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Human Physiology 1 > Lecture 17 & 18 Outline > Flashcards

Lecture 17 & 18 Outline Flashcards

1
Q

What are the 3 types of muscle?

A
  1. Skeletal muscle
  2. Cardiac muscle
  3. Smooth muscle
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2
Q

Skeletal muscle

A

make up muscular system

- muscles that allow you to move about; arms, legs, & fingers & also your diaphragm is 1 of these

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3
Q

Cardiac muscle

A

found only in the heart

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4
Q

Smooth muscle

A

appears throughout the body systems as components of hollow organs & tubes
- key part of blood vessels of your arteries that allows them to contract

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5
Q

What are the 2 different ways that muscle is classified into?

A
  1. Striated or unstriated (much better)

2. Voluntary or involuntary

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6
Q

Describe the skeletal muscle features

A

MULTInucleated

Striated

Long, stacked in parallel

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7
Q

What does multinucleated mean?

A

means each individual muscle cell contains a # of cell nuclei

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8
Q

What is the reason that mutlinucleated is organized in this way?

A

is that during dev. a # of muscle cells will fuse

- as they fuse they will contain more & more nuclei

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9
Q

What does striated mean?

A

has stripes that occur at regular intervals

- alternating dark & light bands

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10
Q

What does long, stacked in parallel mean?

A

means each individual muscle cell or muscle fibre is generally a long skinny cell & in order to make up a muscle, is that a # of them are stacked in parallel
- so generally go from 1 end of the muscle to the other end of the muscle

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11
Q

Describe the Cardiac muscle features

A

UNInucleated

striated

stacked end to end intercalated disk

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12
Q

What does uninucleated mean?

A

means each cell contains a single nucleus

- 1 nucleus per cell

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13
Q

What does stacked end to end intercalated disk mean?

A

joined 1 cell to the next by these regions called intercalated disk
- region where 1 cardiac muscle cell contacts another 1 at their ends

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14
Q

Describe the Smooth muscle features

A

uninucleated

not striated

sheets or tube

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15
Q

What does not striated mean?

A

instead, their often spindle shaped or cigar shaped

  • not as long as skeletal muscle cells
  • each 1 of them has a single nucleus
  • not striated (no alternating bands of light & dark)
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16
Q

Controlled muscle contraction allows:

A
  1. movement of joints, limbs & whole body
    - locomote - move about
  2. propulsion of contents through various hollow organs
    - Ex: allows propulsion of blood through your circulatory system
    - Ex: allows movement of food through various parts of your digestive system
  3. emptying of contents of certain organs to external environment
    - muscle in particular; sphincters - can act as falz, & can allow the emptying of contents of certain organs to the external environment
    - Ex: they allow expulsion of urine from your bladder
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17
Q

What is skeletal muscle controlled by?

A

controlled by neurons the CNS (brain & spinal cord)

- neuronal control

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18
Q

What is apart of the two neuron chain?

A
  • Upper Motor Neurons

- Lower Motor Neurons

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19
Q

Upper Motor Neurons

A

with cell body in the motor cortex synapse on motor neurons in the SC

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20
Q

Lower Motor Neurons

A

with cell body in spinal cord send axons to synapse on muscle cells

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21
Q

Activation of this lower motor neuron will ultimately cause through a series of events…

A

activation of the synapse on muscle cell & ultimately contraction of those muscle cells

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22
Q

The group of muscle cells controlled by a Lower motor neuron is a…

A

motor unit

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23
Q

Neurons in the motor cortex synapse on…

A

motor neurons in the SC

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24
Q

Motor neurons…

A

send axons out the ventral roots & make synapses on muscle cells

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25
Q

Nerve muscle synapse is called…

A

neuromuscular junction (NMJ)

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26
Q

Synapse that’s going to happen b/t lower motor neuron & the muscle cell is called a…

A

NMJ

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27
Q

Describe the neuronal control pathway of skeletal muscle

A
  • from the primary motor cortex
  • send axons on the ipsilateral side
  • through brainstem on same side
  • then in the medulla oblongata, about 90% of those axons are going to cross over
  • make synapse on lower motor neuron, down in SC & that axon will exit through the ventral root & ultimately make a synapse on a muscle cell & cause contraction of that muscle
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28
Q

