca2+ pump
- - resequesteres intracellular Ca2+ from
- the SR
- - rate of resequestration is modulated by phospholamban (PLB)
- - process uses ATP
- 2. Sodium-Calcium Exchanger
- - extrudes extracellular portion of Ca2+
- - 3Na/1Ca, no ATP used
- 3. T-Tubule Ca-pump
- - extrudes extracellular portion of Ca2+
- mediate the release of calcium ions from the sarcoplasmic reticulum
- releases calcium upon calcium binding
what type of regulation does cardiac and skeletal muscle have?
(hint: think of sigmoidal graph)
Allosteric Regulation (cooperative)
Cardiac & skeletal muscle
have slightly different forms of EC coupling
primarily differentiated by?
the sources of calcium necessary to initiatecontraction.