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Biology 107 > ET: Muscles > Flashcards

ET: Muscles Flashcards

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1
Q

Skeletal Muscle Structure

A
  • Voluntary
  • Striated (sarcomeres main unit of contraction)
  • Single, long, cylindrical cells (up to 35cm)
  • Multiple peripheral nuclei
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2
Q

H-Zone

A

Only thick filaments

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3
Q

I-Band

A

Only think filaments

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4
Q

A-Band

A

All thick filaments over lapping think filaments

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5
Q

M-Line

A

Middle of the sarcomere, holds together thick filaments

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6
Q

Z-Disc

A

Plate of dense material passing through the I-Band anchoring thin filaments and connecting myofibrils to each other
- joins sarcomeres

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7
Q

T-Tublules

A
  • Present in Skeletal and Cardiac muscle
  • Circle the sarcomere at junction of A/I-Band in skeletal muscle and at Z-Line in Cardiac muscle
  • Not present in smooth muscle
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8
Q

Sarcoplasmic Reticulum

A
  • Site of Calcium Storage
  • Extensive in Skeletal muscle
  • Some in cardiac muscle
  • Minimal in Smooth muscle
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9
Q

Thick Filaments

A
  • Myosin
  • 2 subunits - each with a globular head and a tail (tails for a helix)
  • Heads have a binding site for actin
  • Titin anchors thick filaments to the Z-line
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10
Q

Thin Filaments

A
  • Mostly globular actin proteins with a myosin binding site
  • Double stranding helical actin chains
  • Troponin and tropomyosin are regulatory proteins associated with actin in skeletal and cardiac muscle
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11
Q

Sliding Filament Theory

A
  • Sarcomere shortens as thin filaments are pulled over thick filaments
  • Z-Line is pulled toward the M-Line
  • I-Band and H-Zone become narrower
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12
Q

Cross Bridge Cycle

A
  1. Cross bridge formation
    - Myosin head binds to binding site on actin forming a cross bridge (when Ca2+ has bound to troponin and tropomyosin has moved off the myosin binding sites on action)
  2. The power stroke
    - ADP is released
    - Myosin head rotates to low energy state (45 degrees to actin) pulling thin filaments
    - Shortening of sarcomere
  3. Detachment
    - New ATP binds to myosin and myosin detaches from actin
  4. Energisation of the myosin head
    - Myosin hydrolysis the ATP to ADP and P and releases the Phosphate
    - Myosin head moves to high energy conformation (90 degrees to actin)
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13
Q

Calcium Role In Skeletal Muscle

A
  • Ca2+ binds to troponin which elicits a shape change in tropomyosin exposing the myosin binding sites on actin
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14
Q

Isotonic Contraction

A
  • Shortening of muscle
  • Tension constant
  • Velocity variable
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15
Q

Isometric Contraction

A
  • No shortening, muscle is constant length

- Tension is variable

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16
Q

Length Tension Relationship in Skeletal Muscle

A
  • During isometric contraction greatest tension is produced due to maximum number of cross bridges formed at optimal length
  • 2.0-2.2um
  • At lengths less than 2.0um filaments collide and interfere reducing developed force
  • At lengths greater than 2.2um active forces decline as the extent of overlap between filaments declines as the extent of overlap between filaments reduces, reducing number of cross bridges
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17
Q

Passive force in Skeletal Muscle

A
  • As muscle tissue is stretch the connective tissue around muscle cells resist the stretch = Passive force
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18
Q

Motor Unit

A

Motor neuron and all the muscle fibres it innervates

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19
Q

Excitation-Contraction Coupling In Skeletal Muscles

A
  1. ACh is released into the neuromuscular junction
    - At axon terminal Ca2+ channels open which triggers vesicles to release ACh into synaptic cleft
  2. Activation of the ACh receptors
    - ACh binds to receptors on muscle end plate opening non specific cation channels (Ligand gated)
    - Na+ enters muscle cell depolarising it
    - ACh rapidly broken down
  3. Muscle Action Potential is Triggered
    - Voltage gated Na+ open when threshold is reached
    - AP propagated along sarcolemma into T-tubules
  4. Calcium is released from the SR
    - Voltage gated Ca2+ channels opened
  5. Ca2+ binds with Troponin
    - Changing shape of tropomyosin and exposing myosin binding sites on actin
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20
Q

Creatine Phosphate

A
  • Acts as ATP store

- Reacts via Lohmans reaction to give phosphate to ADP forming ATP for muscle contraction