Primary neurons of your motor cortex that are on your right side of body for ex…

A

will control muscle cells on the left side of your body

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29
Q

Each muscle is composed of…

A

a large number of muscle cells

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30
Q

In mammals, each muscle cell receives ____ ___ synapse

A

ONLY ONE

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31
Q

In mammals, each muscle cell receives ONLY ONE synapse that is ALWAYS…

A

EXCITATORY & uses n.t. ACh

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32
Q

The motor unit

A

is one motorneuron & all of the muscle cells it innervates

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33
Q

Sometimes a motor neuron will innervate…

A

only one muscle cell, sometimes many

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34
Q

So the 2 ways a motor neuron will innervate are:

A
  • motor neuron innervating only 1 muscle cell
  • 1 motor neuron is innervating a # of diff. muscle cells but still, each muscle cell receives only 1 synaptic input (more common)
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35
Q

The synapse b/t the lower motor neurons & muscle cells is called the…

A

neuromuscular junction (NMJ)

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36
Q

Why is the NMJ a special synapse?

A
  1. The NMJ is HUGE (1000 micrometers2) vs a central synapse (0.05 micrometers2)
  2. The postsynaptic membrane is FOLDED & has a HIGH DENSITY OF nAChR (hundreds of thousands!!)
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37
Q

Central synapse vs NMJ

A

Central synapse:

  • SIMPLE!
  • 0.5 mV EPSP
  • has GPCR’s & Ligand-gated ion channels

NMJ:

  • NOT simple!
  • Folded to increase the SA!
  • High density of both nAChR (& the crests of these synaptic folds) & VG Na+ channels (fold in the trophs)
  • # of peaks & valleys (trophs & crests) & the NMJ
  • LARGE EPSP ~40mV
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38
Q

So the NMJ, when this motor neuron releases its ACh you got a huge EPSP. But then, you got a whole bunch of Na+ channels located in that very same area. Result of that is that:

A

when the muscle cell; postsynaptic muscle cell sees this large EPSP, that’s always enough to bring these VG Na+ channels to their threshold & they will fire an AP

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39
Q

So, what are the 4 reasons why the NMJ is a special synapse?

A
  1. The NMJ is HUGE (1000 micrometers2) vs a central synapse (0.05 micrometers2)
  2. The postsynaptic membrane is FOLDED & has a HIGH DENSITY OF nAChR (hundreds of thousands!!)
  3. The EPSP in muscle cell is LARGE (30-50 mV), whereas the EPSP at a central synapse may be 0.5-1 mV
    - b/c a lot of ACh binding to a lot of nAChR
  4. High density of VG Na+ channels within the post synaptic folds
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40
Q

What is the result of the 4 points for why NMJ is a special synapse?

A

is that a single AP in a motor neuron will ALWAYS cause an AP in the postsynaptic muscle cell (no summation of EPSP)
- HIGH SAFETY FACTOR!

Described in more dets:

  • when there’s an AP in a motor neuron, it releases ACh, it diffuses across the cleft & binds to the nicotinic ACh receptors on the muscle cell membrane - that causes a huge EPSP & that is always enough to cause an AP in that postsynaptic muscle cell
  • result of that: since there’s an AP that always follows from the EPSP, we see that there’s no summation of EPSP’s at the NMJ
  • an AP will always result in contraction of that skeletal muscle (very special feature of neural muscular synapse)
  • has a very high safety factor
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41
Q

Muscle consists of…

A

a number of muscle fibers (AKA muscle cells) lying parallel to one another and held together by connective tissue

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42
Q

Muscle cells

A

elongated cells - multinuclear & generally lie the whole length of the muscle

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43
Q

Single skeletal muscle cell is known as a

A

muscle fiber

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44
Q

Muscle fiber

A

– Multinucleated
– Large, elongated, and cylindrically shaped
– Fibers usually extend entire length of muscle

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45
Q

Tendon

A

very tough colajadece connective tissue

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46
Q

Muscle fascicle

A

bundle of fibers

  • a bundle of muscle cells
  • all wrapped up to form this 1 single muscle
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47
Q

