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Physiology > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

Name the three varieties of muscle in the body

A
  • Skeletal
  • Cardiac
  • Smooth
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2
Q

The contractile cells of muscle tissue

A

Myocytes/Myofibres

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3
Q

Another name for the skeletal muscle

A

Striated muscle

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4
Q
A

Skeletal muscle

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5
Q
A

Epimysium

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6
Q
A

Muscle fascicles

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7
Q
A

Muscle fascicle

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8
Q
A

Perimysium

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9
Q
A

Endomysium

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10
Q
A

Muscle Fibres

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11
Q
A

Muscle fibre

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12
Q
A

Sarcolemma

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13
Q

Fibril diameter

A

100 - 1000 µm

(1mm)

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14
Q

Myocyte diameter

A

10-100µm

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15
Q

Myofibril diameter

A

1µm

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16
Q

What is located between two Z-bands?

A

1 sarcomere

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17
Q
A

A-band

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18
Q
A

H-zone

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19
Q
A

1/2 I-bands

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20
Q
A

Z-bands

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21
Q
A

M-line

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22
Q
A

Sarcomere

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23
Q
A

Sarcoplasmic reticulum

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24
Q
A

Actin filament

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25
Q
A

H-zone

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26
Q
A

Z-disc

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27
Q
A

Myosin filament

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28
Q
A

I-band

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29
Q
A

A-band

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30
Q
A

M-line

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31
Q
A

Sarcolemma

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32
Q
A

Sarcoplasmic reticulum

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33
Q
A

Terminal cister

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34
Q
A

T-tubule

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35
Q
A

Triad

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36
Q

What permits the conduction of electrical impulses in the muscle fibre?

A

Narrow T-tubules

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37
Q

What regulates the intracellular levels of calcium?

A

Sarcoplasmic reticulum

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38
Q

The membrane triad of myocytes is composed of…

A
  • 2 x terminal cisternae
  • 1 x T-tubule
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39
Q

List the 3 additional proteins in the sarcomere

A
  • Titin
  • Nebulin
  • Alpha-actinin
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40
Q

Titin

A
  • Largest protein of the body
  • From Z-lines → Myosin bundles
  • Ensures precise return of actin and myosin bundles to original position
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41
Q

Nebulin

A
  • Determines the direction and placement of actin polymerisation (during development)
  • Protects actin fibres from rearranging
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42
Q

Alpha-actinin

A
  • Creates the Z-band
  • Net-like
  • Provides a binding site for actin complexes
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43
Q
A

Nebulin

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44
Q
A

Titin

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45
Q
A

Alpha-actinin

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46
Q

A motor unit

A
  • Motor neuron
  • Skeletal muscle fibres innervated by the neurone’s axonal terminals
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47
Q

Summarise the pathway from neural activation to muscle contraction

A
  1. Generated AP→ Myoneural junction
  2. ACh-containing vesicles open at synaptic knobs
  3. ACh attach to the sarcolemma ACh-R
  4. ACh channel opens
  5. Na+ enters inner surface → Local end plate potential generated
  6. AP generated → Activates SR though T-system
  7. Ca2+ release into sarcoplasm → Actin-myosin contraction
  8. Ca2+ repumping into:
  • SR
  • Mitochondrium
  • EC
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48
Q

AP on the myolemma is generated only if…

A

The AP is stimulated through a nerve

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49
Q

Transmission of neural AP to the muscle takes place in the…

A

Myoneural junction

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50
Q

Give the summary of the processes that occur at the neuromuscular junction

A
  1. AP reaches nerve terminal → ACh release
  2. ACh → Nicotinic receptors on muscle membrane
  3. Ligand-activated cationic channels open
  4. EPP produced
  5. Voltage-gated Na+ channels open
  6. AP formed in myolemma
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51
Q
A

Synaptic Vesicle

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52
Q
A

Synaptic Cleft

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53
Q
A

ACh receptor

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54
Q
A
  • ACh binding to its receptor
  • Ligand-activated cationic channel opens
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55
Q
A

ACh released by synaptic vesicle

Exocytosis

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56
Q

Lifecycle of neurotransmitter

A

Neurotransmitter synthesis

  • In cell body (cytosol)
  • In the terminal
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57
Q

Lifecycle of neurotransmitter

A

Neurotransmitter packaged into vesicles

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58
Q

Lifecycle of neurotransmitter

A

Neurotransmitter released

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59
Q

Lifecycle of neurotransmitter

A

Neurotransmitter binding

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60
Q

Lifecycle of neurotransmitter

A

Neurotransmitter diffused away

  • Catabolysed or transported back into the terminal
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61
Q

Give the actions when AP reaches the NMJ

A
  • Voltage-gated Ca2+ channels open, influx from EC space
  • [Ca2+] increases 100x → ACh exocytosis initiated
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62
Q

Clathrin

A
  • Protein on inner membrane
  • Stimulates endocytosis
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63
Q

What is shown?

