Muscle Flashcards
Skeletal Antagonist Muscle Pair
- flexor
- extensor
What is Isotonic Contraction
Muscle length changes but tension remains the same.
Eccentric = lengthening
Concentric = shortening
What is Isometric contraction?
Muscle length stays the same but tension changes
Describe Skeletal Muscle structure
Bundles of muscle form myofibres. These are large/cylindrical, multinucleate and packed with myofibrils.
Describe Excitation - contraction coupling in skeletal muscles
1) AP propagates along the myofibril membrane (sarcolemma) and T-tubules
2) Depolarisation activates the dihydropiridice Receptors (DHOR) causing a conformational change in the DHPR
3) This change allows contact between DHPR and Ryanodine Receptor (RyR) on the SR.
4) This leads to conformational change on the RyR and causes Ca2+ release from SR
Sarcomere Components
Actin, Myosin, Myosin Heads, Titin, Nebulin, Tropomyosin, CapZ and Tropomodulin
Describe the Sliding Filament Theory
1) In Ca2+ presence, movement of troponon from tropomyosin chain.
2) Movement exposes myosin binding site on the surface of actin chains
3) ‘Charged’ myosin heads bind to the exposed site on actin
4) This binding and ADP release cause heads to pivot pulling actin filament towards centre of sarcomere
5) ATP binding causes release of myosin head from actin chain
6) ATP hydrolysis provides energy to ‘recharge’ the myosin head
Myofibril Structure Components from Microscope
Z-line, A-band, I-band, Sarcomere
Name of heart muscle cells
Cardiomyocytes (striated)
Internodal Pathway Description
SA node to AV node to purkinje fibres
What is an intercalating disk?
Specialised discs connecting individual cardiomyocytes. They have desmosomes and gap junctions (to allow electrical communication)
Cardiac Muscle EC coupling
AP propagates along sarcolemma and T tubules. Depolarisation opens voltage gated calcium chanels (VGCC) and Ca2+ influx. This causes Ca2+ release from SR by bingding to RyR as well as initate comtraction by binding to troponin.
Smooth Muscle E-C coupling
Depolarisation activates VGCC’s and causes Ca2+ influx. This calcium bings to calmodulin (CaM) forming a Ca-CaM complex. This complex activates Myosin Light Chain Kinase (MLCK). This phosphorylates myosin light chains and muscle contracts (vasoconstriction)
