Muscle Flashcards
Striated muscles
Skeletal, cardiac
Multinucleated muscles
Skeletal only
Motor unit
Group of muscle fibers that function together and the somatic motor neuron that controls them. All muscle fibers in a motor unit are of the same type and this is determined by the somatic neuron during development. Motor units can contain as little as a few fibers. All fibers in the same motor unit fire together and are of the same fiber type.
Antagonistic muscle pairs
Ex: bicep & tricep; skeletal muscles largely exist in antagonistic pairs
Muscle origin
Part of the muscle closest to the trunk or more stationary
Muscle insertion
Part of the muscle that is more distal or mobile
Ligaments
Connect two bones
Tendons
Connect muscle to bone
Muscle “growth”
Satellite cells are muscle stem cells that contribute extra nuclei to skeletal muscles for muscle “growth”
Components of the sarcomere
Sarcomere = basic structural unit of skeletal muscle
Myofibrils are made up of back to back sarcomere.
Sarcomere is composed of thick (myosin) and thin (actin) filaments. Thick filaments are stabilized by titin and nebulous helps align actin filaments.
Each end of the sarcomere is the Z disk. The center of the sarcomere is the M line.
Sliding filament theory
Thick and thin filaments slide past each other in muscle contraction shortening the distance between the M line and Z disk. The myosin heads form crossbridges with actin of the thin filament.
Function of the t-tubule
Brings action potentials into the interior of the muscle fiber
Protein that blocks myosin-actin binding sites
Tropomyosin
Protein that sits atop tropomyosin and moves tropomyosin when bound to Ca2+
Troponin
Relationship between myosin and actin in the relaxed state
Myosin head is cocked and weakly bound to actin
Relationship between myosin and actin in power stroke
Myosin is bound strongly to actin causing actin filament to move in power stroke
Events that lead to the firing of an AP at the neuromuscular junction
Somatic neuron releases ACh which binds to ligand-gated Na+ channels in sarcolemma of motor end plate. Na+ flows into the cell, depolarizing it and causing more voltage-gated Na+ channels to open. Further depolarization causes an AP which travels down the t-tubule to the DHP (dihydropyridine L-type calcium channel).
How does an AP lead to an increase in [Ca2+] in the cytosol?
DHP is stimulated by the AP to “tug” on RyR (ryanodine receptor-channel) which causes the release of Ca2+ from the sarcoplasmic reticulum. Ca2+ then binds to troponin and muscle contraction begins.
What causes a decrease in [Ca2+] in the cytosol which allows the muscle fiber to relax?
Sarcoplasmic Ca2+-ATPase pumps Ca2+ back into the sarcoplasmic reticulum
What occurs during the latent period between muscle fiber AP and development of tension during muscle twitch?
Ca2+ releases, binds to troponin, troponin moves tropomyosin
Types & causes of muscle fatigue
CNS fatigue - largely psychological
PNS fatigue - failure of excitation-contraction coupling, acidosis, elevated inorganic phosphate slows release of inorganic phosphate from myosin or binds to Ca2+, ion imbalances which change sodium potassium pump activity
Ways that muscle cells make ATP
Substrate-level phosphorylation using creative phosphate
Oxidative phosphorylation
Substrate-level phosphorylations of glycolysis
Slow twitch vs fast twitch
Slow - oxidative ATP synthesis which is slower but generates more ATP, requires more oxygen so more vascularized & contains more myoglobin, smaller diameter allows more efficient oxygen diffusion
Fast - glycolytic & creative ATP synthesis which is faster but generates less ATP, not dependent on oxygen so not as vascularized/lighter in color b/c less myoglobin/ larger diameter due to glycogen stores; fatigues more quickly
Fastest source of energy in the muscle fiber
ATP and CP stores
Intermediate source of energy in the muscle fiber
ATP from glycolysis
Slowest but most sustainable source of energy in the muscle fiber
ATP from oxidative phosphorylation
In which type of muscle fiber would you expect to find more mitochondria?
Slow-twitch
Which type of muscle fiber do you expect to undergo glycolytic then oxidative phosphorylation as energy needs continue?
Fast-twitch oxidative-glycolytic (intermediate)
Which muscle fibers are most easily fatigued?
Fast-twitch
Why does too much actin/myosin overlap result in reduced fiber tension?
TBD
Why does too little actin/myosin overlap result in reduced fiber tension?
Too few crossbridge linkages to generate much force
Muscle twitches can undergo ______ summation
Temporal (not spatial)
What determines how long a muscle is contracted?
