7 Muscle Flashcards
Q: What is muscle attached to? In what structure do they function? Example.
A: bone
antagonist muscle pairs consisting of:
- Flexor (e.g. Bicep)
- Extensor (e.g. Tricep)
bicep is antagonistic muscle pair with tricep located on humerus attached by tendons
Q: What are the 2 forms of contraction?
A: Isotonic Contraction = muscle length changes but tension remains the same
Isometric Contraction = muscle length stays the same but tension changes
Q: When it comes to muscle length changing, how do you describe shortening and lengthening?
A: Concentric - shortening
Eccentric - lengthening
Q: Give an example of muscle tone changing (without length changing).
A: when you are carrying a shopping bag with your arm extended
Q: What is skeletal muscle made of? Describe (4). Name and describe 2 functional components.
A: bundle of cells cells: myofibres which are
- large
- cylindrical
- multinucleate
- packed with myofibrils
- T tubules = membranes invaginations that contact the extracellular fluid= allows muscle membrane to come in close contact with myofibrils
- sarcoplasmic reticulum= extensive network of intracellular Ca2+ stores surrounding each myofibril
Q: What are myofibrils? Appearance. Structure (draw).
A: organelle in myofibres that make skeletal muscle
made of myofilaments which create light and dark/ striated appearance
sarcomere= functional unit of muscle between 2 Z lines:
- A band= dark bands, intersected by a darker region
- ^=H zone
- I band= light bands intersected by dark line
- ^ Z line (disc) = made of alpha-actinin and CapZ
Q: Describe the process of excitation-contraction coupling in skeletal muscle. (4) Which steps are the same for cardiac muscle? Overall?
A: 1. AP propagates along the myofibril membrane (sarcolemma) and T-tubules. ***
- Depolarisation activates dihydropiridine receptors (DHPR which are found on T tubule membrane) causing a conformational change in DHPR -> allows DHPR to make physical contact with…
- This change is transmitted to ryanodine receptors (RyR) on SR -> opening of RyR and Ca2+ release from intracellular stores
- This depolarisation -> increase in intracellular Ca2+ -> muscle contraction ***
Depolarisation —> Increase in intracellular Ca2+
Q: What are the components of a sarcomere? (7) Label diagram.
A: -Z lines define lateral boundaries of sarcomere
- actin (thin filament)
- myosin (thick)
- titin= large and spring like
- nebulin= large filaments
- tropomyosin= elongated protein
- CapZ = postive end
- tropomodulin = negative (inner)
Q: What is actin composed of? displays? Labels? (2)
A: polymeric thin filament composed of 2 twisted alpha helices
-polarity
CapZ (positive end touching Z line) and Tropomodulin (negative)
Q: What is myosin? contains?
A: thick filaments-> motor proteins
contains numerous globular heads (that interact with actin)
Q: What is titin? role?
A: VERY LARGE spring like filament - keeps the myosin in place (anchored to Z line)
Q: What is nebulin? role?
A: large filament associated with actin - doesn’t really do anything
Q: Describe the process in the sliding filament theory. (6)
A: 1. In the presence of Ca2+ -> Ca2+ binds to and causes movement of troponin from tropomyosin chain
- Movement exposes myosin binding site on surface of actin chain
- ‘Charged’ (with ADP bound) myosin heads bind to exposed site on actin filament
- This binding and discharge of ADP causes myosin head to pivot (the ‘power stroke’) -> pulling actin filament towards centre of sarcomere
- ATP binding -> releases myosin head from actin chain
- ATP hydrolysis (of ATP attached to myosin head) -> provides energy to ‘recharge’ the myosin head
Q: How do troponin and actin relate?
A: tropinin forms a helix around the actin filament - troponin is what the Ca2+ actually binds to
Q: What does the sliding filament theory not fit with? Explain what actually happens.
A: isometric contraction= no muscle shortening
net force= not getting net shortening of muscle but whole process is happening underneath-> pivoting of heads and pulling in except actin filaments are pulling back out-> result is reattachment of myosin head to same configuration/position on actin
Q: What’s the tension load relationship of isotonic contraction? Contraction? Energy?
A: Muscle tension > force exerted by load
Muscle contracts -> fibres shortens
Energy expenditure (ATP) -> ‘recharging’ of myosin heads
Q: Q: What’s the tension load relationship of isometric contraction? Contraction? Energy?
A: Muscle tension = force exerted by the load
Muscle DOES NOT contract -> myosin heads reattach to the same point on actin chain
Energy expenditure (ATP) -> ‘recharging’ of myosin heads
Q: What are the 2 main types of cardiomyocytes? Role?
A: Pacemaker cells: start AP= responsible for excitation part of excitation contraction coupling within heart
Conducting fibres= transmit electrical current along heart
Q: Give 2 examples of pacemaker cells. Describe (4,3).
A: Sinoatrial (SA) node: small, ‘empty’ (tend to have regular arrangement of actin and myosin), spindle shaped cells, spontaneously active
Atrioventricular (AV) node: spindle-shaped network of cells located at base of right atrium
Q: Give 2 examples of conducting fibres. Describe (2,2).
A: Bundle of His: fast conducting cells adjoining the AV node & Purkinje fibres
Purkinje fibres: large cells that rapidly conduct electrical impulses
Q: What is the wall of the heart called? What is it primarily made of? Cells? describe? (3)
A: myocardium, cardiac muscle
Cardiomyocytes
- striated muscle
- cylindrical shape
- mononucleated
Q: What allows the rapid spread of AP cell to cell in
A: gap junctions
Q: What connects individual cardiomyocytes? Contains? roles?
A: intercalated disks
- gap junctions: allow electrical communication between cells
- Desmosomes: hold the membrane structures together
Q: Describe the process of excitation- contraction coupling in cardiac muscle cells. (4) Which steps are the same in skeletal muscle?
A: 1. AP propagates along the myofibril membrane (sarcolemma) and T-tubules. **
- Depolarisation opens voltage-gated Ca2+ channels (VGCCs) -> Ca2+ influx
- This Ca2+ has three main effects:
- Ca2+ induced Ca2+ release (CICR) by binding to RyR on SR
- Initiate contraction binding to troponin
- Further depolarisation - This depolarisation -> increase in intracellular Ca2+ -> muscle contraction **
Q: How does cardiac and skeletal excitation coupling differ in terms of Ca2+? RyR?
A: for cardiac- comes from both extracelullar and intracellular sources
THERE IS NO CONTACT BETWEEN VGCC and RyR in cardiac
Q: Where is smooth muscle present? examples (3). Structural arrangement? What happens when it contracts? Activation?
A: Present within walls of all hollow organs (e.g. blood vessels, gastrointestinal tract and bladder).
in circular fashion around blood vessels
turns into ball and causes constriction of blood vessels
excitation contraction coupling is not usually activated by electrical signalling-> tend to be hormones
Q: Describe the process of excitation contraction coupling in smooth muscle cells. (4)
A: 1. Depolarisation activates VGCCs-> influx of Ca2+ into cell
- Ca2+ binds to calmodulin and Ca2+-CaM complex -> activates myosin light chain kinase (MLCK)
- MLCK phosphorylates myosin light chains (MLC20)
- Cross-bridges with actin filaments -> CONTRACTION -> vasoconstriction
Q: Why is smooth muscle called such?
A: DO NOT get the striated pattern of actin and myosin that you get in skeletal and cardiac muscle - though it does still contain actin and myosin
Do NOT contain regular arrangement of actin & myosin
