Skeletal and cardiac muscle physiology Flashcards
what are 2 types of striated muscle
skeletal
cardiac
what kind of contraction does skeletal muscle have
voluntary
what kind of contraction does cardiac muscle have
involuntary
dimensions of skeletal muscle
20-100 μm duameter, 12cm length
dimensions of cardiac muscle
brick shaped 10-20 μm diameter, 100 μm length
which is branches and unbranched out of skeletal and cardiac muscle
skeletal = unbranched
cardiac = branches
which one has a motor unit out of skeletal and cardiac muscle
skeletal = The motor unit: multiple fibres can be innervated by a single motor neuron
cardiac = No motor nerve (impulse arrives by conduction)
label this image of striated muscle
where do you find z lines
Z lines repeat along the length of the muscle approximately every 2 µm.
whats found in between 2 adjacent z lines
sarcomere - when we talk about sarcomere length we’re talking about the distance between two adjacent Z lines.
what does sarcomere contain
all of the protein filaments necessary for muscle contraction and these sarcomeric units simply repeat along the length of the muscle fibre.
what 2 structures are within the sarcomere
A band (which is the thick myosin filaments) and the I band (which is the thin actin filament) (which are anchored to the Z-line).
what is the a band
thick myosin filaments
what is the i band
thin actin filament
what are the small holes at every z line called
These are a blind-ended tubes of membrane called T-tubules
which is the thick and thin filaments in this diagram
what is a triad made up of?
1 T-tubule and 2 terminal cisternae
These T-tubules make junctions with the sarcoplasmic reticulum to form triads.
how many cisterns do skeletal cells have compared to cardiac cells
skeletal = triple (triad)
cardiac = double (dyad)
compare the mitochondria elvels in skeletal vs cardiac
more mitochondria in cardiac and bigger
arrangement of sarcoplasmic reticulum
repeating series of networks around myofibrils
where they meet is called terminal cisterna
what are t tubules surrounded by?
two terminal cisternae, called “triad”
what is the function of a t tubule
These t-tubules are necessary in larger cells to bring the action potential down into the centre of the cell and ensure synchronous coordinated contraction.
what cells are t tubules absent in
t-tubules are absent in small cells like atrial cells, neonatal cells and avian heart cells.
the association between Sarcoplasmic Reticulum and t tubule is essential for what
excitation-contraction coupling.
whats the difference between t tubules in skeletal vs cardiac
T tubules in cardiac muscle are fatter and the intracellular sarcoplasmic reticulum is less dense.
what are the 2 important periods in neuronal action potential
refractory period
relative refractory period
what is the refractory period
The refractory period is the period during which the ion channels have opened and inactivated but have not returned to that closed state to be ready and available to fire off another action potential. Remember that ion channels can enter an open state, then an inactivated state and they can only return to the close date to ready for the next action potential when the membrane has repolarized completely - so this period is called the refractory period.
And if a stimulus comes along during that period, we cannot generate another action potential.
what is the relative refractory period
In this period, the sodium channels have recovered from inactivation and they’re available and ready to go. But, because the membrane potential is now much more negative than it was at rest, during this green period, it is going to take a bigger depolarization to get up to that threshold level. So although the cell is available and able to fire off an action potential, it’s going to take a bigger trigger to get it there to get it up to the threshold voltage
key difference between refractory period and relative refractory period
refractory period - where you cannot fire off another action potential, and the relative refractory period (shown in green), where you can still fire off an action potential but it needs a larger triggering pulse.
in a cardiac action potential, does the ventricular muscle beat spontaneously?
no
in a cardiac action potential where does the wave originate
SA node
what is the refractory period like in cardiac action potential compared to relative refractory period
very long refractory period
what is the action potential like in skeletal muscle
short APD
whats the refractory period like in skeletal muscle
Short refractory period (allows tetany = involuntary muscle contractions ie spasms)
whats is skeletal muscle action potential triggered by
Triggered by activation of a motor neuron
what is skeletal muscle action potential initiated by
Excitation initiated in the neuromuscular junction
what is it called when action potentials happen back to back and cause contractions to fuse together
temporal summation
fused vs unfused tetanus
why do we have a long refractory period in cardiac muscles?
