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ZOOL 461 > Muscles pt. 2 > Flashcards

Muscles pt. 2 Flashcards

1
Q

Describe how muscle function gets complicated in life-like scenarios in terms of residual force enhancement (rFE)

A

Experimental setup: Isometric contraction
1. Muscle is set up at peak length -> force ramps up due to latency, and then plateaus at a consistent level of peak force.
2. Take the same muscle and shorten it. Force ramps up due to latency, but then plateaus at a smaller force (due to force-length curve)
3. Take muscle and stretch it back to peak length.
Expectation: same force as trial 1
Real result: Increase in force (rFE)
Mechanism: maybe titin? But we don’t really know what’s going on which this

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2
Q

Describe how muscle function gets complicated in life-like scenarios in terms of tendon/latch mechanisms

A

The frog ankle illustrates how tendon/latch mechanisms bypass muscle’s force-velocity relationship (explains how a frog jumps - generates a lot of force and quickly)
- There is a mechanism in frogs that is locking the ankle in place (the ankle can’t rotate) -> mechanics of leg act as the latch
- Muscle shortens but ankle can’t rotate, so applying force to stretch a tendon (tendon=elastic like a rubber band; energy stored as stretched)
- Tendon snap back when latch released and we get high force and velocity at the same time (at some point, the mechanics of the leg are going to change and release the latch)
- Stored energy released all at once
- Rapid ankle rotation and high force delivered to ground for hopping

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3
Q

Work general definition, formula and units

A

Energy used to do stuff, or force (F) applied to move something a distance (d)
- W = Fxd (if direction of force and movement are aligned)
- Units: Nm = Joules (J)

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4
Q

Are you doing mechanical work if you’re pushing on a heavy box that’s not moving?

A

No

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5
Q

What kind of contraction are you performing while holding a plank? Are you doing work?

A

Isometric, no

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6
Q

Power definition, formula and units

A

The rate energy is used to do stuff, or work (W) over time
P=W/t=(Fxd)/t=Fxv where v=shortening velocity
Units: Watts (W) = J/t = (Nxm)/t

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7
Q

Draw the force-velocity curve and the power-velocity curve for a single myofibril, a single fiber and a constant number of fibers. Where is peak power?

A

Peak power: 20-40% of Vmax

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8
Q

Assume you are operating at peak power on flat ground. Describe what happens to force and power once you hit a hill and you don’t shift gears

A

Pedaling is harder at the hill, so need more force. Power decreases because we’re moving at a slower velocity (P=F x v) and as force increases, power decreases

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9
Q

If you were to bike up a hill at a lower gear than before, is your leg moving slower or faster than before? is your muscle shortening slower or faster?

A

You’re moving faster cause it’s easier to pedal

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10
Q

If you were to bike up a hill at a lower gear than before, is your muscle producing as much force as before? How does power change?

A

Less force is being produced (because legs are moving faster - force-velocity relationship)
Power increase compared to before because velocity is greater

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11
Q

A muscle fiber has enough ATP for ~3 sec of activity at max power. What are the 3 energy sources for contraction

A
  1. Phosphocreatine-creatine system
  2. Oxidative phosphorylation
  3. Glycolysis-lactic acid system
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12
Q

Describe how the phosphocreatine-creatine system replenishes the muscle fiber’s energy for contraction

A

Phosphocreatine reacts with ADP to form Cr + ATP
- Fast: 4 mol ATP/min, but Cr-Pi is depleted in 5-8 sec

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13
Q

Describe how oxidative phosphorylation replenishes the muscle fiber’s energy for contraction

A
  • Replenishes muscle’s energy at <70% of muscle’s max intensity
  • Supplies 95% of all long-term contraction energy
  • Muscle glycogen supplies glucose for 5-10 mins for oxidative phosphorylation
  • To sustain energy for hours: up to 1/2 of fuel is glucose from the blood for 2-4 hours. Then, fatty acids (less efficient fuel source)
  • Slow to start, and slow ATP supply (1 mol ATP/min)
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14
Q

Why do runners “hit the wall” when running?

A

There is a fuel change from blood glucose to fatty acids. Since fatty acids are a less efficient fuel source, runners experience exhaustion and pain.