A

Clathrin-dependent endocytosis

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64
Q

Composition of the nicotinic acetylcholine receptor

What does this allow?

A
  • Two alpha subunits
  • Two beta subunits
  • One delta subunit

Allows blocking effect of curare and bungarotixin

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65
Q

Give the 3 possible conductance states of the nicotinic acetylcholine receptor

A
  • Closed
  • Open
  • Inactivated
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66
Q

Which potential is amplitude-coded?

A

EPP

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67
Q

Which potential is frequency-coded?

A

AP

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68
Q

Decremental conduction

A

Decrease of signal strength with distance travelled

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69
Q

Role of Mg2+ in muscle contraction

A
  • Antagonises ACh receptor
  • Blocking function of sarcomere
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70
Q

Give the importance of Mg2+ in cattle

A
  • High Ca2+ secretion after calving → Low plasma Ca2+ levels
  • [Mg2+] becomes relatively high
  • Muscles relax: Parturient paresis
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71
Q
A
  • AP from axon
  • Ca2+ enters from EC, ACh vesicle release
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72
Q
A

Filling up with ACh

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73
Q
A
  • ACh binds to the receptor
  • EPP generated
  • AP generated, Ca2+ influx, contraction
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74
Q

Effect of nicotine on the neuromuscular junction

A
  • Same effect as ACh
  • Cannot be degraded by cholinesterase
  • Conc. therefore increases → Permanent depolarisation
  • Intensive spasm
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75
Q

Effect of cholinesterase inactivators on the neuromuscular junction

A
  • ACh not hydrolysed
  • High ACh accumulation
  • Repetitive stimulation of muscle fibres
  • Spasm/laryngeal spasm
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76
Q

Effect of curariform drugs on the neuromuscular junction

A
  • ACh receptor blocked
  • No depolarisation → No contraction
  • Paresis
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77
Q

Effect of botulin toxin on the neuromuscular junction

A
  • Blocking of ACh release
  • Pareisis
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78
Q

Effect of myasthenia gravis (autoimmune disease) on the neuromuscular junction

A
  • ACh receptor blocked by antibodies
  • No ACh binding
  • Paresis
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79
Q

Depending on the task of the given muscle, there can be variations in…

A

Nerve:muscle fibre ratio

  • Occular muscles (1:1)
  • Skeletal muscles (1:100)
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80
Q

The fusimotor system

A
  • Intrafusal fibres
  • Modified muscle fibres → Stretch detection
  • Also located in tendons → Golgi tendon receptor organs
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81
Q

Static fibres

A

Sensitive to static changes of tension (Length)

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82
Q

Dynamic fibres

A

Sensitive to dynamic changes of tension (length & velocity)

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83
Q
A

Intrafusal fibres

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84
Q
A

Extrafusal fibres

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85
Q
A

Sensory fibres

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86
Q

Myotatic reflex

A
  • (Contraction of stretched muscle)
  • Efferentation returns to the same muscle where afferentation occurs
  • Monosynaptic
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87
Q

Give the responses of Myotactic reflex

A
  1. Increased stretching causes increased tension (Servo-mechanism)
  2. Fusimotor activation
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88
Q

Give the steps of the servo-mechanism

A
  1. Muscle stretching → Muscle spindles stimulated
  2. Sensory neuron activated
  3. Information processing at motor neurone
  4. Motor neurone activation
  5. Muscle contraction
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89
Q

Co-activation

A

CNS participation (+servo-mechanism) in fusimotor system activation

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90
Q

Describe Co-Activation mechanism

A
  • α- + γ- motorneurones stimulated by cerebral centre (Co-__acitivation__)
  • Intrafusal & extrafusal fibres contract with the same rate and strength
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91
Q

Describe Co-Activation in the case of sudden increased load

A
  • Extrafusal fibre tension is stronger than intrafusal
  • AP frequencies accelerate in Ia and II afferents
  • Locally adjust the tension of extrafusal fibres (fine tuning)
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92
Q

