L 14 - Muscle II

Question 1

AP vs Contractions

Answer 1

Single stim = twitch

Longer duration due to the process of calcium release and uptake is simply slower than the processes involved in an action potential.

Question 2

Twitch and tetanus

Answer 2

Single AP → twitch

Summation & unfused tetanus with increased rate

Higher rates → fused tetanus
o How most muscles operate
o Produced by multiple Aps

Question 3

Henneman’s Size Principle

Answer 3

Cell bodies diff size – bigger more muscle fibres it enervates.

Stimulation coming from brain (W) if it reaches X – wont takes high frequency for X as its small vice versa for Z

Question 4

Slow fibres (oxidative)

Answer 4

Used for posture maintenance etc. Have myoglobin (red) as oxygen store. Many mitochondria.

red

Question 5

Fast fibres (Oxidative)

Answer 5

fast myosin isoform, fast Ca transient (high SR Ca pump). Allows rapid shortening but at high energy cost as ATP hydrolysed quickly

red

Question 6

Glycosidic fibres (fast)

Answer 6

Lactate accumulation & acidosis can limit contraction

white

Question 7

Use of fibres in sports:

Answer 7

Use – oxidative in marathon; glycolytic in boxing; marathon runner 82% slow, average slob 45%, sprinter 37%

Question 8

Duchenne Muscular Dystrophy

Answer 8

X linked disorder: mutation in the dystrophin gene (about 1:3600 male births)

Skeletal muscle fibres are not linked to extracelluar matrix properly

Excess calcium enters and muscle fibres die

Progressive muscle weakness

Average life expectancy 25-30 years

Question 9

How to cardiac muscle differ from skeletal? (8)

Answer 9

Cells incompletely fused

Joined by intercalated discs into a branched syncytium - Gap junctions

Control mechanisms different

Different subtypes of myosin, actin etc.

Action potentials different

Excitation-contraction coupling different

Only found in the heart

Have t tubules

Question 10

Remember the AP graph of cardiac

Answer 10

.

Question 11

Cardiac Excitation Contraction Coupling

Answer 11

Calcium comes in by primarily from L-type Calcium

No RyR = Ca induced Ca release

Ap in membrane – Ca enter cytoplasm.

CICR

Question 12

Three features of the SAN and ions

Answer 12

Slow, continuous and spontaneous.

Sodium and a bit of calcium enter cell.

Question 13

2 mechanisms of controlling contractions

Answer 13

Cronotropic – changing timings on heart beats

Inotropic – changing force of contraction
o Degree of stretch of cardiac muscle (Starling’s Law of the Heart)
o Concentration of cytoplasmic Ca2+

Question 14

Cardiac Muscle Energy Metabolism

Answer 14

Heart needs to beat continuously so can’t use glycolytic ATP production

Uses oxidative metabolism

Cardiac muscle needs a good blood supply

Deprivation of blood (O2) supply -> angina, heart attack

Question 15

Features of Smooth Muscle

Answer 15

No striations

No t-tubules

Small, spindle-shaped cells

Cells often electrically coupled by gap junctions (“unitary” – acts as syncytium) but can be independent (“multiunit”)

Question 16

Where are smooth muscle found?

Answer 16

Hollow organs:
–	Blood vessels
–	Gut
–	Bladder 
–	Uterus
–	Bronchi

Question 17

2 functions of SM

Answer 17

– Propel contents (gut, bladder, uterus)
– Regulate flow (blood vessels, bronchi)

• Controlled by autonomic nervous system
• Considerable variety

Question 18

How does SM contraction differ?

Answer 18

Contracts slowly

More energy efficient

Contracts well over greater range (important in terms of function e.g. bladder)

Different mechanism of E.C. coupling

Question 19

what is Excitation-Contraction Coupling in SM and diffs

Answer 19

Ca still involved

o Troponin not involved

o Not all smooth muscle requires action potential to contract

o Source of calcium: extracellular and SR

o Release from SR via RyR and IP3

o Store Operated ChannelS

Question 20

Sources of Calcium in SM

Answer 20

1. L type channels CICR
2. G – protein couple receptor – GQ – inositol triphosphate (IP3).
3. SOC

Question 21

Stages in Contraction in SM

Answer 21

1. Ca binds to a protein called calmodulin.
2. Calmodulin interacts with myosin light chain kinase (MLCK), converting MLCK to an active state
3. MLCK then phosphorylates the regulatory light chains of myosin, switching on the ATPase activity of the myosin heads.
4. cross bridge formation take place

Question 22

How is the signal switched off (SM)

Answer 22

calcium needs to be removed

RLC needs to have their phosphate groups removed (myosin light chain phosphatase)

Question 23

What slows down SM contraction?

Answer 23

Involvement of enzymes