Muscle Contraction

Excitation-Contraction Coupling Mechanism

Nerve impulse at neuromuscular junction induces muscle contraction.

Process:

1. Nerve impulse reaches the synaptic terminal causing the nerve's synaptic knobs to release acetylcholine, ACh crosses the synaptic cleft and binds to the motor endplate receptors causing a depolarization that travels over the sarcolemma and down into the T-tubule system
2. Impulse travels to SR cisternae and causes Ca⁺² release channels to open briefly, Ca⁺² flows out into sarcoplasm
3. Increase of Ca⁺² above 10^-6M exposes binding sites on actin filaments (1 msec)
4. Sliding filament mechanism
5. Impulse ends and Ca⁺² release channels close
6. Ca⁺² active transport pumps return Ca⁺² to SR or into ECF.  Requires ATP expenditure
7. When Ca⁺² level falls below 10^-6M, myosin binding sites on G-actin are covered and crossbridges cannot form

Sliding Filament Mechanism

Sliding is produced by making and breaking crossbridges between actin and myosin. Myosin heads link to actin, swivel pulling actin filaments toward H-zone, disconnect and reconnect.  Each cycle shortens muscle length.

Process:

1. Relaxed muscle: ATP attaches to myosin heads, which act as ATPase splitting ATP into ADP +  P  .  Myosin heads are activated or cocked
2. When SR releases Ca⁺² , it combines with a troponin subunit and weakens the troponin-actin bond, troponin moves pulling tropomyosin away and exposes myosin binding site on G-actin monomers
3. Activated (cocked) myosin heads spontaneously bind to exposed myosin binding site on G-actin forming crossbridges
4. Power stroke: Myosin heads swivel (conformational change), which pulls actin filaments toward H-zone, then myosin releases the ADP + P
5. New ATP binds to myosin heads causing heads to detach from actin filaments and heads swivel back to their original position (conformation change) as ATPase splits ATP

Length-Tension Relationships

• Amount of tension generated during contraction depends on the number of crossbridges (on all sarcomeres of myofibril) that can form and is based on the degree of overlap of actin and myosin in resting muscle
• Resting muscle length (see fig. 9-21 in text)
  • At short sarcomere lengths there is too much overlap, actins collide and interfere with each other, myosin hits Z-line
  • At long sarcomere lengths too little overlap reduces number of potential crossbridges
  • At about normal resting length the maximal number of crossbridges form producing highest tension

Muscle Relaxation

• Result of active transport of calcium back into the SR (Steps 6 and 7 above), requires ATP

Muscle Lengthening

• Passive process, no active mechanism for returning muscle fibers to normal resting length
• Depends upon:
  1. Elastic forces of extracellular fibers in tendons and connective tissues called series elastic elements
  2. Antagonistic muscle contraction
  3. Gravity