1

A

AP → Myolemma

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93
Q

2

A
  • AP reaches L-type Ca2+ channels in the T-tubuli
  • L-type channels open
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94
Q

3

A

Ryanoid-Ca2+ open

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95
Q

4

A

Ca2+ enters the IC from the SR

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96
Q

5

A
  • Ca2+ channels open on myolemma
  • Ca2+ influx from the EC
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97
Q

6

A
  • IC Ca2+ high in and around the sarcomere
  • Contraction
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98
Q

Contraction and relaxation of muscle require…

A

ATP

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99
Q
A

The triad

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100
Q

Cardiac equivalent to the triad

101
Q

Triad

A
  • Basis of excitation-contraction coupling
  • Where t-tubule is closest to the SR IC
102
Q

What occurs at the triad?

A
  • AP → Change in L-type Ca2+ receptors
  • T-type ryanodin Ca2+ channels open
  • High amount of Ca2+ released from SR to IC space
  • Positive feedback:
    • Ca2+ opens SR Ca2+ channels
  • Increase in [Ca2+] → Cross-bridge cycle triggered
  • Calcium signal stimulates its own inactivation
103
Q
A

Potential dependent DHP proteins

104
Q
A

T-type (Ryanodin) calcium channel

105
Q

Briefly describe the figure

A
  • Receptors in the T-tubule changing from their closed state to their opened state
  • Influx of Ca2+ ions into the triad
106
Q

What is the main component of the actin-complex?

107
Q

Give the function of tropomyosin

A

Used in stimulation of ATPase activity of myosin

108
Q

What is shown?

A

F-actin α-helix

109
Q
A

G-actin subunit

110
Q
A

Myosin binding site

111
Q
A

Tropomyosin (Inactive)

  • Blocks 7 binding sites
112
Q
A

Tropomyosin (Active)

  • Slides into the groove of α-helix, leaving binding sites free
113
Q

What is shown?

A

Troponin-complex

114
Q
A

Troponin-C

115
Q
A

Troponin-T

116
Q
A

Troponin-I

117
Q

Describe activation of tropomyosin

A
  • Ca2+ binding → Removes tropomyosin to grove (Active)
  • Tn-complex binds to the tropomyosin attached to actin
  • Tropomyosin-troponin complex kept on the helix surface (inactive)
118
Q

Describe the structure of myosin

A

1 bundle = 6 myosin molecules

  • 2 heavy chains (HC)
  • 2 light chains (LC)
  • Globular part (head/cross bridge)
119
Q

Angle of myosin head with alpha helices

120
Q

Maximum bend angle of myosin heads

121
Q

Give the three types of ATPases

How do they differ in function?

A
  • LC-1
  • LC-2
  • LC-3

Difference determines the speed of ATPase activity

122
Q

LC-2 ATPases are found in…

A

Fast twitch muscle

123
Q

LC-3 ATPases are found in…

A

Slow-twitch muscle

124
Q
A
  • Tail / Heavy chain
  • Formed by α-helix
125
Q
A

Head Cross-bridge

126
Q
A

Actin binding site

127
Q
A

ATP binding site

128
Q

Myosin filament composition

A

200 miosin units

129
Q

Calcium transient

A
  1. IC [Ca2+] increased x1000
  2. Calcium (re)pumping mechanisms
  3. Calcium elimination from cytoplasm
  4. Ca2+ levels decrease near the sarcomere
130
Q

Give the steps of the Cross-bridge cycle

A
  1. Relaxation/Resting
  2. Ca2+ release from AP
  3. Tropomyosin removed → myosin binding sites exposed
  4. Cross bridge binds to actin
  5. Contraction (head tilts, ADP released)
  6. Ca2+ removed from outside → Myosin detaches
131
Q

ATP in the cross bridge cycle

A
  • Myosin head binds to ATP
  • Energy deliberated → ADP + P
  • Head tilts back to 90° (Cocked head)
132
Q
A
  • Myosin head detached
  • ATP hydrolysed
133
Q
A

ADP + P bound to myosin as myosin head attaches to actin

134
Q
A
  • ADP + P release
  • Head changes position
  • Actin filament moves
135
Q
A
  • ATP binding to head
  • Head returns to resting position
136
Q

When ATP isn’t present in the muscle

A
  • Myosin cannot dissociate from actin
  • Muscle becomes contracted and inactive

Rigor mortis → Autolysis follows after

137
Q

When Ca2+ isn’t present in the muscle

A
  • Tropomyosin slides over myosin
  • Activating part of the actin
  • Muscle relaxes
  • Myosin heads can’t bind
138
Q

