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Physiology 201 > Unit 3 Lecture > Flashcards

Unit 3 Lecture Flashcards

1
Q

What are the three types of muscle?

A
  • Skeletal muscle
  • Cardiac muscle
  • Smooth muscle
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2
Q

What is the basic function of all muscles?

A

Generate tension

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3
Q

What are the four functions of skeletal muscles?

A
  • Locomotion
  • Facial expression
  • Posture and body position
  • Regulation of body temperature
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4
Q

Is skeletal muscle contraction voluntary?

A

Yes; can be automatic but we have the ability to change skeletal muscle activity

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5
Q

What does skeletal muscle contraction always require?

A

Always requires nervous system input

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6
Q

What is an example of a muscle that can be automatic or voluntary action?

A

Contraction of the diaphragm is usually automatic, but you can take a deep breath or hold your breath whenever you choose

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7
Q

Define origin

A

Where the muscle starts on a bone (stays stationary)

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8
Q

Define insertion

A

Where the muscle ends on a bone (moves towards origin)

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9
Q

How do the origin and insertion work together?

A

The insertion moves towards the origin

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10
Q

How do you name a movement?

A

Include the action and the name of the segment that moves:

  • Flexion of the forearm
  • Adduction of the thigh
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11
Q

Define flexion

A

This is the movement to reduce the angle between articulating bones at a joint

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12
Q

Define extension

A

This is the movement to increase the angle between articulating bones at a joint

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13
Q

What is common about both flexion and extension movements?

A

Motions typically in a sagittal plane (anterior/posterior)

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14
Q

Define abduction

A

Movement away from the longitudinal axis (midline)

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15
Q

Define adduction

A

Movement toward the longitudinal axis (midline)…you ADD something back to your midline

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16
Q

Define Reverse Muscle Action (RMA)

A

When the insertion is anchored, the origin moves toward insertion

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17
Q

Classify a Muscle based on action:

  • Action: Leg extension (increasing the angle at the knee)
  • Origin: femur
  • Insertion: tibial tuberosity
A

Muscle group: quadriceps

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18
Q

Define agonist

A

Muscle primarily responsible for movement

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19
Q

Define antagonist

A

Muscle which opposes the action of the agonist

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20
Q

Define synergist

A

Assists the agonist in making the action more efficient

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21
Q

Define fixator

A

Special synergists which help to prevent movement at muscle origin

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22
Q

Example of classification of muscle by action:

Flexion of forearm

A
  • Agonist: brachialis
  • Antagonist: triceps brachii
  • Synergist: biceps brachii
  • Fixator: pectoralis minor
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23
Q

Example of classification of muscle by action:

Abduction of the arm

A
  • Agonist: deltoid
  • Antagonist: latissimus dorsi
  • Synergist: supraspinatus
  • Fixator: trapezius
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24
Q

What is a first class lever (EFL)?

A

Balanced level system like the human skull on the neck

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25
Q

What does E, F, and L stand for in class levers?

A

E= Effort

F= Fulcrum

L= Load

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26
Q

What is a second class lever (FLE)?

A

Sacrifices speed and range of motion for force

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27
Q

What is a third class lever (FEL)?

A

Favors speed and range of motion over force

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28
Q

What are groups of muscles covered by?

A

Deep Fascia

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29
Q

What are each individual (not a group of) muscles covered by?

A

Epimysium

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30
Q

What are fascicles in muscles covered by?

A

Perimysium

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31
Q

What are individual muscle fibers (cells) in fascicles covered by?

A

Endomysium

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32
Q

What are the four structural levels of skeletal muscle?

A
  1. Organ level: muscle
  2. Tissue level: Fascicles
  3. Cellular level: muscle fibers (cells)
  4. Chemical (subcellular) level: myofibrils
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33
Q

Two facts about muscle fibers

A
  1. Muscle cells are called fibers
  2. Muscle fibers are typically ‘multinucleate’ due to the fact that they develop from the fusion of myoblasts
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34
Q

Define hypertrophy

A

Growth of muscle due to an increase in muscle cell size (think body building)

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35
Q

Define hyperplasia

A

Growth of muscle due to an increase in muscle cell number (think little kids)

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36
Q

How do muscle fibers grow after birth?

