Muscular System - NMJ, action potentials/muscle contraction, muscle performance

electrochemical control of muscular contraction

1. arrival of a nerve impulse at terminal ends of axon stimulates exocytosis of acetylcholine through vesicles

2. ACh diffuses across synapse, binds to receptor sites on effector, and electrical stimulation causes depolarization of the muscle membrane resulting in muscle action potential

3. muscle fiber contracts in response to one or more action potentials moving along its sacrolemma via T-tubules

4. muscle action potentials resulting in contraction arise at the NMJ

5. ACh binding to its receptors in the sarcolemma cause release of calcium from the sarcoplasmic reticulum into the cytosol of the cell

contractile proteins

• thick filaments = myosin

• thin filaments = actin

actin filament

contains mainly actin, also contains tropomyosin and the troponin complex

contraction of muscle

1. tropomyosin prevents actin from attaching to the myosin by masking the binding sites during resting state

2. when calcium ions are released from sarcoplasmic reticulum, they are picked up by the calcium binding sites of the troponin complex

3. binding of calcium to the troponin complex causes a shift in position of the tropomyosin, which ceases its inhibition of actin

4. actin is now able to mind with myosin and contraction occurs

sliding filament theory/contraction cycle

1. when calcium concentration rises, binding sites along the length of the actin filament are exposed

2. heads of the myosin (containing ADP and P) attach to the actin forming myosin cross-bridges between thick and thin filaments

3. when binding occurs, ADP and P stored within myosin head are released causing a change in the angle of the myosin head

4. cross bridges bend and pull thin actin filaments toward the H zone

5. As a result of binding, myosin binds to another ATP molecule and detaches from the actin filament

rigormortus

body is stiff because myosin cannot detach from actin and muscles remain contracted