The ratchet mechanism

A

Myosin filament cannot fall back

  • Myosin heads need to work asynchronously to contract
139
Q

How is calcium removed from the cytosol

A

All are ATP dependent:

  • Na+/Ca2+ ion antiporter
    • Secondary active transport
  • Ca2+ repumping into the SR
  • Other
    • Cell organelles
    • Mitochondria
140
Q

Composition of muscle tissue

A
  • 75% water
  • 20% protein
141
Q

Describe the importance of the macroscopic structure of muscles

A
  • Most sarcomere orientations aren’t parallel to the direction of macroscopic contraction
  • Skeletal muscle is wasteful but provides extreme spatial flexibility
142
Q

Which metabolism is expressed in red/slow twitch muscle?

143
Q

Which metabolism is expressed in white muscle?

144
Q

Which metabolism is expressed in pink muscle?

145
Q

Fast twitch muscle types

A

Pink and White

146
Q

Atrophy

A
  • Decrease in skeletal muscle size
  • Myonuclear loss
  • Decreased myofibrillar proteins
  • Decreased CSA
147
Q

Muscle Hypertrophy

A
  • Increase in skeletal muscle size
  • Myonuclear addition
  • Increased myofibrillar proteins
  • Increased CSA
    *
148
Q

The fibre spectrum of an individual is determined by…

A
  • Genetic factors
  • Usage of specified muscle
149
Q

Which two factors contribute to hypertrophy

A
  • Sarcoplasmic hypertrophy - Increased glycogen storage
  • Myofibrillar hypertrophy - Increased myofibril size
150
Q

Remodelling of ‘slow’ muscles

A

Mass of fibres increase slower than nutrient/energy storage of myocytes

151
Q

Myocyte ATP concentration

152
Q

List the energy sources of muscle contraction

A
  • Creatin-phosphate
  • Anaerobic glycolysis
  • Oxidative phosphorylation
153
Q

Creatin phosphate

A

ADP + CrP → ATP + Cr

154
Q

Creatin phosphate conc. in myocytes

155
Q

Anaerobic Glycolysis as muscle energy source

A

In cases of outstanding load

  • Glycogen
  • Glucose

4 ATP produced

  • If more ATP is used than produced → Oxygen debt
  • Produced lactic acid inhibits contraction
156
Q

Oxidative phosphorylation as a muscle energy source

A

Pyruvate → Acetyl-Coenzyme A

36 ATP produced

Process and contraction are slow

No oxygen debt

157
Q
A

Working in an oxygen-free environment

158
Q
A

Oxygen debt

159
Q

Muscle can replenish glycogen and creatine phosphate by…

A

Oxygen consumption

160
Q

Give the types of muscle contraction

A
  • Isotonic
  • Isometric
  • Mixed
    • Auxotonic
    • Preload
    • Afterload
161
Q

Isotonic contraction

A

Contraction with constant tension

162
Q

Isometric contraction

A

Contraction when only tension is changed, no length changes

e.g lifting an unliftable load

163
Q

Auxotonic contraction

A

Working against increasing tension and resistance

e.g against a spring

164
Q

Preload contraction

A
  • Muscle length is adjusted until equilibrium
  • Isotonic contraction follows

e.g locomotion related muscle work

165
Q

Afterload contraction

A
  • Isotonic contraction until the contraction is blocked
  • Isometric contraction follows

e.g. m. masseter

166
Q

The sum of observable and biological latency

A

Virtual latency

167
Q

Which muscle elements reach equilibrium with the load first, why?

A

SEC elements, dues to the contraction of the contractile components

(only tension is increased at this stage)

168
Q

Summation of muscle contraction

A

Addition of muscle contraction forms

  • Increase the contractile capacity of individual fibres
  • Recruits more fibres
169
Q

Give the types of Summation

A
  • All or none law
  • AP Frequency
  • Quantal summation
  • Contraction summation
  • (Staircase effect)
  • Tetanus
170
Q

All or none law

A
  • Applies for a single fibre
  • Adequate stimulus causes maximal contraction
  • Stimulus strength can’t influence amplitude of contraction
171
Q

AP frequency summation

A
  • Increased frequency
  • Prolonged Ca2+ release
  • Stronger contraction
172
Q

Quantal summation

A
  • Increased AP frequency
  • More fibres contract
173
Q

Contraction summation

A
  • Additional Ca2+ release before the end of Ca2+ transient
  • Increased amplitude of contraction
174
Q

Staircase effect summation

A
  • Warmup phenomenon - not graded contraction
  • If new stimuli arrive after the end of the first twitch
  • Increased efficiency of ion channels
  • Ca2+ accumulation
  • Increased amplitude of contraction
175
Q

Tetanus summation

A
  • Stimuli applied with increasing frequency
  • Muscle eventually reaches max contraction state (tetanus0
176
Q

How is the length-tension curve obtained?