prevents tetany
protects against re-entrant arrythmias (, it stops the heart beating in that gap in between beats in a way that would compromise the hearts ability to pump. So if an arrhythmia comes along during the refractory period, is not going to trigger another action potential and another beat)
what happens if you remove calcium from the outside of a single ventricular myocye vs skeletal muscle
skeletal muscle can continue beating for at least 25 minutes without any extracellular calcium . Cardiac muscle, on the otherhand, is arrested almost immediately. Within milliseconds of removing external calcium cardiac muscle arrests.
what is the calcium transient
Within the time course of the action potential the calcium concentration returns to its resting level and hence this change is called the calcium transient.
in the cardiac muscle in excitation-contraction coupling, the action potential, when it sweeps down the surface membrane, sweeps into the T-tubule and in the T-tubule are voltage-gated calcium channels, this allows calcium to enter by diffusing across what
This calcium, when it enters the cell, diffuses across the very small space between the T-tubular membrane and the sarcoplasmic reticulum - the dyadic cleft.
in cardiac muscle excitation- contraction coupling, when Ca is elevated in this dyadic cleft, it binds to another channel (this time in the sarcoplasmic reticular membrane) what is the channel called
This channel is called the calcium release channel or the
ryanodine receptor because it binds a drug called ryanodine. (RyR)
the entire process of excitation-contraction coupling in cardiac muscles depends on what
started by calcium entering the cell through L-type calcium channels and triggering that release of a much larger amount of calcium from those intracellular stores.
excitation-contraction coupling in cardiac muscles is known as
calcium-induced calcium-release.
relaxation in cardiac muscle is brought about by what
Relaxation is brought about by this elevated Ca concentration being reversed when Ca is taken back into the SR through an ATP driven Ca pump called the Sarco endoplasmic reticulum Ca ATPase (more commonly known as SERCA).
In addition to Ca uptake into the intracellular stores, that small amount of Ca that entered the cell via the Ca channels is removed from the cell via what
the surface membrane Na/Ca exchanger
that the primary mechansism for removing Ca from the cytoplasm is
Sarco(Endo)plasmic Reticulum Calcium ATPase (SERCA)
what is SERCA regulated by
phospholamban
what happens when an action potential arrives at the calcium channels in t-tubular membrane in skeletal muscle
the voltage-gated calcium channels change their conformation (just as they do in cardiac muscle). Howver, this time calcium entry is not required. In skeletal muscle, the channel is physically linked to the ryanodine receptor – you can se this indicated in blue on this diagram.
in skeletal muscle when the conformation of the calcium channel changes, in response to the change in voltage what happens
When the conformation of the calcium channel changes, in response to the change in voltage, this literally pulls the plug on the ryanodine receptor. This allows release of calcium into the cytoplasm. Calcium becomes elevated and that calcium binds to the myofilaments and brings about contraction.
what happens in relaxation in skeletal muscle vs cardiac muscle
Relaxation in skeletal muscle – same as in cardiac muscle apart from all the Ca goes back into the SR
what is excitation-contraction coupling in skeletal muscle known as
voltage-induced calcium release.
what 2 things are required for cross bridge formation
Two things are required for cross-bridge formation –
Ca binds to troponin C which pulls tropomyosin out of the actin groove
ATP provides the energy to allow the myosin head to release from actin and swing forward and bind to the exposed actin binding site.
what is troponin
Troponin is the calcium binding protein. It is made up of three individual protein subunits called troponin I, troponin C and Troponin T.
what is a cross bridge
an extension for the myosin thick filament that links to actin
what happens in rigor mortis
in the absence of ATP, the myosin heads remain attached to actin forming ‘rigor bonds’
what 2 things do you need to form a cross bridge
- Calcium needs to bind to troponin C. When calcium binds to troponin C, it changes its conformation and pulls tropomyosin out of the groove formed between the actin filaments. This exposes the actin binding site.
- ATP is necessary to break that bond between actin and the myosin head and to provide the energy to swing the myosin head forward to bind to the next binding site on the actin filament.
OVERALL In the presence of both ATP and Ca, the myosin head can release and move forward, and Ca binding to troponin C will expose the next actin binding site.
what is the number of cross bridges formed, proportional to?
The number of crossbridges formed is directly proportional to the calcium concentration in the cytoplasm.
