(Lectures 7-9, Chapter 11) Muscular System Flashcards
3 types of muscle
- Skeletal
- Cardiac
- Smooth
Characteristics of skeletal muscle
- attached to bones
- striated
- voluntary contractions
Characteristics of cardiac muscle
- found only in the heart
- striated
- involuntary contractions
Characteristics of smooth muscle
- lines hollow internal structures
- nonstriated
- involuntary contractions
Functions of muscle
- Producing body movements
- Stabilizing body positions
- Storing/moving substances within the body
- Thermogenesis (generating heat)
Properties of muscle (3)
- Electrical excitability (ability to respond to stimuli by producing action potentials)
- Contractility (can contract forcefully when adequately stimulated)
- Extensibility (can stretch without being damaged)
Shape of skeletal muscle fibers (cells)
Long, cylindrical
3 layers of connective tissue in skeletal muscle
- Epimysium (surrounds muscle tissue)
- Perimysium (divides skeletal muscle into bundles)
- Endomysium (thin sheath that covers individual fibers)
Myosatellite cells
Mononucleated stem cells; precursors to skeletal muscle cells
What happens to myoblasts as they differentiate into muscle fibers?
Align, elongate, fuse together; forms long multinucleated cells
T/F: muscle cells don’t have/need many mitochondria
False
What happens to a muscle when it’s damaged?
Inflammation, swelling
Axial vs Appendicular Muscies
Axial: located along the body’s axis (i.e. along the center; head, neck, core)
Appendicular: located along the body’s limbs
Myofibrils
Filaments containing muscle fibers
Sarcoplasmic Reticulum (SR)
“Smooth ER” of the muscle, containing a lot of Ca2+
What are the names for the plasma membrane and cytoplasm of muscle cells?
Sarcolemma. sarcoplasm
Transverse Tubules
Invaginations of the sarcolemma, filled with ECF
Terminal Cisternae/Lateral Sacs`
Sacs on the end of the SR, located near the T-tubules, containing Ca2+
Triad
Structure consisting of a T-tubule and the two terminal cisternae on either side of it
Why do muscle fibers need many nuclei?
- Muscle fibers consist mostly of protein, which degrade over time
- More nuclei = more transcription/translation (i.e. more protein is made)
Describe the charge distribution on either side of the sarcolemma.
Negative on the inside, positive on the outside
What causes the uneven distribution of charges across the sarcolemma?
Leak channels, which allow for the movement of ions
How do muscle action potentials trigger the start of muscle contractions?
- Travel along sarcolemma and into T-tubules
- Triggers release of Ca2+ from the SR
What structure separates individual myofibrils?
Z disc
Sarcomere
- Unit of contraction in myofibrils (one myofibril has many sarcomeres)
- Contain thick and thin filaments
Thick Filaments
Myosin fibers
Thin Filaments
Actin fibers
How are myofibers in the sarcomere attached to the plasma membrane?
What happens to the membrane when a muscle contracts?
Membrane proteins
Myofiber shortens, putting stress on the membrane
Myoglobin
- Protein that binds oxygen from RBCs
- A muscle that needs to use more oxygen will have more myoglobin, giving it a red appearance
Glycogen
- Stored in the muscles
- Broken down when an energy source is needed
M line
The middle of a sarcomere
H zone
- Middle region of a sarcomere, containing the M line
- Contains only thick filaments
A band
- Found on either side of the H zone
- Contains both thick and thin filaments
I band
- Found between A band and Z disc
- Contains only thin filaments
Name the two contractile proteins in muscles.
Actin, myosin
Name the two regulatory proteins in muscles.
Troponin, tropomyosin
What are the purposes of the 3 types of proteins in muscles?
Contractile: formation of filaments
Regulatory: regulate contraction
Structural: hold the sarcomere complex together so the muscle can function
Name two structural proteins in muscles.
Titin, alpha-actinin
Actin
Consists of globular proteins, each with a binding site for myosin
How do troponin and tropomyosin regulate contraction?
- Tropomyosin covers the binding sites on actin, preventing myosin from binding there when contraction isn’t occurring
- During contraction, troponin binds two Ca2+ and undergoes a conformational change, making tropomyosin do the same so it twists and uncovers the binding sites on actin
Myosin
Each fiber contains 2 myosin heads with two binding sites:
- Actin binding site
- ATP binding site; ATPase that results in the hydrolysis of ATP
Titin
- Large filament that attaches to myosin, anchoring filaments between the M line and Z disc
- Provides structural support and elasticity; stretches when sarcomere contracts
T/F: Structural proteins are part of the sarcomere
False; they hold the contractile units to the sarcolemma
Regarding the proteins that make up the sarcomeric complex, what must they do to ensure that the muscle can function properly? What happens if this isn’t accomplished?