A

After birth, growth of muscle fibers happen by hypertrophy, muscle fibers cannot undergo mitosis

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37
Q

How can satellite myoblasts grow after birth?

A

Satellite cells have the ability to undergo mitosis after birth to aid in muscle regeneration

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38
Q

What are the three C’s of skeletal muscle physiology

A
  1. Conduction of electrical signals
  2. Control of muscle contraction
  3. Contraction of muscle
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39
Q

Discuss the conduction of electrical signals

A
  • It is the result of excitation of a muscle fiber
  • Occurs along the sarcolemma (the plasma membrane of skeletal muscle fibers)
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40
Q

Discuss the control of muscle contraction

A
  • Is accomplished by regulation of the activities of the smooth ER of skeletal muscle fibers (in muscle fibers, the smooth ER is called the ‘sarcoplasmic reticulum’ or ‘SR’):
  1. Ca2+ release (by E-C COUPLING) from the SR starts contraction
  2. Ca2+ recovery later by the SR stops contraction
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41
Q

Discuss contraction of muscle

A
  • Is carried out by the CROSS BRIDGE CYCLE
  • Results from the shortening of organelles called myofibrils in the cytoplasm of skeletal muscle fibers
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42
Q

Define excitation

A

The events that transmit an electrical signal from a motor neuron to a muscle fiber

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43
Q

What does the arrival of the motor neuron AP result in in excitation?

A

Results in the generation of an AP in the skeletal muscle fiber membrane (sarcolemma)

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44
Q

Define excitation-contraction (EC) coupling

A

The events that connect excitation to contraction

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45
Q

What does skeletal muscle AP trigger?

A

Triggers release of Ca2+ from the sarcoplasmic reticulum (SR) into the sarcoplasm of the skeletal muscle fiber

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46
Q

Define contraction in the terms of physiological events of skeletal muscle fiber contraction

A

The events that cause the sarcomeres of the muscle fiber to shorten

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47
Q

When enables the contraction cycle to begin?

A

Ca2+ binds to torponin

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48
Q

Define relaxation

A

The events that cause the sarcomeres of the muscle fiber to return to resting length

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49
Q

What triggers the end of the contraction cycle

A

Removal of Ca2+ from the sarcoplasm

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50
Q

Since the activation of skeletal muscle is voluntary, what is required?

A

Requires an action potential to be sent from the central nervous system (CNS)

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51
Q

What does the arrival of the motor neuron AP at the neuromuscular junction always result in?

A

Always results in the generation of an AP in the skeletal muscle fiber’s sarcolemma. This is called neuromusclar transmission

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52
Q

Difference between the endomysium and sarcolemma

A

Endomysium is the external covering of the muscle fibers and the sarcolemma is the internal membrane covering of the muscle fiber

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53
Q

What does the neuromuscular junction look like and what is its function?

A

It governs the muscle fiber to contract and without it the muscle fiber dies

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54
Q

What do somatic motor neurons synapse with?

A

Skeletal muscle

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55
Q

What is a critically important fact about neuromuscular junction?

A

There is only one connection (one NMJ) between any skeletal muscle and the alpha-motor neuron that triggers its contractions

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56
Q

What is an alpha (a)-motor neuron also called?

A

Axon collateral of somatic motor neuron

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57
Q

Where does neuron send the nerve impulse?

A

Down each axon branch to the end of all the axon terminals where the NMJs are

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58
Q

What is the first event in neuromuscular transmission?

A

Action potential arrives at the synaptic end bulb of motor neuron and causes opening of voltage gated Ca2+ channels

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59
Q

What is the second event in neuromuscular transmission?

A

Synaptic vesicles containing the neurotransmitter acetylcholine (ACh) undergo exocytosis

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60
Q

What is the third event in neuromuscular transmission?

A

ACh is released into the synaptic cleft and rapidly diffuses across to bind to ACh receptors on the sarcolemma (motor end plate).

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61
Q

What is the fourth event in neuromuscular transmission?