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15
Q

Describe how the glycolysis-lactic acid system replenishes the muscle fiber’s energy for contraction

A
  • Fills time between the phosphocreatine-creatine system and oxidative phosphorylation when <70% of muscle’s max intensity is being used
  • primary energy source at >70% max
  • intermediate speed - 2.5 mol ATP/min
  • uses muscle glycogen to make ATP faster than oxidative phosphorylation
  • consumed supply in ~1.5 mins (much faster than oxidative phosphorylation, makes ATP much faster)
  • End products (lactic acid) may impact contraction?
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16
Q

What are two ATP uses in muscle?

A
  1. Myosin head (Cross-bridges)
  2. Ca2+ pumps on the SR
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17
Q

Only the ATP use at the myosin head can count toward…

A

Useful, mechanical work
- the myosin head is the only thing that’s tagging on something and moving a certain distance in the muscle

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18
Q

Max energetic efficiency of human muscle and what this means

A

25%
- that means, at max, 25% of muscle energy goes to useful mechanical work.
- The rest is converted to heat (Ca2+ pump is counted as heat)

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19
Q

True or false: the muscle is usually much less efficient than 25% (max energetic efficiency of human muscle)

A

True
- we don’t use muscle optimally

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20
Q

How efficient is an isometric contraction?

A

0% efficient because work isn’t being done at all (no energy is going to useful mechanical work)

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21
Q

Why do your muscles get warm during use?

A

Our muscles are poorly efficient -> a lot of our energy ends up producing heat.

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22
Q

Some individuals have genetic mutations affecting DHPRs and RyRs. When exposed to certain anesthetics, these abnormal receptors stop regulating Ca2+ release, leading to constant, high levels of Ca2+ in the cytoplasm.
- how might this affect the cross-bridge cycle?

A

Cross-bridge cycle just keeps going

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23
Q

Some individuals have genetic mutations affecting DHPRs and RyRs. When exposed to certain anesthetics, these abnormal receptors stop regulating Ca2+ release, leading to constant, high levels of Ca2+ in the cytoplasm.
-What impact does this have on muscle energy use?

A

Use lots of energy

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24
Q

Some individuals have genetic mutations affecting DHPRs and RyRs. When exposed to certain anesthetics, these abnormal receptors stop regulating Ca2+ release, leading to constant, high levels of Ca2+ in the cytoplasm.
- What symptoms do you think you would see in an affected individual? (4)

A
  • Muscle rigidity (due to continuous contractions)
  • Stop breathing (all muscles are tensed up)
  • Heat up
  • Depleted glycogen stores
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25
Q

Describe slow oxidative vertebrate muscle fibers in terms of the following:
- Speed of MHC ATPase and Ca2+ pump in SR
- Max power
- Metabolism
- Aerobic support (mitochondria, blood supply, myoglobin)
- Glycogen stores
- Fatiguability
- Use

A
  • Speed of MHC ATPase and Ca2+ pump in SR: Slow
  • Max power: good
  • Metabolism: oxidative (aerobic)
  • Aerobic support (mitochondria, blood supply, myoglobin): High (red)
  • Glycogen stores: Low
  • Fatiguability: Fatigue resistance (oxidative metabolism can run for hours)
  • Use: Posture, slow walk
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26
Q

Describe fast oxidative glycolytic vertebrate muscle fibers in terms of the following:
- Speed of MHC ATPase and Ca2+ pump in SR
- Max power
- Metabolism
- Aerobic support (mitochondria, blood supply, myoglobin)
- Glycogen stores
- Fatiguability
- Use

A
  • Speed of MHC ATPase and Ca2+ pump in SR: Fast
  • Max power: High
  • Metabolism: Primarily oxidative, but also glycolytic (anaerobic)
  • Aerobic support (mitochondria, blood supply, myoglobin): Good (pink)
  • Glycogen stores: medium
  • Fatiguability: Fatigue resistance (because they primarily use oxidative phosphorylation)
  • Use: Rapid but sustained (e.g. fast walking)
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27
Q

Describe fast glycolytic vertebrate muscle fibers in terms of the following:
- Speed of MHC ATPase and Ca2+ pump in SR
- Max power
- Metabolism
- Aerobic support (mitochondria, blood supply, myoglobin)
- Glycogen stores
- Fatiguability
- Use

A
  • Speed of MHC ATPase and Ca2+ pump in SR: Fast
  • Max power: Very high
  • Metabolism: Glycolytic (anaerobic)
  • Aerobic support (mitochondria, blood supply, myoglobin): Low (white)
  • Glycogen stores: high (supporting glycolytic-lactic acid system)
  • Fatiguability: Rapidly fatigued
  • Use: Sprint
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28
Q

True or false: fiber types have different force- and power-velocity curves
- If true, draw them

A

True
- Same general relationship, but shape is slightly different

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29
Q

If fast glycolytic fibers can achieve more force at slow velocities, why use slow oxidative fibers? Give 2 answers and use the power-shortening velocity curve in one of them.