MORE CALCIUM = MORE TENSION
what is the length tension relationship in cardiac and skeletal muscles - what is it based on?
The longer the muscle (the more we stretch a muscle) the stronger it will contract.
In striated muscles like cardiac and skeletal muscles, this is based on sarcomere length (distance between Z-lines)
what is the relationship between sarcomere lenghts and cross bridges
short sarcomere length = few cross bridges
long sarcomere length = more cross bridges
what is the optimal length for sarcomeres for cross bridges to form
2.25 µm
what is skeletal muscle optimal length
around 2.05-2.25 µm
what is cardiac muscle optimal length
around 2.05 µm
why do skeletal muscle and cardiac muscle operate at different optimal lengths
Skeletal Muscle is held in place by bones, which usually keeps it at an optimal length for strong contractions.
Cardiac Muscle (heart muscle) isn’t held by bones; it’s more flexible and usually operates around the midpoint of the length-tension curve. This allows it to change its length easily.
what is the frank starling mechanism
The Frank-Starling mechanism is the way the heart naturally adjusts the strength of its contractions based on how much blood fills it.
When more blood flows into the heart, it stretches the heart muscle. This increases the overlap between the thick (myosin) and thin (actin) filaments in the heart muscle cells, allowing more cross-bridges to form.
As a result, the heart muscle contracts more forcefully, pushing more blood out of the heart. The opposite happens when there’s less blood.
In short, the Frank-Starling mechanism ensures that the heart pumps out whatever blood it receives, helping it adapt to the body’s needs without requiring extra signals.
what kind of relationship on a graph does ca concentration and tension have
sigmoidal
larger ca transient gives you what compared to a smaller ca transient?
force is regulated by regulating the size of what?
Force is regulated by regulating the size of the Ca transient in EVERY cell.
whats the name of the relationship on a graph with ca concentration and tension
pCa-tension relationship where tension is on the Y-axis and calcium concentration (or pCa) on the X-axis
Q: What is a “skinned fiber preparation” in the context of studying cardiac muscle?
A: A skinned fiber preparation is a technique where the cell membrane is removed chemically, and the myofilaments are placed in a low-calcium “relaxing” solution to study the calcium-tension relationship.
Q: What does the term “pCa” mean, and how is it related to calcium concentration?
pCa is the negative log of calcium concentration, similar to the pH scale. For example, a pCa of 6 is 10⁻⁶ M, or 1 micromolar.
At what pCa value is calcium concentration equal to 1 micromolar?
A pCa of 6 corresponds to a calcium concentration of 1 micromolar (10⁻⁶ M).
What unique feature does cardiac muscle have compared to skeletal muscle regarding calcium sensitivity?
Cardiac muscle shows increased myofilament sensitivity to calcium as muscle length increases, unlike skeletal muscle.
In the calcium-tension relationship graph, what does the X-axis represent, and what does the Y-axis represent?
The X-axis represents calcium concentration in micromolar, and the Y-axis represents forc
What does a leftward shift in the calcium-tension curve indicate?
A leftward shift in the curve indicates an increased calcium affinity in the muscle filaments, allowing more force to be generated at a given calcium concentration.
This leftward shift is unique to cardiac muscle and is generally not observed in skeletal muscle
What does the Frank-Starling law of the heart state?
The Frank-Starling law states that the more the heart is stretched (filled with blood), the stronger it will contract.
What kind of pump is the heart described as under the Frank-Starling law?
The heart is described as a “permissive pump,” meaning it only pumps out what comes back to it.
What is the relationship between cardiac output and venous return according to the Frank-Starling law?
Cardiac output equals venous return; the heart pumps out the amount of blood that returns to it.
How does an increase in venous return affect the heart’s contraction?
An increase in venous return stretches the heart more, leading to a stronger contraction.
What happens to heart contraction if venous return is restricted?
If venous return is restricted, the heart stretches less and contracts less vigorously.
What is the major determinant of cardiac output?
The major determinant of cardiac output is venous return.
what other relationship does the frank sterling law of the heart relate to?
The length-tension relationship underlies the Frank-Starling law, which states that the more we stretch cardiac muscle, the stronger it will contract.
What are the two cellular mechanisms that explain the Frank-Starling law?