A

ACh receptors open and allow Na+ to enter into the muscle sarcoplasm, generating an action potential along the sarcolemma

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62
Q

What is the fifth event in neuromuscular transmission?

A

ACh is quickly broken down to acetate and choline by Acetylcholine Esterase (AChE) for recycling. (ACh also diffuses away)

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63
Q

Summarize the Neuromuscular Transmission (Excitation)

A
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64
Q

What is step 1 in EC Coupling?

A

Skeletal muscle sarcoleema forms tunnels (T-tubules) which travel into the cell.

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65
Q

What do T-tubules do in EC Coupling?

A

T-tubules travel between ‘terminal cisternae’ of the SR

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66
Q

What is the second step of EC Coupling

A

AP runs along the sarcolemma and T-tubules

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67
Q

What is step 3 of EC Coupling?

A

AP Triggers release of Ca2+ from SR. Ca2+ diffuses into sarcoplasm and myofibrils

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68
Q

What is the fourth step of EC Coupling?

A

Ca2+ binds to troponin, which changes shape and pushes tropomyosin over on thin filament to reveal myosin binding sites

69
Q

What happens at the end of the EC Coupling?

A

Contraction cycle starts and SR Ca2+ recovery starts

70
Q

Summarize Exitation-Contraction coupling

A

1) AP Runs along sarcolemma, continues into T-tubules
2) Triggers release of Ca2+ from SR
3) Ca2+ diffuses into sarcoplasm and myofibrils
4) Ca2+ binds to troponin on thin filament
- Myosin binding sites on actin are exposed
5) Crossbriges form -> tension is generated

(Starts contraction cycle)

71
Q

What is the first step of relaxation

A

When APs stop arriving at the NMJ, the repeating ‘trigegrs’ to release Ca2+ from the SR stop

72
Q

What is the second step of relaxation

A

Active Ca2+ transporters in the SR membrane pump Ca+ back into the SR

73
Q

What is the third step of relaxation?

A

Cytoplasmic Ca2+ decrease

74
Q

What is the fourth step of relaxation?

A

As Ca2+ falls, Ca2+ comes off troponin - the myosin binding sites on actin are re-covered by tropomyosin.

75
Q

What is the fifth step of relaxation

A

Crossbridge cycling stops and tension drops

76
Q

What is the final step of relaxation?

A

Titin brings the sarcomere back to resting position

77
Q

What is the main anatomical part of the muscle fiber that is involved in conduction?

A

‘Sarcolemma’ (plasma membrane)

  • Surrounds ‘sarcoplasm’ (cytoplasm)
  • Forms ‘transvers tubules’ (T-tubules) that tunnel through the muscle fiber
78
Q

What is the main anatomical structure involved in control (second C in muscle physiology) and what are its functions?

A

‘Sarcoplasmic Reticulum’ (Smooth ER) - stores Ca2+

  • Close proximity to T-tubules
  • Surrounds myofibrils
79
Q

What are some primary functions of skeletal muscle?

A
  • Does what we tell it to
    • Eat when we tell it to
    • Contract when we tell it to
    • Relax when we tell it to
80
Q

What is the purpose of an action potential?

A

To open a calcium channel where acetoholine is then released

81
Q

What causes an action potential to start?

A

Sodium ions rush into the structure

82
Q

What is the immediate source of energy to support development of tension?

83
Q

What does hydrolysis by myosin head group fuel?

A

Fuels tension generation using ATP

84
Q

What does hydrolysis by the Ca2+ pump of the SR support?

A

Supports relaxation using ATP

85
Q

What two processes make up energy metabolism in the cell?

A

Anaerobic (glycolysis) and aerobic (glycolysis and oxidative phosphorylation)

86
Q

Does aerobic or anaerobic metabolism make more energy?

A

Aerobic metabolism

87
Q

Where are the 4 places ATP come from?

A
  1. Cell ‘pool’ of ATP
  2. Creatine phosphate (CP) ‘pool’
  3. Anaerobic Glycolysis (glucose breakdown)
  4. Aerobic metabolism
    1. Glucose (from glycogen)
    2. Fatty Acids (from lipids)
    3. Amino Acids (from proteins
88
Q

Is ATP ‘stored’?