Sarcoplasmic reticulum

A

specialized endoplasmic reticulum for storing Ca++ ions thats found in muscle cells

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48
Q

Sarcoplasmic reticulum is specialized b/c of a # of reasons:

A
  1. Way its organized, it always sits in these certain positions, always sits with its middle here at the middle of the sacromere, & it extends
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49
Q

T-Tubules

A
  • imp. b/c they form a mesh network of canals & tubules that traverse all the way through the muscle
  • lie directly adjacent to the sarcoplasmic reticulum - - continuous with the sarcolemma itself
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50
Q

Sarcolemma

A
  • membrane of the muscle cell

- basically just cell membrane of muscle cell

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51
Q

Myofibril

A

bundles of the contractile proteins

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52
Q

Thick filaments

A

thick lines –> dark purple

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53
Q

Thin filaments

A

thin lines –> light pink

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54
Q

Why is the thick & thin filaments always organized in the same structure?

A

so the dark & light bonds that make striated muscle have that unique appearance b/c of the presence of these thick & thin filaments

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55
Q

What is the most basic fundamental unit?

A

the sarcomere (goes from 1 Z-line (Z-disk) to another Z-line (Z-disk)

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56
Q

A band

A

represents the length of those thick filaments

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57
Q

H zone

A

surround M line

- area where there are NONE of these myosin crossbridges

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58
Q

M line

A

middle of sacromere

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59
Q

What are the thick filaments made up of?

A

made up PRIMARILY just of myosin molecule

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60
Q

Where are the thick filaments?

A

in middle of sarcomere

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61
Q

What are the thin filaments made up of?

A

made up of this actin chain

- # of proteins come together to make this

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62
Q

Where are the thin filaments located?

A

on each side or end of sacromere

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63
Q

What is the major component of thick filament?

A

myosin

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64
Q

Myosin

A

Protein molecule consisting of two identical subunits shaped like a golf club
– Tail ends are intertwined around each other
– Globular heads project out at one end

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65
Q

Describe where the tails & heads of myosin go

A

Tails oriented toward center of filament and globular heads protrude outward at regular intervals

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66
Q

Heads form…

A

cross bridges (molecular interactions) b/t thick & thin filaments

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67
Q

Myosin head has 2 important sites critical to contractile process:

A
  • An actin-binding site

- A myosin ATPase

68
Q

Thin filaments made up of…

A

actin, tropomyosin, troponin, nebulin, titin

69
Q

What is the primary structural component of thin filaments?

A

actin

70
Q

What is actin made up of?

A

G-actin monomers are spherical, but assemble into long chains

71
Q

Each actin has a special binding site for…

A

attachment with myosin head

- binding results in contraction of muscle fiber

72
Q

What are tropomyosin & troponin?

A

regulatory proteins

73
Q

Tropomyosin

A

Thread-like molecules that interacts with actin along its spiral groove

74
Q

Tropomyosin covers…

A

myosin binding sites

75
Q

What is troponin made of?

A

3 polypeptide units
• One binds to tropomyosin
• One binds to actin
• One can bind with Ca2+

76
Q

When NOT bound to Ca2+

A

troponin stabilizes tropomyosin in blocking position over actin’s cross-bridge binding sites

77
Q

When Ca2+ binds to troponin

A

tropomyosin moves away from blocking position

With tropomyosin out of way, actin and myosin bind, interact at crossbridges

Muscle contraction results

78
Q

Whole purpose of troponin is that it…

A

simultaneously combines with tropomyosin, actin & Ca2+

79
Q

Titin

A

– Giant, elastic protein (1 of the largest proteins that we know of)
– Joins M-lines to Z lines at opposite ends of sarcomere

80
Q

What are 2 important roles of Titin?

A

• Helps stabilize position of thick filaments in relation to thin filaments
- keeps thick filaments in the middle

• Improves muscle’s elasticity
- sarcomere can get longer & shorter; what titin does is it even looks like a spring & contributes to the elasticity of these proteins sliding past each other)

81
Q

Nebulin

A
  • aligns actin filaments
82
Q

Myomesin

A
  • M-line
  • main protein here that forms the M-line
  • a structural element to keep those thick filaments at the regular stacings
83
Q

What is the sliding filament hypothesis?

