Muscle Physiology and Cardiac Muscle (L3) Flashcards

1
Q

4 ways we control muscle cells

A

Electrical (action potentials can propagate like in the heart); hormonal/chemical (epinephrine, acetylcholine release can modulate muscle activity); stretch/force (stretch can modulate the force of contraction); innervation by nerves (NMJ)

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2
Q

Types of muscle and subtypes

A

Striated (skeletal; cardiac); smooth (single unit, multiunit)

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3
Q

How do striated muscles control the force/power the muscle is able to put out vs the length of time that muscle may need to be active?

A

Fiber types
There are slow (which rely on oxidative metabolism), medium-fast (which are oxidative), and VERY fast (rely on glycolysis for energy)

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4
Q

What kind of metabolism do cardiac cells rely on

A

Slow oxidative metabolism (in fact they prefer beta-oxidation over anything)

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5
Q

Muscles are organized into _(fasicles/fibers)__ which can further be subdivided into individual __(fasicles/fibers)__

A

Fasicles, fibers

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6
Q

What is a muscle fiber?

A

A muscle cell

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7
Q

If you were to cut into a myofibril, what would you see it was made of?

A

Each myofibril (muscle cell) has, on the inside, tons of individual sarcomeres organized into cylindrical tubes

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8
Q

What is the sarcomere, and describe the components of one?

A

The sarcomere is the basic mechanical unit of a muscle cell. It spans from z-disc to z-disc by convention.
The I-bands span across Z discs. They are lighter in color and represent where there is only actin, no myosin. The darker A band is present wherever there is thick filament (contains myosin). The point in the middle of the A band, the H band, where there is a lighter coloration while still in the darker zone, is where there is only myosin containing thick filaments, but no actin-containing thin filaments. The M line is the center of the sarcomere. The Z bands represent a structural anchoring area where thick filaments are anchored by titin. The z discs have tons of structural proteins present. during muscle contraction the thick filaments pull themselves across the thin filaments.

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9
Q

If we have thousands of sarcomeres per muscle fiber, how do we make sure contraction occurs uniformally and that it penetrates to the same level of the cell?

A

this is because of the t tubules, invaginations of the plasma membrane that allow for depolarization and SR release to be located closer to sarcomeres, which allows EC coupling to be rapid. Seth described the T Tubules as wrapping around the sarcomere bundles “like a sock”

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10
Q

Parts of the SR/ER in cardiac cell

A

Terminal cisternae - the part of the SR with the business end stuff (for example, RYR2) that directly participate in muscle contraction.

Longitudinal cisternae - the part of the SR that does not directly participate in muscle contraction; is thought to be potentially involved in re-uptake of calcium

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11
Q

What is Titin?

A

It is a massive protein that acts as an anchoring center, holding the thick filaments against the Z disc like a spring.

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12
Q

Which bands shorten during sarcomere contraction?

A

The I band is the primary shortening band (because thick filaments pull against the thin filaments) but the H band (the area with only thick filaments) will also shorten somewhat as the crossover between filaments becomes more pronounced.

The A band stays the same because this is just where thick filaments are. This will not change during contraction.

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13
Q

What is troponin C? (Not what it does, just what it is)

A

A component of thin filaments that acts as a calcium sensor. It is part of a larger complex called the troponin complex.

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14
Q

How are myosins positioned along the thick filament?

A

Two myosins are bundled together so heads are apposed and opposed. The enzymatic activity is in the head. the tails wrap around one another and several of these polymerize together to make the thick filament. This polymerization of ““dimers”” allows for the thick filament to work together.

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15
Q

Skeletal muscle is under (voluntary/involuntary) control

A

Voluntary

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16
Q

Neurotransmitter which is released from a neuron to activate muscle cells

A

Acetylcholine

17
Q

Can one neuron activate many muscle cells, or can one muscle cell be activated by many neurons?

A

One neuron can activate many muscle cells but NOT the other way around

18
Q

What happens at the neuromuscular junction (skeletal mucle)

A

Acetylcholine is released from a neuron and binds to nicotinic acetylcholine receptors. These receptors then let in sodium which depolarizes the cell to cause an action potential by eventually triggering VG Na channels. This leads to a cascade of events which will activate the DHPR and subsequently RYR to release calcium into the cytosol. This will lead to contraction.

19
Q

How does the DHPR work in skeletal muscle?

A

The exact mechanism isn’t known but it acts as a voltage sensor and changes conformation to let the RYR know to turn on when voltage is high. In skeletal muscle the DHPR (dihydropyridine receptor) is actively touching the ryanodine receptor. It is analagous to the L-Type calcium channel of cardiac muscle cells

20
Q

What brings calcium back into the ER/SR once it has been released

A

SERCA

21
Q

What kind of pump is SERCA

A

Calcium pump that is activated by ATP (it is pumping calcium against its concentration gradient)

22
Q

Difference between skeletal and cardiac muscle modulation of force

A

In skeletal muscle, the force of contraction and can be modulated by fiber (cell) recruitment but in the heart every cell must contract every time. In cardiac muscle therefore the force of the contraction is modulated by extrinsic factors such as PSNS/SNS input, that will then modulate contractile parameters such as SERCA and thin filament aspects (like TnI)

23
Q

How does magnitude of calcium release equate to a force output?

A

This has to do with troponin C (see slide about actin/mysoin interaction regulation in skeletal muscle

24
Q

Describe actomyosin interaction regulation in skeletal and cardiac muscle

A

In skeletal and cardiac muscle, on thin filaments there is a protein called tropomyosin that normally blocks myosin from interacting with actin. To allow for cross-bridge cycling this protein must be moved to allow the interaction. This is done by the troponin complex. One of these proteins, Troponin C, acts as a calcium sensor. When calcium is bound, it changes conformation and nudges Tropomyosin out of the way to free the interaction between actin and myosin to allow crossbridge cycling to occur.

25
Q

Basic steps of the cross-bridge cycle

A
  1. ) ATP binding
    - this leads to release of the myosin heads from actin
  2. ) ATP hydrolysis
    - this leads to myosin getting into a conformation that is able to bind to actin
  3. ) Actomyosin interaction
    - Actin interacts with myosin in the case of calcium being present
  4. ) Release of phosphate
    - occurs as myosin is pulled along/pulls along actin
26
Q

Describe the length-tension relationship of muscle

A

As you increase sarcomere length, you increase the force that can be produced (thought to be a consequence of the increased overlap of thick/thin filaments). This of course is only in the duration of a sweet spot until you surpass that overlap and things cannot move anymore. This point is not seen in normal physiology.

27
Q

Describe what’s going on in this picture

A

As you increase the frequency of the action potential you’re increasing the duration of calcium release and thus the duration of the cross-bridge cycling, leading to a greater generation of force. Slow twitch muscles have slow, long contraction. Fast twitch muscles have very rapid kinetics and are not built for endurance.

28
Q

Describe the relationship between force on a sarcomere and contraction velocity.

A

At a given sarcomere length, as more load is put on the muscle cell the lower the contraction velocity. At the Y intercept this is the maximum contraction speed (no weight). At X intercept this is when the weight exceeds the maximum load the muscle cell can move. This point where it dips is isometric contraction, where you’re contracting but no sarcomere shortening is occurring (you’re trying to lift a car). At this point you aren’t doing any “work” which is why the work line dips here as well.

29
Q

Difference between EC coupling in skeletal and cardiac muscle cells

A

Skeletal: you can modulate the contraction by fiber recruitment

Cardiac: You modulate the strength of contraction by variation in the SR calcium release (modulate the EC coupling duration/etc). This happens through beta adrenergic stimulation