A

No, ATP is not stored. There is only enough to support a person for 2 seconds of maximal forc at a time in the cell ‘pool’ of ATP

89
Q

What does Creatine phosphate do?

A

Creatine phosphate stores ‘high energy phosphate. Thid pool had enough phosphate to support 15 seconds of maximal contractions

90
Q

What is the reaction of CP and ATP after a meal vs during exercise

A

After a meal

: ATP + C -> ADP + CP

During and excersciencee

: ADP + CP -> ATP + C

91
Q

What is creatine?

A

A small amino acid-like molecule that is synthesized in the liver kidney snd psncrease and transported to muscle fibers

92
Q

What happens in a relaxed muscle fiber?

A

Creatine phosphate is 3-6 times more plentiful in ATP

93
Q

Discuss glycogen

A
  • Occurs in the cytoplasm
  • Occurs rapidly
  • Cans support for roughly 2 min of contraction
  • Used anaerobically - glycolysis
94
Q

Discuss aerobic metabolism

A
  • Occurs in glycogen, fat, and protein
  • Can support 40 min to several hours of contraction (intensity dependent)
95
Q

Discuss resting, moderate, and peak activity and aerobic production of ATP

A
  1. Resting - aerobic production of ATP
    1. Supports activity and buildup of CP pool
  2. Moderate - aerobic production of ATP increases
    1. Supports activity, but no CP buildup
  3. Peak - aerobic production of ATP maximal; as O2 becomes limiting, anaerobic metabolism fills need
    1. CP depleted - lactic acid builds up (increase of H+)
96
Q

What are three sources of fatigue?

A

Psychological -> Nervous system -> Muscle

97
Q

What is the major cause of fatigue?

A

Failure of EC coupling because of increase in [Pi]cell

  • Due to breakdown of creatine phosphate
  • Inhibits Ca2+ release from SR
98
Q

What are other factors that increase fatigue?

A

Includes insufficient oxygen, depletion of glycogen, ADP and lactate build up

99
Q

What is the Cori Cycle?

A

The contribution of lactic acid from the muscles to the liver that converts to glucose in the liver that fules the muscles.

  • Aerobic cellular respiration in the heart, kidneys, and skeletal muscle also contributes to the elimination of lactate
100
Q

What is the cost of resetting the system after exercise?

A

O2 debt aka. excess post-exercise oxygen consumption

Two things that happen:

  1. Metabolizing lactic acid
  2. Repair of tissue
101
Q

What are some reasons for elevated O2 consumption after exercise?

A
  1. Lactic acid conversion back to glycogen in the liver (cori cycle)
  2. Resynthesize creatine phosphate
  3. Replace oxygen remobed from myoglobin
  4. Repair
  5. Other reasons…
102
Q

Define muscle twitch

A

Contraction arising from a single electrical stimulus. Ex. an action potential

103
Q

What are the three periods of a muscle twitch?

A
  1. Latent
  2. Contraction
  3. Relaxation
104
Q

What happens during the latent period and how long does it last?

A
  • 2 msec or less
  • Action potential sweeps over the sarcolemma
  • Ca2+ is released from the sarcoplasmic reticulum
  • No change in tension
105
Q

What happens during the contraction period and how long does it take?

A
  • 10-100 msec
  • Ca2+ binds to troponin
  • Myosin-bindinh sites on actin are exposed
  • Crossbridge cycle begins and continues
  • Peak tension develops
106
Q

What happens during the relaxation period and how long is it?

A
  • 10-100 msec
  • Ca2+ transported back into sarcoplasmic reticulum
  • Myosin-binding sites on actin are covered by tropomyosin
  • Crossbridge cycle ends (Myosin can no longer to sites on actin)
  • Tension decrease
107
Q

Observe tension vs time chart for different anatomical parts

108
Q

Define tetanus

A
  • ‘Summation over time (Temporal summation) of individual twitches
  • Tetanus (temporal summation) is a mechanism for increasing tension
  • Each hump in the charts show that more and mpre Ca2+
109
Q

Define motor unit

A

A motor neuron and all the muscle fibers (cells) it innervates

110
Q

How can summation be spatial?