A

Muscle shortens when actin and myosin slide past each other

84
Q

When muscle is relaxed…

A

stretched

- thick filaments barely overlapping on the thin filaments

85
Q

When the muscles contracted…

A

the thick & thin filaments are gonna slide past each other
- then we’ll see a greater degree of overlap (sarcomere is going to shorten & that’s causing greater degree of overlap b/t thick & thin filaments)

86
Q

What happens when troponin & tropomyosin is in the RELAXED state?

A
  • myosin head cocked (ready-in position)
  • tropomyosin partially blocks binding sites on actin
  • myosin is weakly bound to actin

no Ca2+ ions

87
Q

What happens when troponin & tropomyosin is in the initiation of contraction?

A

a calcium signal initiates contraction

  1. Ca2+ levels increase in cytosol
  2. Ca2+ binds to troponin (TN)
  3. Troponin-Ca2+ complex pulls tropomyosin away from actin’s myosin-binding site
  4. Myosin binds strongly to actin & completes power stroke
  5. Actin filament moves
88
Q

What is the difference b/t myosin in the relaxed state & the initiation of contraction?

A

in the initiation of contraction it is starting to bend & it’s pulling/moving the actin

89
Q

Describe the pathway of the sliding of the thick filament past the thin filament & the shortening of that sarcomere

A

BINDING Myosin cross bridge binds to actin molecule

POWER STROKE Cross bridge bends, pulling thin myofilament inward

DETACHMENT (Ca2+ concen. is going to lower again) Cross bridge detaches at end of power stroke & returns to original conformation

BINDING Cross bridge binds to more distal actin molecules; cycle repeated
- will eventually allow this to bind all the way to the very middle (2-line)

90
Q

Actin & myosin…

A

DO NOT CONTRACT

- only the sarcomere can contract

91
Q

Myosin is properly called a…

A

motor protein: a protein that hydrolyzes ATP to convert chemical energy to carry out mechanical work

92
Q

What is the role of ATP in this whole process (utilization of ATP)

A

TIGHT binding in the rigor state
- myosin head is bound very tightly to the actin molecule

  1. ATP binds to myosin. Myosin RELEASES actin
  2. Myosin hydrolyzes (breaks down) ATP. Energy from ATP rotates the myosin head to the cocked position. Myosin binds WEAKLY to actin
    - ADP & Pi remain bound
  3. Ca2+ signal. Power stroke begins when tropomyosin moves off the binding site
  4. Myosin releases ADP at the end of the power stroke
    - actin filament moves toward M line
    - head swivels
    - myosin releases Pi

ADP releases

93
Q

Muscle cells have extensive network of endoplasmic reticulum:

A

sarcoplasmic reticulum (SR)

94
Q

SR has…

A

very high Ca2+ concentration

95
Q

How does the SR achieve this high concentration of Ca2+ concentration?

A
  • SR has a powerful Ca++ ATPase transporter

* SR also has a Ca++ binding protein called Calsequestrin.

96
Q

What does the SR’s powerful Ca2+ ATPase transporter use?

A

Uses ATP to pump Ca++ from cytoplasm into SR

97
Q

What does SR’s Ca2+ binding protein called calsequestrin help with?

A

Helps maintain high Ca++ concentration

98
Q

T-tubules run…

A

perpendicular from surface of muscle cell membrane into

central portions of the muscle fiber

99
Q

T-tubules aligned on the…

A

edges of the A band (thick filaments, myosin)

100
Q

T-tubules is continuous with…

A

surface membrane – action potential on surface

membrane also invade T-tubule

101
Q

Spread of action potential down a T tubule triggers…

A

release of Ca2+ from SARCOPLASMIC RETICULUM into cytosol

- when it’s in the cytoplasm of the muscle cell - that’s when it will be free to interact with the tryponin

102
Q

Why is the voltage gates Ca2+ channel (=dihydropyridine receptor)?

