Muscle Physiology

Front 1

What are the types of muscle?

Back 1

1. Smooth

2. Skeletal

3. Cardiac

Front 2

Which types of mucle are striated?

Back 2

Skeletal and cardiac

Front 3

What is the monomeric divisions of a muscle fibre?

Back 3

Fasicles --> muscle fibres --> myofibrils --> protein filaments.

Front 4

Back 4

1. Z Line

2. Thick Filaments

3. H-Zone

4. I-Band

5. A Band

6. Thin filaments

Front 5

What is the H zone made up of?

Back 5

Only thick filaments (Heavy zone)

Front 6

What is the A band made up of?

Back 6

Overlap of thin and thick filaments

Front 7

What is the I band made up of?

Back 7

Only thin filaments

Front 8

How is actin arranged in the thin filaments?

Back 8

Double helical arrangements.

Front 9

What is the role of the troponin complex?

Back 9

Binds calcium to reveal myosin binding sites.

Front 10

Label this thin filament

Back 10

1. Actin (double helical)

2. Tropomyosin

3. Ca++ binding sites

4. Troponin complex

5. Calcium ions (Ca++)

6. Exposed myosin binding site.

Front 11

What are the subunits of the troponin complex?

Which binds calcium?

How many calcium?

Back 11

GICTT - gerald is coming to town

1. G-actin

2. Troponin I

3. Troponin C - binds 4x Ca++

4. Troponin T

5. Tropomyosin

Front 12

What is the critical area of the myosin (thick) filament?

Back 12

The binding head areas.

Front 13

What are the critical areas of the myosin head?

Back 13

1. The ATP binding site

2. The Actin binding site

Front 14

How do the sarcomere bands change size during contraction?

Back 14

1. I-Band shortens

2. H-zone shortens

3. A-band remains the same

Front 15

Describe the steps of the crossbridge cycle.

Back 15

1. Calcium binds to the troponin complex on the thin filaments exposing the myosin head binding sites.

2. Myosin binds to the thin filaments and an inorganic phosphate (previously associated with ADP on the head) is released.

3. Release of inorganic phosphate changes the conformation of the head causing it to pull the actin filament inwards, towards the centre of the sarcomere.

4. ADP dissociates from the myosin head which exposes the ATP binding site in the myosin head.

5. ATP binds to the now exposed myosin head ATP binding region

6. ATP is hydrolysed into ADP + Pi releasing the myosin head and cocking it into its high energy form

Front 16

What is the role of transverse (T) tubules in excitation coupling?

Back 16

Transverse tubules carry AP to the sarcoplasmic reticulum which releases Ca++ to initiate contraction.

Front 17

Biochemically how does a T-Tubule cause its effect?

Back 17

T-Tubule is connected to the DHP protein receptor which is linked to a Ryanodine receptor (an ion channel) bound to the membrane of the sarcoplasmic reticulum which is filled with calcium)

Activation of DHP by an AP flowing down the T Tubule -> Activation of RyR -> release of calcium from sarcoplasmic reticulum lateral sacs.

Front 18

How is calcium reuptaken after the muscle contraction?

Back 18

Actively pumped back into the sarcoplasmic reticulum channel - SERCA

Front 19

What are sources of energy are available for muscle contraction?

Back 19

1. Creatine phosphatase

2. Oxidative phosphorylation

3. Glycolysis directly

Front 20

How does creatine phosphatase allow for an instant source of energy?

Back 20

Conversion to creatine coupled to phosphorylation of ADP.

Front 21

What are the myosin fibre types?

Back 21

1. Slow oxidative

2. Fast oxidative

3. Fast glycolytic

Front 22

What distinguishes a slow oxidative myosin fibre?

Back 22

1. Generally small physical features

2. low amounts of substrates

3. high in cellular components

4. appears red

5. slow contraction speed

Front 23

What distinguishes a fast oxidative myosin fibre?

Back 23

1. Generally intermediately sized physically

2. intermediate substrates and alternatives to oxidative phosphorylation pathway and glycolysis

3. high in cellular components to supply oxidative phosphorylation

4. Red

5. Fast contraction speed

Front 24

What distinguishes a fast glycolytic myosin fibre?

Back 24

1. Physically very large

2. High substrates and alternatives to oxidative phosphorylation for high levels of glycolysis

3. Few cellular components (no need to support oxidative phosphorylation)

4. White

Front 25

What types of muscle fibres are recruited to a contraction first?

Back 25

Slow oxidative --> fast oxidative --> fast glycolytic

Front 26

What is myotonia?

Why does it happen?

Back 26

Myotoia is the inability to relax voluntary muscle after full contraction.

Results from over firing of multiple action potentials.

Front 27

Where is smooth muscle mainly found?

Back 27

1. Vascular system

2. GI tract

3. Ocular system

Front 28

How is smooth muscle innervated?

Back 28

Autonomic innervation

Front 29

What are the key features of a smooth muscle which distinguishes it from a skeletal muscle?

Back 29

1. Many individual myocytes linked by gap junctions

2. Neuron stimulates across all the muscle rather than at the neuromuscular junctions of skeletal

3. Smooth muscle is the slowest to contract and relax

Front 30

How are thick and thin filaments arranged in smooth muscle?

Back 30

Myosin filaments are surrounded by actin filaments which connect to dense bodies

Front 31

What is the difference between multi and single unit smooth muscle?

Where can each be found?

Back 31

1. Smooth unit muscles aer not electrically linked and must be stimulated independently - found in the iris of the eye

2. Single unit smooth muscle cells are connected by gap junctions and the cells contract as a single unit - Can be found in the small intestine

Front 32

What does a 'Varicosity' refer to in terms of smooth muscle?

Back 32

A varicosity is a lump in neurons surrounding smooth muscle which acts as an unliked synapse which secretes neurotransmitters.

Front 33

What is the signal which causes smooth muscle contraction?

Back 33

Increased cytosolic Ca++ is the signal for contraction.

Front 34

What is the biochemical process which activates contraction of smooth muscle?

Back 34

1. Calcium enters the cell after release from sarcoplasmic reticulum

2. Calcium binds to calmodulin

3. Ca++ - calmodulin complex activates the Myosin light chain kinase (MLCK) protein

4. MLCK phosphorylates light chains in myosin heads, increasing myosin ATPase activity.

5. myosin ATPase activates crossbridge cycling

6. Activated myosin crossbridges slide along actin - creating muscular tension

Front 35

How does smooth muscle ultimately relax following contraction?

Back 35

1. Excess calcium in cytosol pumped out of cell into extracellular matrix and sarcoplasmic retriculum via primary active channels.

2. Calcium - calmodulin complex unbinds

3. MLCK activity decreases

4. Myosin Light Chain Phosphatase (MLCP) dephosphorylates myosin light chains

5. Myosin ATPase activity decreases

6. Decreases crossbridge cycling = decreased smooth muscle tension