A
  1. Slow oxidative fibers are fatigue resistant.
  2. Slow oxidative fibers have a higher peak power at a slower speed _. deliver force and energy at a higher rate at slower velocities
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30
Q

Why do you run a marathon slower than a 50m dash?

A

Need to provide energy for many hours -> need to use oxidative metabolism -> provide energy slower so we have a limit to our speed

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31
Q

Describe how fiber type location differs across vertebrate muscle

A

Fishes: separated
Other vertabrates: mixed within muscle (different types of fibers all in one muscle)

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32
Q

Describe the impact of athletic training on the following:
- The number of myofibrils
- The ATP and Cr-Pi stores
- The glycogen stores in muscle and liver
- The number of mitochondria (SO, FOG)
- Converting fibers

A
  • Increase the number of myofibrils (but not the number of cells)
  • Increase ATP and Cr-Pi stores
  • Increase glycogen stores in muscle and liver
  • Increase number of mitochondria in slow oxidative and fast oxidative glycolytic fibers
  • <10% of fast-twitch fibers can change to slow-twitch (but most of our fibers stay the same identity)
  • Some fast glycolytic fibers convert to fast oxidative glycolytic fibers
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33
Q

What are 4 purposes of skeletal muscle control systems?

A
  1. Voluntary motion
  2. Coordination of multiple muscles
  3. Get graded levels of force (so we’re not producing max force all the time, e.g. contracting gravity)
  4. Provide some automatic systems (don’t think about which muscles to contract when doing certain things like walking)
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34
Q

Where do signals for voluntary motion originate?

A

The motor cortex

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35
Q

Cerebellum function

A

Coordinates timing of complex motions

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36
Q

Where is the origin of central pattern generators (big patterned signals that coordinate different muscle movements) and reflex arcs?

A

The spinal cord

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37
Q

Describe the arrangement of motor control neurons

A

Sensory neuron and axons in descending pathway from motor cortex synapse at interneuron in spinal cord. Interneuron in spinal cord synapses onto alpha motor neuron which synapses to a muscle. Ascending axons are also present, bringing sensory info to the brain.

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38
Q

What do temporal and spatial summation allow for in general?

A

Summation lets us modulate the level of force produced by a muscle
- Graded levels of force are achieved through summation: control force over time (scale=fractions of second) and control force over space

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39
Q

Describe temporal summation in muscles and what causes it

A

Temporal summation occurs when the frequency of twitches is so high that subsequent twitches occur when all the previous Ca2+ hasn’t been sequestered into the SR yet and cross bridges are still occurring upon the second stimulation.
- More Ca2+ is released -> even more cross bridges

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40
Q

Difference between incomplete tetanus and fused tetanus

A

Fused tetanus: can no longer see individual twitches anymore
Incomplete twitches: can still kind of see individual twitches

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41
Q

What is a motor unit?

A

An alpha motor neuron and all fibers it connects to; only have 1 type of fiber within unit

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42
Q

Describe the variation in motor units

A

More and smaller motor units in areas where we need fine control

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43
Q

Where might you find large motor units?

A

Big muscles that you need a lot of force for, e.g. quads, hamstring, etc.

44
Q

Where might you find small motor units?

A

Muscles required for fine control (e.g. hands, face, eyes, etc).

45
Q

We have 1000s of motor units, which is too many for the brain to individually control. How do we deal with this?

A

The brain has a single axon that innervates different cell body sizes
- Alpha motor neurons with smallest cell bodies are innervated first, which innervate slow oxidative (SO) fibers.
- Alpha motor neurons with medium-sized cell bodies are innervated second, which innervate fast oxidative glycolytic (FOG) fibers
- Alpha motor neurons with largest cell bodies are innervated last, whcih innervate fast glycolytic fibers.
*Increase stimulation rate of brain on alpha motor neurons to recruit faster fibers

46
Q

Describe the force- stimulation rate of SO, FOG and FG fibers

A

SO recruited first, then FOG, then FG.
- All forces plateau due to tetanus
- SO has smallest force plateau, then FOG, then FG

47
Q

What are the 5 elements of reflex arcs?