A

By activating (aka recruitinhg) increasing numbers of motor units, tension can be increased…. “spatial summation”

111
Q

Discuss motor units and the ‘Size Principle’

A
  • The first motor units recruited are small (innervate few fibers)
    • The result is fine, carefully controlled increase in tension
  • As more force is required, larger motor units are recruited
112
Q

Analyze the size principle graph for standing to jumping

113
Q

Define isometric contractions

A

‘Same length’

  • Muscle generates tension but does not shorten
  • every contraction begins isometrically…
114
Q

Define isotonic contraction

A
  • ‘same tension’
  • after sufficient tension is generated to move the ‘load’ the muscle shortens
  • Two types: 1) concentric; 2) eccentric
115
Q

Define concentric contraction

A

When developed tension is sufficient to move the load, the muscle shortens

Effort > Load

116
Q

Define eccentric contraction

A

As tension decreases and the load exceeds tension, the muscle lengthens

Load > effort

117
Q

What are three strategies to increase force?

A
  1. Increase motor unit recruitment = spatial summation
  2. Increase frequency of stimulation = temporal summation
  3. Optimal muscle length as start of contraction
    1. Peak tension is developed at an intermediate muscle (or sarcomere) length. This is due to the length-tension relationship
118
Q

Look at the length-tension relationship

119
Q

Isometric vs isotonic concentration

120
Q

Discuss conduction

A
  • Is the result of excitation of a muscle fiber
  • Sarcolemma (plasma membrane)
    • Surrounds ‘sarcoplasm’ (cytoplasm)
    • Forms ‘transverse tubules’ (‘T-tubules’) that tunnel through the muscle fiber
121
Q

Discuss control of skeletal muscle physiology

A
  • by Ca2+ (released by EC Coupling and later recovered)
  • Sarcoplsmic reticulum
    • Close proximity to T-tubules
    • Surrounds myofibirils
      *
122
Q

Look at the relationship between SR and myofibrils

123
Q

Discuss contraction

A
  • Thanks to the cross bridge cycle
  • Myofibrils
    • Longitudinal bundles of protein filaments (primarily made of the proteins actin and myosin) inside muscle fibers
    • Each myofibril has repeating units called ‘sarcomeres’
124
Q

What is the cause of the striated appearance?

A

The banding (striated) appearance of a muscle fiber is due to the alignment of all sarcomeres in all myofibrils inside the sarcoplasm

125
Q

Three muscle proteins

A
  • Contractile proteins
    • Actin and myosin
  • Regulatory proteins
    • Troponin and tropomyosin
  • Structural proteins
    • Titin, dystrophin, a-actinin, myomesin, nebulin
126
Q

Discuss Actin in contractile proteins

A
  1. Actin
    1. Found in thin filaments
    2. Has myosin binding sites for crossbridge formation with myosin
127
Q

Discuss myosin in contractile proteins

A
  1. Myosin
    1. Motor protein found in thick filaments
    2. Has myosin head that binds to the myosin binding site on actin and forms crossbridge during muscle contraction
128
Q

Discuss tropomyosin and troponin in regulatory proteins

A
  1. Tropomyosin
    1. Found in thin filaments
    2. Covers the myosin binding sites on actin when muscle is relaxed
  2. Troponin
    1. Found in thin filaments
    2. Holds tropomyosin in place when muscle is relaxed
    3. During contraction, calcium binds to troponin and causes a conformational change that shifts tropomyosin away from the myosin binding sites on actin -> exposes the binding sites to allow crossbridge formation
129
Q

Discuss titin in structural proteins

A
  • Spans half of each sarcomere from Z disc to M line
  • Stabilizes the position of the thick filament; gives muscle its elasticity and extensibility; and helps the sarcomere return to resting length after contraction
130
Q

What is strong evidence for exercise benefits?