[Ca2+] is continually high in the cytosol
Tetanus & difference between infused and complete tetanus
Tetanus - Continuous maximum muscle tension
Unfused - brief moments of slight relaxation occur during this period
Complete - no relaxation - complete maximum tension until muscle fatigue causes the muscle to lose tension despite continuing stimuli
How to lift heavy :)
Recruit more motor units
Isotonic vs isometric contractions
Isotonic - muscle contracts, shortens, and creates enough force to move a load
Isometric - muscle contractions, does NOT shorten, force does NOT move the load
Elastic tendons compensate for muscle shortening in isometric contractions
Types of smooth muscle + examples
Phasic that is usually relaxed; ex: esophagus
Phasic that cycles between contraction and relaxation; ex: intestine
Tonic that is usually contracted; ex: sphincter
Tonic that contracts variably; ex: vascular smooth muscle
Contracted smooth muscle appears _____
Bulky instead of shortened
Why are single unit smooth muscle cells connected by gap junctions?
Allows the signal from the autonomic neuron varicosity to travel between cells so they all contract as a unit. Ex: small intestine
Why are multi-unit smooth muscle cells electrically independent?
Each cell can be stimulated independently which allows for more precise movements. Ex: eye
Which muscle cells have the longest contraction-relaxation cycle?
Smooth (then cardiac, and skeletal is fastest)
Slow wave potential vs pacemaker potential
Periodic subthreshold depolarization which may eventually reach threshold causing an AP
Periodic suprathreshold depolarization which causes an AP to fire every time. Present in cardiac and smooth muscle cells.
Steps involved in smooth muscle contraction
- Signal arrives for Ca2+ to enter the cell (vague, but roll with it)
- Entry of Ca2+ initiates release from the SR (aka calcium spark)
- Ca2+ binds to calmodulin
- Calmodulin activates MLCK (kinase)
- MLCK phosphorylates the myosin head and increases myosin ATPase activity
- Crossbridge cycling is enabled
How does smooth fiber myosin differ from skeletal fiber myosin?
Smooth fiber myosin does not have an ATP binding site
Why does smooth muscle have lower ATP requirements than skeletal muscle?
TBD
Troponin exists in which muscle fiber types?
Skeletal and cardiac, not smooth
Steps involved in smooth muscle relaxation
- Ca2+ is removed from the cytosol by: a) primary active transport into SR, b) primary active transport into ECF, c) secondary active transport using Na+ gradient into ECF
- Ca2+ is released from calmodulin (law of mass action)
- MLCK activity decreases
- MLCP removes phosphates from myosin heads and decreases myosin ATPase activity
- Cross-bridge cycling decreases
Why do cardiac muscle cells have larger t-tubules?
Spread the depolarization faster
Why do cardiac muscle cells have intercalated disks?
Contain demsmosomes and gap junctions which help in cell-to-cell communication and thus coordinated muscle contraction and provide mechanical strength to the small cardiac fibers
Why do cardiac muscle cells have smaller SR?
Some Ca2+ comes from outside of the cell
Pacemaker cells
A patch of cells independent of the CNS which fire action potentials at a given rate and depolarize the cardiac fiber
Process of excitation-contraction coupling in cardiac muscle
- Depolarization/Na+ entry —> fires AP
- Depolarization opens DHP Ca2+ channels in T-tubules
- Small amount of Ca2+ Enters cell binding to RyR in SR membrane causing it to open
- Ca2+ flows into cytosol
- Ca2+ binds troponin, enables crossbridge cycling/sliding filaments
- Ca2+ pumped back into SR/ECF via primary/secondary active transport
- Membrane is repolarized when K+ exits cell and ends AP
Biggest difference between cardiac and skeletal excitation-contraction coupling
DHP physically tugs on RyR in skeletal muscle while in cardiac muscle, DHP allows a trigger amount of Ca2+ into the cell to bind to RyR
Why does cardiac muscle have a long refractory period and action potential?
Influx of Ca2+ contributes to the formation of the AP
TBD
What activates the myosin head for cross-bridge cycling?
ATP!
What breaks the bond between myosin head and actin filament to end cross bridge cycling?
ATP!
What is on the myosin head when in the cocked position?
ADP and inorganic phosphate
What is released from the myosin head to bind it more strongly to actin?
inorganic phosphate
What is released from the myosin head to make the head pivot, performing the full cross bridge?
ADP
What is the cause of rigor mortis?
Tension requires ATP…but so does relaxation! Lack of ATP means that myosin heads remain bound to actin, so your muscles tense up completely. That’s why a corpse is called a ‘stiff’.
Tight binding in rigor state for myosin head
Myosin is tightly bound to actin, but has already pivoted and not yet cocked. NO ATP, NO Pi, NO ADP. NOTHING!