A
  1. Sensor
  2. Sensory neuron
  3. Interneuron
  4. Alpha motor neuron
  5. Muscle
48
Q

What advantage is there to bypassing the brain through a reflex arc?

A

Fewer steps, so takes less time for muscle action
- Prevents tissue damage, for example

49
Q

True or false: the information involved in a reflex arc never reaches the brain

A

False
- There are ascending axons bringing sensory info to the brain, so we will eventually process the stimulus

50
Q

Describe and draw the diagram of the withdrawal reflex/flexor reflex (6 steps)
- Describe reciprocal innervation

A

Pulls the limb back in response to pain
1. Sensor detects pain
2. AP in sensory neuron goes to spinal cord
3. Excites IN1 and sends signal to brain
4. Branch 1.1 excites alpha neuron to flexor (e.g. hamstring- bends knee to lift lower leg)
5. Branch 1.2 excites IN2
6. Inhibits alpha motor neuron to extensor (e.g. quads)
Reciprocal innervation: one signal excites one muscle and inhibits its opposition at the same time

51
Q

Describe and draw the cross-extensor reflex (6 steps)

A

Withdrawal reflex plus keep the other leg straight (helps us stay upright so that we lift up our foot but we don’t want to fall over and hurt ourselves even more)
1. Signal to spinal cord like before
2. Excite first interneuron and signal to brain
3. Finish withdrawal reflex with reciprocal innervation in pain leg
4. Third branch from first interneuron crosses to the other side of the spinal cord and excites a third interneuron
5. First branch from third interneuron excites an alpha motor neuron of the extensor (quad) -> extends quad which prevents us from falling over
6. Second branch from third interneuron excites fourth interneuron, which inhibits alpha motor neuron to flexor (hamstring)
- Opposite of withdrawal reflex

52
Q

Some neurons have tone. What is tone?

A

Always active, and we change the level of activity

53
Q

Neural tone

A

Stimulating (sending APs) all the time, but pacing changes

54
Q

Less tone vs. default tone vs. more tone

A

Less tone: APs are being sent slower
Default tone: normal level of tone
More tone: APs are being sent faster

55
Q

Muscle response to increase in tone

A

Increased tone -> increased stimulation -> more signals to contract -> more contraction

56
Q

Muscle response to decrease in tone

A

Decreased tone -> decreased stimulation -> fewer signals to contract -> less contraction

57
Q

What allows for the stretch (myotactic) reflex?

A

Muscle spindles

58
Q

Muscle spindle

A

Special muscle fiber wrapped by stretch-sensitive neuron

59
Q

On a muscle spindle, the ends of the muscle fiber have…

A

Contractile filaments innervated by gamma motor neurons (but center doesn’t have any myofibrils)

60
Q

Describe a stretch neuron’s tone

A

Always firing

61
Q

What changes the AP firing rate in a muscle spindle? Be specific

A

Stretch
- Stretching increases tone, and compression decreases tone

62
Q

Where do signals from the muscle spindle go to?

A

Goes to spinal cord and synapses directly on alpha motor neurons for the same muscle

63
Q

Describe and draw the stretch (myotactic) reflex (6 steps)

A
  1. Whole muscle stretches, and spindle stretches too
  2. Increase firing rate of stretch neuron (i.e. increase its tone)
  3. Excites alpha motorneuron to same muscle that the spindle is embedded in
  4. Muscle contracts and shortens
  5. Spindle length is reduced, which decreases the tone of the stretch neuron
  6. Decrease in tone reduces the firing rate of the stretch neuron
64
Q

True or false: if the whole muscle is stretched, this allows the spindle muscle to also stretch

A

True

65
Q

Give two examples of a stretch (myotactic) reflex

A
  1. Knee-jerk reflex (hit causes a momentary stretch in the quad muscle)
  2. Holding position (e.g. carrying a box and don’t want our arms to drop -> myotactic reflex is keeping you from dropping your arms without thinking if yourarm slightly shifts while holding the box)
66
Q

What do gamma motor neurons do to the set point of the muscle spindle?

