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Muscle Structure and Contraction (Sarcolemma (outside muscle cell)…
Muscle Structure and Contraction
Sarcolemma (outside muscle cell)
Sarcoplasmic Reticulum (inside muscle cell)
Surrounds each myofibril
End of segments form "terminal cisternae" which store calcium
Segments do not touch and T-tubules do not touch
Muscle cell
Myofibril
Sarcomere
A band (dark)
Thick
Myosin
2 heavy chains
4 light chains
Crossbridge with hinges
I band (light)
Thin
Actin
G-actin which polymerizes into F-actin
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Titin
From M line to Z disc
Biggest protein
Scaffold
Acts as elastic spring
Participate in signaling for muscle enlargement
T- Tubules
Penetrate deep into each muscle
Run transverse to the myofibrils
Action potentials travel into them
Depolarization
Changes conformation of dihydropyridine receptor (DHPR)
Changes conformation of ryanodine receptor (RYR) on SR
Opening of Ca++ channel and release of Ca++ from SR
Neuromuscular Junction
One axon terminal with one muscle cell
Axon terminal splits into many branches and each ends in a terminal button
Motor end place under muscle cell
Action potential travels along motor nerve to NMJ
Nerve ending releases ACh
ACh receptor activated; is a gated sodium channel
Na+ enters muscle cell
Depolarization and action potential
SR releases CA++ into cytoplasm
Muscle contraction
Ca++ pumped back into SR and contraction stops
Calcium binds to troponin
Troponin-tropomyosin complex pulled aside
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Energetics and Fatigue
Energetics
Energy consumption
Sliding of filaments
Pumping of calcium into SR after contraction
Pumping of sodium and potassium across sarcolemma
Fatigue
Metabolic
Depletion of energy supply (ATP, phosphocreatine, carbohydrate)
Accumulation of metabolites (ADP, inorganic phosphate)
Interferes with SR release of calcium
Interferes with calcium effect on actin
Interferes with cross-bridge powering production
ADP competes with ATP for myosin head
Nervous
Limited capability for motor nerve to generate sustained high-frequency action potential
After a period of maximum contraction, the nerve's signal reduces in frequency and the force generated by the contraction diminishes; some channels change in density
Can be reduced by strength training