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