A

Gamma motor neurons change the “set point” of the muscle spindle
- Ex: let’s say we’ve shortened the whole muscle. This makes it so we hav slack, so we can’t detect small length changes. Solution: gamma motor neurons control spindle length to let stretch neurons work effectively (gamma motor neurons fire on the ends of the spindle and do contraction-coupling to lengthen it out)

67
Q

Describe smooth muscle structure

A
  • Smaller, spindle-shaped cells (not long rope-like fibers like skeletal muscle)
68
Q

Smooth muscle cells are (uninucleate/multinucleate)

A

Uninucleate

69
Q

Describe smooth muscle tissue

A

Very stretchy

70
Q

True or false: smooth muscle cells are striated

A

False
- Because thin and thick filaments are not arranged in sarcomeres

71
Q

True or false: smooth muscle cells have T-tubules, DHPRs and RyRs

A

False

72
Q

Describe how sliding filaments are arranged in smooth muscle

A

Filaments in lattice arrangement throughout cell, and are held together by dense bodies on the cytoskeleton.

73
Q

What are attachment plaques in the sliding filaments?

A

They attach filaments to the cell membrane in smooth muscle

74
Q

What way do thin filaments slide during smooth muscle contraction?

A

In opposite directions

75
Q

True or false: Thick filaments in smooth muscle have bare zones

A

False

76
Q

Describe what it means to say that smooth muscle filaments experience “change of partners” during stretch

A

After smooth muscle cell is stretched, the cell is longer and thinner so original filament sets no longer overlap with their original thick filaments, but they overlap with neighbouring thick filaments (different thin filaments are nearby, cross-bridges move to these)

77
Q

Why does change of partners occur in smooth muscle but not skeletal muscle?

A

Possible in smooth muscle because all myosin heads point the same way in smooth muscle

78
Q

Why is the process of “change of partners” useful in the bladder?

A

Bladder stretches when filled with pee, need to be able to contract the bladder to pee

79
Q

Describe the stress-relaxation property in smooth muscle that results from change of partners

A
  • As length of muscle initially increases, so does the force; this is due to the resistance from cross-bridges that haven’t detached from the original filament yet and the elasticity of the myosin neck
  • Decrease in force aka “stress-relaxation” occurs as myosin heads move to new, closer thin filaments (so smooth muscle cell isn’t being stretched anymore)
80
Q

True or false: there is a defined length-tension relationship in smooth muscle, similar to skeletal muscle

A

False

81
Q

True or false: the number of cross-bridges before and after a smooth muscle cell is stretched is the same due to the “change of partners”

A

True

82
Q

Describe single vs. multi-unit smooth muscle

A

Single-unit: electrical synapses are connecting together through gap junctions and cells are being excited together as one
- postganglionic axon of the autonomic nervous system doesn’t connect to every cell due to presence of gap junctions
Multi-unit: No gap junctions, cells are acting separately
- postganglionic axon of the autonomic nervous system connects to every cell

83
Q

Describe phasic vs tonic smooth muscle

A

Phasic: Rhythmic contractions
Tonic: Muscle has tone - it is always on, it’s just a matter of “what degree of on it is”

84
Q

Myogenic vs neurogenic excitation

A

Myogenic: Contraction originates in the muscle itself
Neurogenic: Contraction originates in the neuron

85
Q

What 2 smooth muscle classifications are common? Give examples for each

A
  1. Single unit, phasic and myogenic: gut, urinary bladder
  2. Multiunit, tonic and neurogenic: blood vessels, hair, iris
86
Q

In late pregnancy, smooth muscle in the uterus changes from multiunit to single unit. Why might this be important?

A

Ensures uterine muscle cells contract simultaneously.

87
Q

What are the two forms of myogenic excitation? What do both forms ensure?

A
  1. Pacemaker potential
  2. Slow wave potential
    In both, the ANS modifies contraction by moving baseline potential closer to/farther from AP threshold (changes baseline potential by changing the ion fluxes across the membrane)
88
Q

Describe pacemaker potential
- Draw it

A

Potential starts with a drift, due to leaky ion channels in the membrane which leads to slow depolarization in the membrane over time. Once drift reaches AP threshold, single AP fires.
- Spikes come from Ca2+ influx, not Na+

89
Q

Describe slow wave potential and give an example of an organ where this is seen
- Draw it

A

Potential starts with a random drift, that comes from the following:
- Leaking across the cell membrane
- Random speeding up/slowing down of ion channels, especially Na+ channels (greatest contribution)
- Random speeding up/slowing down of ion pumps

Then, once AP threshold is met, there is a burst of APS before the potential goes back down.