A
  • Lower risk of early death
  • Lower risk of coronary heart disease,

stroke, high blood pressure, adverse

blood lipid profile

  • Lower risk of type 2 diabetes
  • Lower risk of metabolic syndrome
  • Lower risk of colon and breast cancer
  • Prevention of weight gain
  • Weight loss, particularly when

combined with reduced calorie intake

• Improved cardiorespiratory and

muscular fitness

  • Prevention of falls
  • Reduced depression and better

cognitive function (for older adults

131
Q

What is moderate to strong evidence for exercise benefits?

A
  • Better functional health (for older

adults)

• Reduced abdominal obesity

132
Q

What is moderate evidence for exercise benefits?

A
  • Lower risk of hip fracture
  • Increased bone density
  • Lower risk of lung and

endometrial cancer

• Weight maintenance after weight

loss

• Improved sleep quality

133
Q

What does exercise affect?

A
  • Natural pain relievers
134
Q

What are some CDC Physical activity recomendations for adults?

A

Aerobic activity

  • 150 min/week at moderate intensity
  • Split into >10 min block

Muscle strengthening activity

  • At least one set of 8-12 repetitions
  • 2 days/week at moderate to high intensity working major muscle groups

Balance activities for older adults

-3 or more days per week

135
Q

What is the basic principle of exercise and response of muscle:

A

Muscle will change in response to the stresses it encounters

136
Q

What two things does exercise require?

A
  1. Increase energy utilization (endurance training)
  2. Increased force production (strength training)
137
Q

Look at the exercise effects on muscles

A

Increased angiogenesis (development of new blood vessels)

138
Q

What are some effects of exercise on muscle?

A
  • Increased angiogenesis
  • Higher density of mitochondria
  • Increased cross sectional area
139
Q

What is muscle hypertrophy?

A

Each muscle fiber increases in diameter -> increased # of myofibrils

More sarcomeres in parallel = more cross bridges = more force

140
Q

What is the role of satellite cells in muscle hypertrophy?

141
Q

What factors activate the satellite cells?

A
  • Strength training causes micro tears in the myofilaments, z-lines and connective tissues
  • Damage attracts macrophages
    • Macrophages release cytokines and growth factors
    • Cytokines and growth factors stimulate proliferation and differentiation of satellite cells
142
Q

Who does Nicy waub?

143
Q

What are muscle changes in strength vs endurance training?

144
Q

Speed (velocity) X strength (force) =

A

= Power regarding muscle performance

145
Q

What is endurance?

A

Sustained activity: Type of metabolism (aerobic vs anaerobic)

146
Q

What are three different fiber (skeletal muscle) types?

A
  1. Slow fiber: slowly contracting; aerobic metabolism
  2. Fast fibers: rapidly contracting; anaerobic metabolism
  3. Intermediate fibers: relatively fast contracting; primarily anaerobic

***Within a motor unit, all fibers are the same type

147
Q

Discuss slow fibers

A

(called SO for slow oxidattive or type I)

  1. Low speed - slow myosin ATPase
  2. High resistance to fatigue - relies on aerobic metabolism
    1. High aerobic capacity
      1. Many mitochondria
        1. High myoglobin content
          1. Dense capillary supply (for O2 delivery)
148
Q

Discuss fast fibers

A

(Called FG for fast-glycolytic or type IIX)

  1. High speed - fast myosin ATPase
  2. Low resistance to fatigue - relies on anaerobic glycolysis
    1. Low aerobic capacity
      1. Few mitochondria
        1. Low myoglobin content
149
Q

What is myoglobin and what is it responsible for?

A
  • 152 amino acid protein containing a heme (iron containing) prosthetic group for O2 binding
  • Binds or releases on molecule of oxygen at a time
  • Responsible for muscle’s red color
  • Abundant in diving mammals
150
Q

Discuss intermediate fibers

A

(called FOG for fast-oxidative/glycolytic or Type IIA)

  1. Moderate speed - intermediate myosin ATPase
  2. Intermediate resistance to fatigue
    1. Primarily relies on glycolysis, but has much high aerobic capacity than FG fibers
151
Q

What are slow oxidative fiber characterists?

152
Q

What are fast oxidative glycolystic fiber characteristics?

153
Q

What are fast glycolytic fiber characteristics?