A

called this b/c their blocked by a class of drugs called dihydropyridine

103
Q

Why is the ryanodine receptor that is the Ca2+ release channel called this?

A

b/c its blocked by a drug called ryanodine

104
Q

VG Ca2+ channel (= dihydropyridine receptor) & ryanodine receptor are…

A

PHYSICALLY connected by part of the ryanodine receptor called the foot

105
Q

Why is the foot called this?

A

b/c its a big piece of globular protein & it literally interacts with this VG Ca2+ channel

106
Q

What happens with the t-tubules?

A
  1. We have an AP & it’s traveling along the membrane of that muscle cell & it travels into the t-tubules of that muscle cell
  2. As it travels into those t-tubules its gonna depolarize the membrane, & this is a VG Ca2+ channel so when it depolarizes it will open
    - so the depolarization causes the VG Ca2+ channel to open
  3. Immediately what happens is a little bit of Ca2+ will enter the cytoplasm of that muscle cell
  4. As this channel opens, its connected to the foot of the ryanodine receptor, & that physically pulls open the ryanodine receptor (it’s a Ca2+ release channel)
  5. When this ryanodine receptor opens, its going to allow a flood of Ca2+ into the cytoplasm of that muscle cell
107
Q

Putting it all together

A
  1. An AP invades the presynaptic terminal and causes release of ACh
  2. ACh binds to the receptor, allows entry of Na+, causes EPSP large enough to trigger an AP
  3. The AP invades the T-tubule system
  4. The AP causes the DHP receptor to open, and in turn, open the RyR channel. This causes a massive release of Ca++, and increase in intercellular Ca++ concentration
  5. Ca++ binds troponin. Troponin pulls tropomyosin
    away from the myosin binding site on the actin protein
  6. Power stroke
  7. Actin filaments slide towards centre of the sarcomere
  8. Free Ca++ pumped back into SR
108
Q

Explain Rigor Mortis

A

• ~3-4 hours after death, peak at ~12 hours
- muscle starts to become stiff

  • After death, intracellular Ca++ rises (leaks out of SR)
  • Ca++ allows troponin-tropomysin complex to move aside and allow myosin cross bridges to bind to actin.

• But….
– ATP is needed to separate myosin from actin.
– Dead cells don’t produce more ATP.
– So once bound, cross bridges can’t detach.

• Rigor mortis subsides when enzymes start to break
down myosin heads

109
Q

Relaxation of muscle

A

• Action potentials stop arriving at NMJ
• ACh dissociates from AChR, gets degraded
• Ca++ ATPase pumps FREE Ca++ back into SR
• Ca++ dissociates from troponin, pumped back into SR
• Tropomyosin moves back into position, blocking
cross bridge binding site (will block that site where the myosin & actin can form that very tight bond)
• Muscle ceases to maintain tension
• Actin and myosin (are free to) slip past each other
– Pulled by titin
– Pulled by antagonistic muscle

110
Q

Titin is a protein…

A

with some elastic properties that will actually tend to pull that sarcomere apart a bit

111
Q

Antagonistic muscle

A

muscles will be pulled - stretched back out by the antagonist muscle

112
Q

Steps in the Contraction-Relaxation process that Require ATP

A
  1. Splitting of ATP by myosin ATPase for power stroke
    - when muscles die, this is no longer able to keep happening (this will be to a state of rigor mortis)
  2. Active transport of Ca2+ back into sarcoplasmic reticulum
    - once Ca2+ is released into the cytoplasm of that muscle cell (when that muscle no longer needs to contract) , we’ve got to pump that Ca2+ back into the SR & get ready for the next muscle contraction
  3. Na+/K+ ATPase
    - imp. b/c neurons & muscle cells need to have a RMP if their gonna generate APs)
113
Q

Main Energy Sources for Muscle Contraction

A
  1. Stored ATP (very little stored)
    - just a couple of secs worth
  2. Creatine phosphate
    - First energy storehouse tapped at onset of contractile activity
  3. Oxidative phosphorylation
    - Takes place within muscle mitochondria if sufficient O2 is present
  4. Glycolysis
    - Supports anaerobic (absence of O2) or high-intensity exercise
114
Q