90
Q

Varicosity and orientation relative to muscle cells

A

Swellings along long ANS axon.
- Each swelling is near a smooth fiber cell, but not as close as synapses

91
Q

Describe the interactions between varicosities and smooth muscle fibers

A

Diffuse “shower” of neurotransmitter over the smooth muscle fiber
- more room for diffusion of neurotransmitters compared to synapse

92
Q

True or false: there are junctional folds in the smooth muscle fiber
- Explain a consequence of the answer

A

False
- There are neurotransmitter receptors all over the fiber
- Receptors all over means that muscle sensitive to hormones and compounds in the blood (i.e. stuff outside of the junction)

93
Q

What are the 3 pathways that can connect excitation to an increase in cytoplasmic Ca2+ in smooth muscle?

A
  1. Sarcolemma, voltage-gated Ca2+ channels opened by AP
  2. SR, triggered by second messenger
  3. Sarcolemma, Ca2+ channel opened by second messenger
94
Q

Describe how Ca2+ comes from the SR, triggered by a second messenger (4 steps)

A
  1. neurotransmitter binds to GPCR on cell membrane
  2. G-protein activates enzymes
  3. Enzymes make inositol triphosphate (IP3)
  4. IP3 opens Ca2+ channel on SR
95
Q

Kinases

A

Enzymes that split ATP and phosphorylate stuff to activate things

96
Q

Phosphatases

A

Enzymes that remove Pi from stuff to deactivate things

97
Q

What turns the ATPase in the myosin head on/off?

A

Regulatory myosin light chain (MLC)
- depends on phosphorylation state of MLC

98
Q

What controls the phosphorylation state of MLC?

A

MLC kinase (MLCK) and MLC phosphatase (MLCP) control whether MLC is phosphorylated

99
Q

MLCK and MLCP (are/are not) always present and operating, so smooth muscle is (always/sometimes) on
- Explain why

A

MLCK and MLCP are always present and operating, so smooth muscle is always on (always have some phosphorylated MLC)

100
Q

What does the “degree of on” of a smooth muscle depend on?

A

Which enzyme (MLCK or MLCP) is currently working faster

101
Q

Describe how ATPase is switched on, increasing contraction (control at the thick filament) (4 steps)

A
  1. Ca2+ binds to a protein called calmodulin (CaM)
  2. Ca2+-CaM complex activates MLCK
  3. MLCK phosphorylates MLC, which swithces the ATPase on
  4. Cross-bridge cycle runs = contraction
102
Q

Describe how ATPase is switched off, decreasing contraction (control at the thick filament) (6 steps)

A
  1. Ca2+ is removed from cytoplasm through several pumps
  2. Low Ca2+ concentration promotes unbinding of Ca2+ from CaM
  3. So, MLCK deactivated
  4. MLCP dephosphorylates MLC
  5. So, ATPase switched off
    6, Cross-bridge cycle stops = relaxation
103
Q

True or false: Troponin and tropomyosin are present in both smooth and skeletal muscle

A

False
- it’s only present in skeletal muscle

104
Q

Describe the control at the thin filament by Ca2+-CaM

A
  1. Myosin binding site on g-actin is blocked by caldesmon (instead of tropomyosin)
  2. Ca2+-CaM also binds to caldesmon, removing it
  3. And other enzymes can phosphorylate caldesmon, which also removes it from the thin filament.
105
Q

What 4 things promote smooth muscle contraction?

A
  1. Stimulation from the parasympathetic autonomic nervous system (uses Ach)
  2. Stimulation by the sympathetic autonomic nervous system (uses norepinephrine + epinephrine, which also influence contractino if they come from somewhere other than the sympathetic nervous system) -> binds to α1 receptors
  3. Serotonin slows down MLCP
  4. Stretch
106
Q

What 2 things promotes relaxation/decreases contraction in smooth muscle?

A
  1. Sympathetic autonomic nervous system (norepinephrine + epinephrine)
    - binds β2 receptors -> inhibits MLCK
  2. Hormones from the blood
107
Q

What are 5 other things that influence contraction?

A
  1. O2
  2. CO2
  3. pH
  4. Nitric oxide (NO)
  5. Heat

ZOOL 461 (11 decks)

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