L 14 - Muscle II Flashcards
AP vs Contractions
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.
Twitch and tetanus
Single AP → twitch
Summation & unfused tetanus with increased rate
Higher rates → fused tetanus
o How most muscles operate
o Produced by multiple Aps
Henneman’s Size Principle
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
Slow fibres (oxidative)
Used for posture maintenance etc. Have myoglobin (red) as oxygen store. Many mitochondria.
red
Fast fibres (Oxidative)
fast myosin isoform, fast Ca transient (high SR Ca pump). Allows rapid shortening but at high energy cost as ATP hydrolysed quickly
red
Glycosidic fibres (fast)
Lactate accumulation & acidosis can limit contraction
white
Use of fibres in sports:
Use – oxidative in marathon; glycolytic in boxing; marathon runner 82% slow, average slob 45%, sprinter 37%
Duchenne Muscular Dystrophy
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
How to cardiac muscle differ from skeletal? (8)
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
Remember the AP graph of cardiac
.
Cardiac Excitation Contraction Coupling
Calcium comes in by primarily from L-type Calcium
No RyR = Ca induced Ca release
Ap in membrane – Ca enter cytoplasm.
CICR
Three features of the SAN and ions
Slow, continuous and spontaneous.
Sodium and a bit of calcium enter cell.
2 mechanisms of controlling contractions
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+
Cardiac Muscle Energy Metabolism
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
Features of Smooth Muscle
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”)
Where are smooth muscle found?
Hollow organs: – Blood vessels – Gut – Bladder – Uterus – Bronchi
2 functions of SM
– Propel contents (gut, bladder, uterus)
– Regulate flow (blood vessels, bronchi)
- Controlled by autonomic nervous system
- Considerable variety
How does SM contraction differ?
Contracts slowly
More energy efficient
Contracts well over greater range (important in terms of function e.g. bladder)
Different mechanism of E.C. coupling
what is Excitation-Contraction Coupling in SM and diffs
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
Sources of Calcium in SM
- L type channels CICR
- G – protein couple receptor – GQ – inositol triphosphate (IP3).
- SOC
Stages in Contraction in SM
- Ca binds to a protein called calmodulin.
- Calmodulin interacts with myosin light chain kinase (MLCK), converting MLCK to an active state
- MLCK then phosphorylates the regulatory light chains of myosin, switching on the ATPase activity of the myosin heads.
- cross bridge formation take place
How is the signal switched off (SM)
calcium needs to be removed
RLC needs to have their phosphate groups removed (myosin light chain phosphatase)
What slows down SM contraction?
Involvement of enzymes