Most of the energy for sustained contraction is gonna come from…

A

oxidative phosphorylation or glycolysis

115
Q

Creatine phosphate

A
  • During times of rest when ATP demand is low, muscle stores energy in the form of creatine phosphate
  • First store of energy tapped to fuel muscle contraction. (technically after “stored ATP” but it runs out after a few secs)
  • Provides 4-5 times the energy of STORED ATP

• Limited supply (only a few minutes)
- of activity that can be fuelled by creatine phosphate

116
Q

Creatine phosphate

A

the substrate for an enzyme called creatine kinase

117
Q

The Creatine Kinase enzyme is…

A

bidirectional

  • in times of rest, it’s able to use ATP to phosphorylate creatine to give you this reserve of phosphate in the form of creatine phosphate
  • but when use of muscle begins & it starts to use up its ATP then the creatine kinase enzyme can work in reverse & it can phosphorylate an ADP from the creatine phosphate to generate ATP
118
Q

Creatine Kinase can take…

A

1 reactant ATP & a 2nd reactant a molecule called creatine & it can transfer 1 of the P’s from the ATP to the creatine & you end up with a creatine phosphate molecule
- product is a creatine phosphate & an ADP

119
Q

At rest, creatine kinase:

A

goes to the left

slide 50

120
Q

During the 1st few minutes of exercise, creatine kinase:

A

goes to the right

ATP can be used for muscle contractions
- & then the concentration of ATP gets low in the cell - that’s gonna favour the creatine kinase enzyme to work in reverse, allow the transfer of the phosphate on the creatine phosphate back to the ADP & create ATP which can now be used for muscle contraction

121
Q

Oxidative phosphorylation is…

A

the process that provides energy during light to moderate exercise
– Uses stores of glycogen (polymer of glucose) in muscle (30 min)
– Good yield of ATP (38 per glucose molecule)
– Aerobic exercise (b/c its using O2)
– Adequate supply of oxygen

122
Q

How does Oxidative phosphorylation maintain adequate oxygen?

A

– Increase ventilation (increase breathing rate)
– Increase heart rate and force of contraction
– Dilate skeletal (muscle) blood vessels

All of these processes will provide an increase blood flow to provide increase O2

123
Q

Anaerobic Glycolysis is the…

A

Primary source of ATP when oxygen supply is limited (during intense exercise)
- blood can no longer supply the amount of O2 thats needed to fuel the activity of your muscles

124
Q

Describe Anaerobic Glycolysis

A

• Rapid supply of ATP
– (b/c) Only a few enzymes involved

BUT
• Very low ATP yield
– Only 2 per glucose molecule (remember oxidative phosphorylation gets you 38)
– (end up with production of) Lactic acid, acidifies muscle and contributes to fatigue

• Duration of anaerobic glycolysis is limited

125
Q

What causes muscle fatigue?

A

Pyschological & Peripheral

126
Q

Describe Central fatigue (psychological)

A

happens after you’ve been working hard & you say I just can’t do it anymore

  • different from person to person
  • who has it in them to dig a little bit deeper to be able to push just a little bit harder to get to the finish line
  • differences in ELITE ATHLETES
127
Q

Describe Peripheral muscle fatigue

A

for the rest of us plays a more immediate role

(physiologists not really sure which is the most important)
– Decrease in release of ACh 
– Receptor desensitization 
– Changes in of muscle RMP
– Impaired Ca++ release by SR
– Intracellular pH of muscle
– Others…
128
Q

Describe what decrease in release of ACh implies

A

from those lower motor neurons with sustained activity

129
Q

Describe what receptor desensitization implies

A

idea that when receptors are exposed to a n.t. or their ligand for a long period of time they can lower their affinity for that very ligand

130
Q

Describe what changes in of muscle RMP implies

A

if muscle is very active for a long period of time then it will be firing a lot of APs - EVENTUALLY over a long period of time you may see slight changes in extracellular K+ & if that happens then a little bit higher concen. of extracellular K+ in the ECF is gonna depolarize those cells & those changes in RMP can lead to inefficiencies in being able to contact the muscle

131
Q

Describe what impaired Ca2+ release by SR implies

A

after a while maybe the ryanodine receptors won’t be as effective at allowing that muscle flow of Ca2+ into the cytoplasm of muscle cell

132
Q

Describe what intracellular pH of muscle implies

A

remember anaerobic activity can generate lactic & that can lead to acidification of muscle

133
Q

What does development of tension during one muscle twitch tell us?