The proteins have to assemble properly, as the interaction/association/binding needed to make muscles work is specific
Functional/clinical issues can occur when parts of the sarcomere aren’t expressed or assembled properly.
Name one muscle disease that is caused by an issue with a protein.
Muscular Dystrophy: muscle breaks down due to truncation in dystrophin protein
What happens to the thick/thin filaments and the bands/zones of the sarcomere during contraction?
- Filaments slide past each other, but do not change in length
- A band does not change in length
- H zone, I band, sarcomere all shorten; Z discs move closer together
Steps of the Cross-Bridge Cycle
1) ATP hydrolysis on myosin head puts it in a high-energy state; ADP and P are still attached
2) Myosin head binds to actin and P is released, forming a cross bridge
3) Power stroke: myosin head changes position, pulling the actin filament towards the M line, ADP is released
4) Another ATP binds to the myosin head, making it detach from the actin
What is excitation-contraction coupling? What are two things that are required for it?
The sequence of events where an action potential in the sarcolemma causes a muscle contraction; EPP spreads to sarcolemma.
- Requires neural input from motor neuron to NMJ (chemical signal becomes mechanical energy)
- Requires release of Ca2+ from SR
Dyhydropyridine Receptor (DHPR)
Voltage-sensitive protein on the membrane of T-tubules
Ryanodine Receptor (RyR)
Voltage-gated channel on the SR membrane that gates the flow of Ca2+ from the SR. It’s physically linked to DHPR
What is the role of DHPR and RyR?
When the DHPR senses an action potential in the T-tubule, it causes a change in RyR that makes it open and lets Ca2+ exit the SR
What is required to stop contraction?
- Turn off the motor neuron
- Remove Ca2+
How is Ca2+ removed from the sarcoplasm?
Ca2+-ATPase pumps Ca2+ into the SR by active transport
What does calsequestrin do?
Hold Ca2+ in the SR, so it doesn’t diffuse out.
Motor Unit
Somatic motor neuron + the fibers that it innervates
T/F: muscles contract in a synchronous manner
False
Muscle Twitch
Recorded measure of force/tension a muscle (can be a single cell or a group of muscles) produces
What are the 3 phases of a muscle twitch?
1) Latent Phase
2) Contraction
3) Relaxation
Latent Phase of a muscle twitch
- No tension develops
- Lasts for 2msec after stimulus
- AP travels across SR and into T-tubule, Ca2+ is released
Contraction (muscle twitch)
- Ca2+ binds to troponin, cross-bridge cycle occurs
- Encompasses the development of tension to the start of peak tension
Is Ca2+ released continuously from the SR?
No, it’s released in bursts
Relaxation (muscle twitch)
- Ca2+ levels in the sarcoplasm decrease as it returns to the SR
- tropomyosin covers actin binding sites again
- Encompasses peak tension to the end of the twitch (~25msec)
Treppe
Type of tension where stimulus is repeatedly applied when muscle is at rest, with a stepwise increase in tension between each application
Summation
Application of a stimulus before the muscle relaxes causes an increase in tension
Incomplete Tetanus
- Stimulus is applied before muscle can rest, and even afterwards when tension can’t increase anymore
- Max. tension isn’t sustained
Complete Tetanus
- Stimulus is applied before muscle can rest, and even afterwards when tension can’t increase anymore
- Max. tension is sustained
What factors can lead to increased muscle tension? (5)
- High frequency of action potentials
- Optimal sarcomere length
- Large muscle fiber diameter
- Large motor unit
- High motor unit recruitment
Length-Tension Relationship
- Optimal length of sarcomere is needed to allow for maximum # of cross bridges and greatest tension
- No overlap of filaments = no tension, as myosin can’t bind to actin
- Too much overlap = no tension, as the sarcomere won’t be able to shorten
Muscle Tone
- Tension that’s always present in muscles, established by alternatively active and inactive motor units
- Helps maintain blood pressure and posture
Isotonic Muscle Contraction + 2 types
- Movement occurs, muscle length changes
- Concentric = muscle shortens
- Eccentric = muscle lengthens
Isometric Muscle Contraction
- No movement, muscle length doesn’t change, but energy is still expended
- Tension generated by the muscle doesn’t exceed the load
What are the 3 types of skeletal muscle fibers?
- Slow Oxidative Fibers (SO)
- Fast Oxidative-Glycolytic (FOG)
- Fast Glycolytic (FG)
T/F: most skeletal muscles only contain one type of fiber
False; the way we train our muscles influences the type of muscle fibers we have (to an extent)
Which type of fiber is most resistant to fatigue?
Slow Oxidative
What is the main method + capacity of ATP generation for each type of fiber?
SO: aerobic respiration, high capacity
FOG: aerobic respiration and anaerobic glycolysis, intermediate capacity
FG: anaerobic glycolysis, low capacity
Which type of skeletal muscle fiber has both the biggest diameter and the most glycogen storage?
