Module 17 - Muscle II Flashcards
How long do action potentials and muscle contraction last?
AP - 1-2ms
MC –20-100ms
How is muscle contraction induced
Single AP - twitch
Multiple APs fired leads to summation as contraction is stimulated before the last one ends
Higher rates of AP - fused tetanus
Tetanus: what is it and what should it not be confused with?
The summation of multiple APs causing lots of contraction
Tetanus - the disease (they both come from the same greek word)
Types of skeletal muscle types
Slow oxidative fibres (Type I) - used for posture maintenance, etc and myoglobin (red) as oxygen store (many mitochondria)
Fast fibres (Type IIa, IIb): both have fast myosin isoform and fast Ca transient (high SERCA pump) which allow for rapid shortening but at a high energy cost as ATP is hydrolyzed quickly
IIa: oxidative fibres: lots of mitochondria, pretty good blood supply, good glycogen stores. Resist fatigue
IIb: glycolytic fibres: lactate accumulation & acidosis can limit contraction
Slow oxidative muscle fibres: colour, metabolism, myosin ATPase, mitochondria, capillaries, glycogen, myoglobin, fatiguability, diameter, and force
Red
Oxidative
Low
High
Very high,
Low,
Very high
Low
Small
Low
Fast oxidative muscle fibres: colour, metabolism, myosin ATPase, mitochondria, capillaries, glycogen, myoglobin, fatiguability, diameter, and force
Red
Oxidative
High
High
High
High
High
Medium
Medium
Intermediate
Fast glycolytic muscle fibres: colour, metabolism, myosin ATPase, mitochondria, capillaries, glycogen, myoglobin, fatiguability, diameter, and force
White
Glycolytic
High
Low
Low
Very high
Low
High
Large
High
Cardiac muscle: its key features
Branched syncytium
Cells incompletely fused
Joined by intercalated discs
Control mechanisms different
Action potentials different
Excitation-contraction coupling different
Only found in the heart
The 4 stages of cardiac muscle action potentials and the ions involved in each part
1) sharp increase in membrane potential (NA⁺ in)
2) Start of plateau (K⁺ and Cl⁻ out)
3) plateau (Ca²⁺ in and K⁺ out)
4) Slow decline (K⁺ out)
Cardiac Excitation Contraction Coupling
Sources of Ca²⁺:
80~90% from sarcoplasmic reticulum via CICR
10~20% from outside (this is used to access the other 80-90%)
Initiation of contraction: SA node AP
Constantly slowly increasing (can either be quicker or slower by the ANS controlling it) - funny current
After the AP is triggered, K⁺ channels open
Why is smooth muscle histologically distinct from skeletal and cardiac muscle?
- No striations
- No t-tubules
- Small, spindle-shaped cells
- troponin not involved in contraction
- not all smooth muscle requires an AP to contract
- source of calcium: extracellular and SR
Where is calcium obtained from in smooth muscle?
Either:
Depolarisation - AP triggers L-type CaC to open and calcium ions open up calcium stores in the SR
GPCR activation - GPCR activated - Phospholipase C activated - IP3 activated - IP3 receptors in SR membrane activated and opened
Calcium regulation in smooth muscle
Calcium binds to a protein called calmodulin which interacts with myosin light chain kinase (MLCK), converting it to an active state
MLCK then phosphorylates the regulatory light chains of myosin, switching on the ATPase activity of the myosin heads allowing cross-bridge formation
To stop contraction, calcium is removed and then the regulatory light chains have their phosphate groups removed by myosin light chain phosphatase
The involvement of these enzymes means that smooth muscle contraction and relaxation is a slow process.
Skeletal muscle: thick and thin filaments, striations, transverse tubules, SR, control of cross bridges, speed, pacemaker activity, gap junctions, effects of nerve stimulation
Present
Present
Present
Present
Troponin and tropomyosin
Fast and slow
Not present
Not present
Excitation