A

tells us that in this whole experimental setup, what we also got done is the muscle is basically glued in some sort of apparatus that when theirs an AP - we can measure the tension generated

134
Q

Latent period

A
  • the tension that’s generated by the muscle cell - there is a substantial lag from the AP to the actual generation of tension
  • that period of delay from the AP to when it starts to generate tension is the latent period
  • all those events take time & contribute to this
135
Q

Describe the single twitches

A
  • stimulate it at a very low freq.
  • every 200 msec
  • muscle cell is gonna generate some tension, slight latency & then the muscle cell will relax (repeat)
136
Q

Describe summation (of tension)

A
  • stimulated with a duration of 200 msec from 1st to 2nd
  • tension & relaxation but now for this 3rd stimulation (triangle) we’ll do it a little sooner - stimulate that muscle cell before its completely relaxed
  • can generate tension before that single twitch has actually been allowed to relax
137
Q

Describe summation leading to unfused tetanus

A
  • we’re stimulating time after time after time in a repetitive way before it gets a change to relax & eventually we’re gonna stimulate until it gets this point of max tension
  • call it unfused tetanus b/c that muscle cell (that fiber) is getting to relax a little bit from 1 pulse to the next
  • unfused b/c this curve is not smooth
138
Q

Describe summation leading to complete tetanus

A
  • the most tension that a muscle cell can generate - you would generate from this complete (fused) tetanus
  • curve is smooth
    • the most force a motor unit can generate **
  • we’re gonna stimulate this muscle cell a lot faster - so fast that it never gets any of these little opportunities to start to relax, it’s just gonna generate tension in this very smooth fashion
139
Q

Takes several AP to cause…

A

generation of maximal tension (out of a single muscle cell)

140
Q

What are the 2 potential reasons why it takes several AP to cause generation of maximal tension

A

• Some think it takes several APs to increase intracellular Ca++ enough to saturate actin’s myosin binding sites

• Some think intracellular Ca++ reaches its maximum
(saturates) after first action potential.
– Summation and Tetanus develop because SUSTAINED elevation of increased Ca++ allows greater exposure of actin binding sites and therefore maximizes interaction with myosin (effect is time dependent)

141
Q

Length-tension relationships

A

too much or too little overlap of thick & thin filaments in resting muscle results in decreased tension
- the amount of tension that a muscle or muscle cell generate depends on its initial resting state

142
Q

We can generate the most tension from a single muscle fiber, if theirs this amount of overlap - where the thin fibers only overlap until the end of a myosin head…

A

optimal resting length

143
Q

If we basically squish together a sarcomere & we push the thin filaments towards the M line in this sarcomere then its not able to generate as much tension if we got this overlap in C. Reason is…

A

as you push the sarcomere more & more together it’s not empty space - lots of other proteins in there (titin - big protein that takes up space), so the more you scrunch or push together this sarcomere all those other molecules start to push against each other & when that starts to happen - then that’s working against the generation of tension

144
Q

If you stretch out the muscle so theirs less overlap b/t the thin filaments & myosin heads (if that’s the initial state), which is shown in D & E then…

A
  • the muscle cell is not able to generate as much tension b/t theirs not as many myosin heads able to interact with the actin binding sites
  • E is the most extreme ex: if you stretch out muscle fibers so far that theres no interaction/overlap b/t the myosin heads & actin binding sites then it can’t possibly generate any tension
145
Q

In turkey & chicken…

A

fibre types grouped together (white meat, dark meat)

146
Q

In mammals, fibre types are…

A

interspersed

147
Q

Most mammals (including humans) have 3 types of motor units…

A

– Slow twitch oxidative (=red muscle)
– Fast twitch oxidative-glycolytic (=red muscle)
– Fast twitch glycolytic (=white muscle)

interspersed with each other

148
Q

Turkeys have 2 kinds of meat (=muscle):

A

dark meat (=red muscle)

white meat (=white muscle)

149
Q

What are the 3 types of muscle fibres?