Fast Glycolytic
Which fiber type has the most myoglobin, capillaries, and mitochondria? How does this relate to its function?
Slow oxidative; allows for ATP production via aerobic respiration
Where is each type of skeletal muscle fiber commonly found? What are their purposes?
- SO: postural muscles (e.g. neck); maintaining posture, aerobic endurance activities
- FOG: lower limb muscles; walking, sprinting
- FG: upper limb muscles; rapid, intense, short movements
What is smooth muscle formed from? What is its main purpose?
- Formed from sheets of cells in organs
- Acts as barrier; lines the lumen of hollow organs
2 layers of smooth muscle
- Longitudinal Layer: fibers that are parallel to the long axis of the organ, which make the organ shorten when they contract
- Circular Layer: fibers that run around the organ’s circumference, which make the lumen constrict when they contract
- The alternating contraction and relaxation of the layers mixes/squeezes substances through the lumen
How does smooth muscle differ from skeletal muscle?
- Spindle-shaped (thinner/shorter), non-striated, mononucleated
- No sheaths of connective tissue; only has endomysium
- Not organized into sarcomeres (still has actin/myosin)
- Controlled by ANS, not SNS
- Less-elaborate SR, no T-tubules
Which component of smooth muscle acts like Z discs in skeletal muscle?
Dense bodies; anchor myofilaments to the sarcolemma
Innervation of smooth muscle
ANS nerves that innervate smooth muscle contain varicosities, that store neurotransmitters and release them into the diffuse junction (type of synaptic cleft)
Smooth muscle contracts asynchronously. Why is this a good thing?
Reduces stress on the muscle
Single-Unit Smooth Muscle
- Muscle cells are electrically connected by gap junctions and contract together (together =/= synchronously!), as a single unit
- Depolarization of one cell will cause the contraction of many cells
- Found in the intestinal/respiratory tracts and blood vessels
Multi-Unit Smooth Muscle
- Muscle cells individually receive stimuli and contract
- Few/no gap junctions, each fiber is individually innervated
- Found in large airways, arteries, eye (cillary muscle, iris)
For smooth muscle contraction, where does most of the Ca2+ come from?
ECF
Caveolae
Infoldings of sarcolemma (in smooth muscle) that contain voltage-gated Ca2+ channels; when these channels open, there’s a rapid influx of Ca2+ from the ECF
How do myosin filaments in smooth muscle differ from those in skeletal muscle?
- There are fewer myosin filaments in smooth muscle
- Thick filaments in smooth muscle have myosin heads along their entire length
Both of these things make the power stroke in smooth muscle similar in strength to the power stroke in skeletal muscle
There is no troponin complex in smooth muscle fibers. What happens instead?
- Ca2+ binds to calmodulin, forming a complex
- This complex activates the enzyme myosin kinase
- Myosin kinase phosphorylates the myosin head(s), which activates them and lets cross bridge formation occur
How is smooth muscle contraction stopped?
- Ca2+ detaches from calmodulin
- Ca2+ moves into the SR (Ca2+-ATPase) and ECF (Na+-Ca2+ exchanger) via active transport
- Myosin is dephosphorylated
Weightlessness can be detrimental to muscles that we use to walk and support our body weight. What do astronauts do to combat these negative effects, and how does it help?
- Exercise maintains the connection between motor neurons and skeletal muscles
- Weight/resistance training maintains the neuromuscular junction
Spinal Muscular Atrophy
- Genetic disorder where the nerves that innervate muscles break down
- Muscle is smaller, fibers are separated by gaps and are unorganized, fluid accumulates and forms vacuoles/scar tissue
What happens to muscle cells that are innervated by diseased neurons? (+example)
- Muscle isn’t as healthy and ends up atrophied
- All neurons damaged = loss of muscle function
- e.g. leg would look atrophied after removing a cast due to disuse of muscle
Myasthenia Gravis
- Antibodies block ACh receptors (i.e. immune response), reducing the transmission of action potentials
- Muscles fatigue easily when trying to contract (i.e. fatigue isn’t constant)
- Symptoms: droopy eyes/facial muscles, blurred vision, respiratory distress, slumped posture
How does myasthenia gravis lead to respiratory issues?
Tired respiratory muscle = less chest expansion = smaller lung capacity
What is used to treat myasthenia gravis?
Pyridostigmine
Duchenne Muscular Dystrophy
- Occurs when dystrophin doesn’t provide mechanical stability by holding the sarcomere and sarcolemma together
- Muscles easily tear and break apart due to stress
- More common in boys (caused by a mutation on the X chromosome)
What are some of the consequences(?) of DMD?
- Scoliosis
- Respiratory weakness
- Sleep hypoventilation
- Decreased heart function (leads to heart failure)
- Inflammation, fibrosis/scarring