A
  • Stimulation of a muscle which is passively stretched with varying loads
  • Isometric, isotonic, preload and afterload experiments carried out
177
Q

What does the length and tension diagram show?

A

The area where muscles execute normal work

178
Q

Maximal tension value

A

3kg/cm2 muscle cross section

179
Q
A

Tension (g) generated upon stimulation

180
Q
A

Sarcomere length (µm) before stimulation

181
Q
A

Overly contracted

182
Q
A

Optimum resting length

183
Q
A

Overly stretched

184
Q

Length x Tension =

185
Q

Describe obtaining length-tension diagram in isotonic conditions

A
  • Muscle stretched to A, B, C distances (Above L0)
  • Muscle is stimulated with max single stimuli
  • The isotonic maximum (It) curve can be obtained
186
Q

Describe obtaining length-tension diagram in isometric conditions

A
  • Shortening isn’t possible
  • Only changes of tension can be measured
  • Isometric maximum (Im) curve achieved
187
Q

Describe obtaining length-tension diagram in the preload experiment

A
  • Tension increase is followed by contraction
  • Preload maximum (Pm) curve achieved
188
Q

Length-tension diagram in the afterload conditions

A

Afterload-maximum (Am) curve achieved

189
Q

How is working range achieved from the 4 length-tension experiments?

A

Area is constructed on a graph

190
Q

Compare ‘normal working range’ and ‘length measured under max power’ in skeletal muscle

A

Both are identical to eachother

191
Q

Compare ‘normal working range’ and ‘length measured under max power’ in cardiac muscle

A
  • The normal working range is much below the length
  • Ensuring maximal tension
192
Q

Velocity x Tension =

193
Q

As tension is…velocity becomes…during muscle work

194
Q

Unloaded muscle contracts with…velocity

195
Q

Overloaded muscle contracts with…velocity

196
Q

Velocity related to an actual tension is determined by…

A

The type of muscle

  • Phasic (Fast)
  • Tonic (Slow)
197
Q

Using the velocity-tension diagram rather than the length-tension diagram gives a better indication of…

A

The power of the muscle

198
Q

Intermediate tension and intermediate velocity result in…

A

Maximal power

199
Q

Describe the figure

A

Grey rectangles:

  • Small tension = High velocity
  • High tension = Small velocity

Red rectangle:

  • The optimal position where maximum power can be achieved
200
Q

Max speed of muscle contraction

201
Q

Total force of skeletal muscle

A

200N

relative to 100kg mass

202
Q

Efficiency of skeletal muscle

203
Q

Power maximum of skeletal muscle

A
  • Short term: 3-5000 W
  • Long term: 1200 W
204
Q

How do muscles produce heat?

A
  • Contraction: ATP breakdown
  • After contraction: Synthetic processes create heat
205
Q

When do phasic/fast/white fibres produce heat most?

A

During restoration/recovery

206
Q

When do tonic/slow/red fibres produce heat most?

207
Q

Give the phases of heat production

A
  • In resting (Muscle maintenance/BMR)
  • Initial heat production
    • Activation heat
      • Ca2+ release
      • Myosin-activation
    • Contraction heat
      • Sliding filament
      • Ca2+ repumping
  • Restitution heat
208
Q

Muscle fatigue is dependent on…

A

Ratio of phasic and tonic fibres

209
Q

Signs of fatigue on a mechanogram

210
Q

In Vitro fatigue

A
  • Lack of O2
  • Lack of Transmitter
211
Q

In Vivo fatigue

A
  • Peripheral
    • Decreased energy sources
    • Lactic acid
  • Central fatigue
    • Exhaustion of motor-unit
    • Exhaustion of myoneural junction
212
Q

Subjective feelings of fatigue can be caused by…

A
  • Increased heat production
  • Decreased pH
  • Lactic acid
  • Dehydration
  • Hypoglycaemia
213
Q