154
Q

What is a common muscle composition for humans?

A
  • Most muscles are mixtures of fast and slow motor units
    • In humans a 50:50 mix is common with much individual variability
  • The proportion of fast vs slow motor units is determined genetically
155
Q

What is muscle hypertrophy? what is hyperplasia?

A
  • Muscles become stronger when the muscle fibers in them add more myofibrils, a process called hypertrophy
  • To grow a muscle by adding cells (mitosis) is called hyperplasia. Skeletal muscle does not grow/strengthen through hyperplasia
156
Q

What is muscle atrophy?

A

With disuse, muscles become weaker as muscle fibers lose myofibrils, decreasing in diameter. This is called atrophy

157
Q

What type of muscle generates tension?

A

ALL MUSCLE (skeletal, cardia, and smooth)

158
Q

What are the two common themes that are underlying mechanisms that all three muscle types rely on?

A
  1. Sliding filaments (actin and myosin)
  2. Regulation of cytoplasmic [Ca2+]
    1. Needed for contractions
159
Q

What does the heart muscle do?

A

Pumps blood

160
Q

What type of muscle function involves contraction of muscle around a confined volume, increasing the pressure so the fluid can be pushed through the circulatory system

A

Cardiac muscle

161
Q

What are some cardia muscle structural features? (compared to skeletal muscle)

A
  • Smaller cells (branched)
  • Less extensive T-tubule and SR system
  • Myofibrils also organized into sarcomeres
  • Extensive cell-to-cell interactions called interecalated discs, and they contain
    • Sarcoplasm-sarcoplasm channels called gap junctions
    • Desmosomes
162
Q

What does the microscopic anatomy of cardiac muscle look like?

163
Q

What does a sarcomere on a myofibril in a microscopic cardiac muscle picture look like?

164
Q

What are some cardiac muscle functional issues? (similarities to skeletal muscle) regarding sliding filament and Ca2+ release

A
  • The sliding filament model still applies
    • Crossbride cycling occurs
    • Ca2+ interacts with regulatory proteins on the thin filament
  • Ca2+ release by the SR is NOT sufficient to support cardiac muscle concentration!
    • There is an obligatory need for extracellular Ca2+
    • Entry of extracellular Ca2+ is required on a beat-to-beat basis
165
Q

What are some cardia muscle functional issues (differences with skeletal muscles)?

A
  • Contraction is NOT initiated by an electrical signal from the nervous system
    • Cardiac cells show ‘authorhythmicity’
    • Electrical (and contractile) activity is stated by ‘pacemaker cells’ -> spontaneous generation of APs
  • There are no motor units, and every cardiac cell contracts with every heartbeat
    • The electrical signal (the cardiac muscle action potential) moves from cell-to-cell through gap junctions
  • Every contraction is a twitch (no cardiac tetanus)
  • Nervous inpit influences the rate and strength of contraction
    • Rate change is changed by acting on pacemaker cells
    • Strength is changed by altering Ca2+ delivert from the extracellular fluid into the sarcoplasn
  • The single twitch of cardia muscle have a very long time course (hundreds of milliseconds)
    • This reflects the characteristics of the ‘cardiac action potential’ which lasts 300 milliseconds (more than 30 times longer than a skeletal muscle action
166
Q

what does smooth muscle do?

A
  • Smooth muscle fibers control the diameter of ‘tissue tubes’ such as blood vessels, the intestines
    • There are many types of smooth muscle, and they have common structural features
      • One small, single nucleus
      • Lack of a clearly-organized structure
        • Smooth muscle fibers do NOT contrain sarcomeres
        • Smooth muscle fibers do NOT have an extensice T-tubule/SR system
167
Q

Even though smooth doesnt have sarcomeres…

A

There are think (myosin) and then (actin) filaments with a rudimentary overlapping organization

168
Q

What is the key to generation of tension in smooth muscle?

A
  • Regulation of cytoplasmic Ca2+
  • BUTTT that regulation is very different from that in skeletal and cardia muscle
  • Ca2+ does not interatc with regulatory proreins on the thin filament to permit myosin head groups to bind

Physiology 201 (15 decks)

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