1) Stretch increases cross-bridge formation by optimizing myofilament overlap.
2) Stretch uniquely increases the calcium sensitivity of troponin C in cardiac muscle.
What is unique to cardiac muscle regarding calcium sensitivity when stretched?
Stretching cardiac muscle increases the calcium sensitivity of troponin C, which enhances contraction strength.
What does inotropy refer to in cardiac terms?
The strength of contraction.
What does lusitropy refer to in cardiac terms?
The rate of relaxation.
What does chronotropy refer to in cardiac terms?
The heart rate.
What effect do positive chronotropes, inotropes and lusitropes have on the heart?
They increase the strength of contraction.
What effect do negative chronotropes, inotropes and lusitropes have on the heart?
They decrease the heart rate.
What are the three major modifiers of myofilament calcium sensitivity that change early in myocardial ischemia
myocardial ischemia = blood flow to the heart muscle (myocardium) is reduced
ATP, pH, and inorganic phosphate.
What cellular change occurs within seconds of severe ischemia onset?
Breakdown of creatine phosphate, leading to a substantial accumulation of inorganic phosphate.
What impact does ischemia have on cellular redox state?
Ischemia causes changes in the cellular redox state, contributing to ischemic effects on myofilaments.
How does acidosis develop in myocardial ischemia?
Acidosis develops rapidly after the onset of ischemia due to the lack of oxygen.
What happens to ATP levels during severe ischemia, and when is depletion most significant?
ATP levels deplete, especially once glycogen stores run out.
What overall effect do early ischemic changes have on myofilaments?
The changes in ATP, pH, inorganic phosphate, redox state, and acidosis impact myofilament function, affecting contraction and relaxation.
What is “akinetic” tissue in the context of myocardial ischemia?
Akinetic tissue refers to heart muscle that has stopped contracting, as seen within a minute of ischemia onset.
What causes early contractile failure in myocardial ischemia?
Early contractile failure is caused by rapid desensitization of muscle filaments to calcium due to a quick increase in inorganic phosphate and acidosis in ischemic tissue.
How is tension regulated in skeletal muscle?
Tension in skeletal muscle is regulated by the activation of motor units, with each unit contracting in an “all or nothing” manner.
How does skeletal muscle increase the force of contraction?
By recruiting more motor units, which increases the number of fibers contracting and thus generates more tension.
How is contraction in cardiac muscle different from skeletal muscle?
Cardiac muscle contraction is graded and every cell contracts with each heartbeat, regulated mainly by calcium concentration, rather than by recruiting additional motor units.
How is calcium regulation different in cardiac and skeletal muscle?
In cardiac muscle, calcium levels are finely regulated to produce graded contractions, while in skeletal muscle, contractions are “all or nothing.”
What are the two main types of skeletal muscle fibers?
Slow-twitch (Type I) and fast-twitch (Type II) muscle fibers.
What are the characteristics of slow-twitch (Type I) muscle fibers?
Smaller, slower, produce less force, used for sustained activity (e.g., distance running), and fatigue-resistant.
What type of activities are slow-twitch (Type I) muscle fibers best suited for?
Sustained, endurance activities like distance running.
What are the characteristics of fast-twitch (Type II) muscle fibers?
Larger, quicker, produce more force, used for high-intensity activities (e.g., sprinting, weightlifting), and fatigue quickly.
What are Type IIA muscle fibers, and what are their characteristics?
Type IIA fibers are fast oxidative/glycolytic with intermediate force, speed, and fatigue resistance, fewer mitochondria, and intermediate blood supply.
What are Type IIB muscle fibers, and what are their characteristics?
Type IIB fibers are fast glycolytic, produce the most force, contract quickly, fatigue rapidly, have very few mitochondria, and poor blood supply.
Which type of muscle fiber is fatigue-resistant and well-vascularized with many mitochondria?
Slow-twitch (Type I) muscle fibers.
Which muscle fiber type is suited for sprinting and weightlifting due to its large size, quick contraction, and high force production?
Fast-twitch (Type II) muscle fibers.
How does the blood supply differ between Type IIA and Type IIB fast-twitch fibers
Type IIA fibers have intermediate blood supply, while Type IIB fibers have poor blood supply.