Fatigue develops earlier in…

A

Phasic fibres

214
Q

Smooth muscle

A

Used in maintenance and form of visceral organs

  • Single-unit smooth muscles
  • Multi-unit smooth muscles
215
Q

Multi-unit smooth muscle

A
  • Individual fibres not connected with gap junctions
  • Fibres under direct neural control (not by AP)
  • Capable of fast and accurate movements
  • Transmitters cause local depolarisation

Located in the eye

216
Q

Single unit smooth muscle

A
  • Many hundreds of fibres
  • Form a functional syncytium
  • Fibres are innervated by varicosities

e.g muscle of vessels

217
Q

What causes contraction of smooth muscle

A
  • Dense bodies and intermediate filaments
  • Networked through the sarcoplasm
218
Q

Proportion of myosin:actin in smooth muscle

219
Q

Give the steps of contraction in smooth muscle

A
  • If IC Ca2+ is high, MLCK enzyme is used
  • Actomyosin complex formation
  • Contraction stays continuous until MP enzyme triggers relaxation

Most muscles are in weak but continuous contraction

220
Q

Summarise the structure of smooth muscle

A
  • No transverse tubular system
  • Poor blood supply
  • Non-striated
  • Small SR
221
Q

What is shown?

A

Smooth muscle sarcomere

222
Q
A

Calmodulin

223
Q
224
Q

Describe the role of caldesmon in smooth muscle contraction

A
  • Ca2+ binds to the Calmodulin-Ca2+ complex
  • Removes tropomyosin from binding sites
225
Q

Describe smooth muscle myosin

A

Heads contain a unique MLC subunit:

P-LCh

  • Phosphorylated = Actin binding → Contraction
  • Non-phosphorylated = No actin binding
226
Q

In smooth muscle:

If there is no Ca2+

A

MLCK is inactive → P-LCh is not phosphorylated

227
Q

Elimination of Ca2+ activates…

A

Myosin phosphatase (MP)

228
Q

Activation of MP

A

Dephosphorylation of P-LCh → Relaxation

229
Q

Characteristics of smooth muscle contraction

A
  • Prolonged tonic contraction (hours/days)
  • Energetically economic - low energy use
  • Length of contraction 30x longer than skeletal
230
Q

Max contraction length of smooth muscle

A

66% of resting length

231
Q

Varicosities

A
  • Series of axon-like swellings
  • From autonomic neurons
  • Form motor units in the smooth muscle
232
Q

Example of multi-unit smooth muscle

A

m. ciliaris

233
Q

Example of single unit smooth muscles

A

Gastrointestinal muscles

234
Q

What is shown?

A

Special structure of smooth muscle SR

235
Q

Sources of Ca2+ in the smooth muscle

A
  • Minor: SR
  • Major: EC-Space
236
Q

Which channels can be found in the smooth muscle myolemma?

A
  • Voltage-gated Ca2+ channels
  • Ligand-gated Ca2+ channels
237
Q

Describe AP in smooth muscle

A
  • Single-unit only
  • RMP = -50mV
  • Forms of AP:
    • Typical peak potential
    • AP with ‘plato’
238
Q

Importance of extremely prolonged repolarisation of smooth muscle

A

Prolonged contraction:

  • Myocardium
  • Uterus
239
Q

Factors causing contraction of smooth muscle

A
  • AP
  • Binding of chemical ligands
  • IC IP3 release
  • G-Protein or phospholipase C (PLC) mediated Ca2+ influx
240
Q

What stimulates relaxation of smooth muscle?

A

All stimuli which can increase IC cAMP or cGMP levels

  • Sympathetic beta2 receptor agonists
241
Q

Chemical factors influencing smooth muscle contraction

A
  • Lack of O2
  • Excess of CO2
  • Increased H+
  • Increased K+
242
Q

Bayliss effect

A

Extension of smooth muscles results in contraction

Not related to neural or hormonal influences

243
Q

What is the mechanism of the Bayliss effect?

A
  • Stretching opens the mechano-sensitive cation-channels
  • Depolarisation
244
Q

Where would the spontaneous generation of smooth muscle AP be observed?

A

In the gut

245
Q

Spontaneous generation of smooth muscle AP is associated with…

A

The ‘slow wave’ rhythm

246
Q
A

AP (Spike potential)

247
Q
A

Slow wave potential

  • Not AP
  • Local potential
  • If above -35mV, AP is initiated
248
Q

Each slow wave initiates…

A

More than one AP

(Also called pacemaker waves)

Physiology (18 decks)

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