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21
Q

Type 1 Skeletal Muscle

A
  • Slow Twitch (oxidative)
  • Aerobic
  • Slow ATPase rate
  • Small cells
  • High number of mitochondria
  • Moderate glycolytic capacity
  • Moderate SR pumping capacity
22
Q

Type 2 Skeletal Muscle

A
  • Fast twitch (glycolytic)
  • Anaerobic
  • Fast ATPase rate
  • Large cells
  • Low number of mitochondria
  • High glycolytic capacity
  • High SR pumping capacity
23
Q

Temporal Summation In Skeletal Muscle

A
  • Wave
    Low stimulation frequency gives unfused/incomplete tetanus
  • Duration of the AP is much shorter than the ability for Ca2+ to move back into SR so another AP can be initiated before Ca2+ goes completely back to resting levels
    High stimulation frequency gives fused/complete tetanus
  • There is no relation at all between stimuli and results in a constant high tension
24
Q

Spatial Summation

A

Recruitment of multiple motor units to increase muscle contraction

25
Q

Cardiac Muscle Structure

A
  • Involuntary
  • Striated and branched cells
  • 100um x 30um
  • 1-3 central nuclei
  • Connected via inter calculated discs
26
Q

Inter-calculated Discs

A
  • Desmosomes hold the cells together and prevent separation during contraction
  • Gap Junctions allow AP to be carried from one cell to the next (coordinated contract of monocytes)
27
Q

Sino Atrial (SA) Node

A
  • Positioned in the Right Atrium
  • Pacemaker cell
  • Starts contractions of cardiac muscle
  • Unstable RMP so is always drifting to threshold which goes to depolarisation
  • i.e. spontaneous contraction
28
Q

Atrio Ventricular (AV) Node

A
  • Serves as an electrical relay system swing the current sent by the SA node before it passes it to ventricles
  • Pacemaker cell
29
Q

Pacemaker Potential

A

Slow depolarisation due to Na+ If (funny/leaky) current

- Leaking Na+ into the cell making it more positive

30
Q

Ventricular AP

A
  • Long lasting 100ms-300ms
    1. Rapid depolarisation as fast voltage gated Na+ channels open making the cell more positive (+30mV)
    2. Small drop off as Na+ channels close and K+ channels open
    3. Plateau as slow voltage gated Ca2+ channels (ICaL) open
    4. Repolarisation due to the closing of Ca2+ and the opening of K+ (outward) channels
31
Q

Why do when have a Plateau phase?

A

Serves as the refractory period, allows the heart to refill with blood for the next contraction
Premature contractions do not cause wave summation

32
Q

SR in Cardiac Muscle

A

Does not have voltage gated Ca2+ channels like in skeletal muscle
- Calcium induced, calcium release channels

33
Q

Excitation-Contraction Coupling in Cardiac Muscle

A
  1. Depolarisation of the cell opens fast voltage gated Na+ channels in the sarcolemma
  2. Membrane potential moves from -90mV to +30mV
  3. L Type (slow) Ca2+ channels open in the sarcolemma ( DHPR)
    - Balanced by Na+/Ca2+ exchangers
  4. Ca2+ influx triggers opening of Ca2+ sensitive channels in the SR (RyRa) which liberates Ca2+ into the cytosol
  5. Increased conc on intracellular Ca2+ allows Ca2+ to bind to Troponin which turns on contraction machinery
34
Q

Movement of Ca2+ out of the cell in Cardiac muscle

A
  • Pumped back into SR by SR Ca2+ ATPase
  • Pumped out of the cell by sarcolemmal Na+/Ca2+ exchanger
  • Pumped out of the cell by sarcolemmal Ca2+ ATPase
  • Pumped into the mitochondria but the mitochondrial Ca2+ uniport
35
Q

Cardiac Output (CO)

A

CO = Stroke Volume (SV) x Heart Rate (HR)

- CO is around 5L per minute at rest

36
Q

Heart Rate (HR)

A
  • Set by pacemaker cells in the SA node

- Rate can be modifies via autonomic nerves releasing neurotransmitters

37
Q

Vagus Nerve

A
  • Parasympathetic
  • Releases ACh which decreases the rate of spontaneous depolarisation of pacemaker cells but hyper polarising the cells (making them more negative)
  • This means cells take longer to reach threshold
  • Decreases heart rate
38
Q

Sympathetic Cardiac Nerve

A
  • Releases noradrenaline which increases the rate of spontaneous depolarisation by making the cell less negative
  • Cells reach threshold quicker
  • Increases heat rate
39
Q

Stroke Volume (SV)