A
  1. Slow twitch oxidative (slow fatigue resistant)
  2. Fast oxidative-glycolytic (fast fatigue resistant)
  3. Fast twitch glycolytic (fast fatigable)
150
Q

Describe Slow twitch oxidative (slow fatigue resistant)

A

• Small amounts of tension, slowly
• Capable generating tension for long periods of time
without running down energy stores
• Large numbers of mitochondria
• Small fibres
• Well vascularized, Myoglobin (to facilitate oxygen
transfer from blood)

151
Q

Describe Fast oxidative-glycolytic (fast fatigue resistant)

A
  • Generate a lot of tension, moderately fast
  • Somewhat resistant to fatigue
  • Moderate # of mitochondria
  • Fibres are larger than slow twitch
152
Q

Describe Fast twitch glycolytic (fast fatigable)

A 
– White muscle
– Generate the most tension
– Fatigue rapidly
– Few mitochondria (Anaerobic catabolism)
– Fibres are larger than slow twitch
153
Q

The slow twitch are…

A

slower to generate their tension but their fatigue resistant & they can keep going for a long time
- able to generate the same amount of tension - NO change in force up to an hour after we start this exp.

154
Q

The fast fatigue-resistant

A

after just a couple stimulations, it already gets to its peak

  • can do both glycolidic & oxidative phosphorylation
  • can maintain its tension for a while (6 mins later)
  • but by 4-6 mins that tension is starting to decrease
  • pooped out 50 mins later
155
Q

The fast-fatigable…

A

generate more tension, quickly but poop out really fast

  • reaches its peak force much sooner than either the other 2
  • generate a max force for ~ 1 min of activity but then it poops out real fast
  • clearly very fatigable
156
Q

All muscle fibres within the same motor unit are…

A

of the same type

157
Q

In mammalian muscles…

A

different fibre types may coexist side by side

158
Q

But all muscle fibres within the same motor unit are of the…

A

same type

159
Q

Remember muscle fibres can be 1 of 3 types, also fair to say the motor units are 1 of 3 types b/c…

A

it turns out that motor unit will only include fibres of the same type
- motor unit is 1 motor neuron & all the muscle fibres that it innervates

160
Q

Remember muscle fibres can be 1 of 3 types, also fair to say the motor units are 1 of 3 types b/c…

A

it turns out that motor unit will only include fibres of the same type
- motor unit is 1 motor neuron & all the muscle fibres that it innervates

161
Q

Any given motor neuron, it might innovate a # of muscle fibres but their all either gonna be one of the…

A

slow type, fast type or the fatigue resistant type

162
Q

Given a single motor neuron, all of the muscle fibres that it innervates are all gonna be of the…

A

same type

163
Q

Why would the motor neuron & your muscle cells be organized in this way?

A

all has to do with the order in which those muscle cells are gonna be recruited

164
Q

Describe the recruitment of motor units

A

• First Motor units recruited:
– Smallest motorneurons
– Slow twitch fatigue resistant (red; oxidative)
- if you lift a light weight these are the ones that your gonna activate 1st
– Each MU has only a few fibres
- small, weak & generate tension very slowly

• Next recruited
– These motor neurons are slightly larger
– Motor units that include fast fatigue resistant fibres

• Last recruited
– Fast fatigable (= fast twitch glycolytic, white muscle)
- lifting a really heavy weight & you need more strength to be able to finish that curl
– The largest MN, include most fibres

• Size principle

165
Q

Size principle

A

size does matter for muscle fibre recruitment

refers to the idea: that when you’ve got a muscle & its being tasked to do some work - theres 3 sites, 3 general sizes of MN’s (small, med, large)

  • 1st to become activated are gonna be the smallest MN’s & they innervate the slow twitch fatigue resistant fibres
  • the med size MN’s that innervate the fast fatigue resistant fibres get recruited next
  • & the last ones only when you really need them are the largest MN’s & if they innervate the fast twitch glycolytic muscle fibres

Human Physiology 1 (32 decks)

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