A

Reflects the tension developed by the cardiac muscle fibres in one contraction
Can be increased by:
- Increased stretch of ventricles
- Increased HR
- Certain neurotransmitters (stronger force of contraction)

40
Q

Length Tension Relationship in Cardiac Muscle

A

Resting tension in cardiac muscle is much greater than in skeletal muscle

  • Cardiac muscle has more collagen and CT making it very stiff and elastic (passive tension)
  • Can stretch ventricles by having more blood enter the chambers (exercise) which results in more force developed (SV)
41
Q

Automaticity

A

Increasing HR increases the contractile force (SV)

  • Less available time for Ca2+ to be pumped out of the cell
  • More Ca2+ in the cell at the starting point of the next contraction
42
Q

Neural Control of SV

A

Noradrenaline acts on Beta-receptors and via second messengers acts on:

  • L Type channels resulting in more Ca2+ inside the cell
  • Ca2+ pump in the SR so SR takes up Ca2+
  • Results in a bigger/shorter contraction
43
Q

Smooth Muscle Structure

A
  • Involuntary
  • 30-200um x 3-8um
  • Not striated (no sarcomeres)
  • Spindle Shaped
  • Uninucleate
  • Found in walls of internal organs (Gut, blood vessels etc.)
  • Dense bodies act like Z-lines to anchor actin to sarcolemma
  • Caveolae - dimples on surface of the cell to increase its surface area
  • Intermediate filaments are the cytoskeleton element - act like a netting and can’t stretch and contract (can shorten more than skeletal as actin and myosin are not organised)
  • 60-75% shortening possible
  • Regulatory protein is Calmodulin
44
Q

Multiunitary Smooth Muscle

A
  • Discrete bundles of cells which are densely innervated and contract only in response to this innervation
  • Each cell works alone
  • e.g iris, vas deferens
45
Q

Unitary Smooth Muscle

A
  • Sheets of electrically coupled cells (joined by gap junctions) which act in unison, often spontaneously
  • e.g. gut and blood vessels
46
Q

Ca2+ Regulation in Smooth Muscle

A
  • Voltage dependant Ca2+ channels (L Type)
  • Hormones (angio tension 2) or neurotransmitters actin on G-Protein receptors to increase IP3 levels to release Ca2+ from SR
  • Calcium induced Calcium release from SR
  • Ca2+ ATPase in cell membrane
  • Ca2+/Mg2+ exchangers
  • Na+/Ca2+ exchangers
  • Outward rectifying K+ channels (regulate MP)
47
Q

How is smooth muscle contraction brought about

A

Can be neural, hormonal, or spontaneous

  • Myogenic with slow waves of depolarisation (GUT)
  • Neurally induced contraction (iris)
48
Q

Contraction in Smooth Muscle

A
  1. Ca2+ enters the cytosol
  2. Ca2+ binds to and activates Calmodulin
  3. Activated Calmodulin activates Myosin Light Chain Kinase enzymes (MLCK)
  4. MLCK phosphorylates the neck of myosin and activates myosin ATPase
  5. Activated myosin forms cross bridges with actin of thin filaments and shortening begins in the usual fashion
    REGULATION IS MYOSIN BASED
    Smooth muscle contractions are slow and don’t use much energy so can continuously bind
49
Q

Relaxation of Smooth Muscle

A
  • Contraction ends when a Myosin Light Chain Phosphatase (MLCP) dephosphorlates the myosin light chain
  • Balance of MLCK and MLCP working that allows for the level of contraction
  • Ca2+ ATPase in the cell membrane is the primary mechanism for reducing intracellular Ca2+
50
Q

Innervation of Smooth Muscle

A
  • Autonomic nerve fibres branch and form “diffuse junctions” (synaptic cleft) with the underlying smooth muscle fibres
  • Varicosities in the terminal axons contain a neurotransmitter
  • Varicosities release neurotransmitters into the synaptic cleft
  • Neurotransmitter is secreted into the matrix coating and diffuses to the smooth muscle cells
51
Q

Stretch Relax Response

A
  1. When you stretch smooth muscle is will initially contract resisting the stretch
    - stretch-activated Ca2+ channels open raising intracellular concentration
  2. Slowly relax adjusting to the change in length
    - Via Ca2+ dependant K+ channels
52
Q

What leads to cytosol Ca2+ MLCK or MLCP activity?

A
  • Stretch
  • Hormones
  • Neurotransmitters
  • Nitric oxide
  • Histamines
  • Prostacyclin
  • Adenosine
  • Environment (pH, O2 etc.)

Biology 107 (5 decks)

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