Muscle Contraction

EXCITATION: Muscle receives chemical stimulus and responds with an electrical impulse.

  1. The motor neuron stimulates the muscle fiber at the neuromuscular junction. An impulse from the brain travels down the motor neuron axon, causing voltage-gated ion channels in the synaptic knob to open and allow calcium to enter the neuron. Ca++ entry leads to vesicle movement towards the pre-synaptic membrane.

  2. ACh (acetylcholine) is released by exocytosis out of synaptic vesicles held in the pre-synaptic axon terminal. On the other side of the synapse, the muscle fiber sarcolemma has a motor end plate with many ACh receptors (two types: nicotinic and muscarinic).

  3. ACh binds to the receptors. The enzyme acetylcholinesterase immediately breaks down ACh into choline and acetic acid.
    NOTE: Many neurotoxins and drugs work here.

  4. The resting muscle fiber sarcolemma is polarized (-70mv). When ACh binds post-synaptic receptors, Na+ channels open and depolarization occurs. This initial depolarization is called an end plate potential. IF the stimulus is adequate, an action potential will be initiated and propagated.

  5. Repolarization of sarcolemma occurs immediately. Na+ channels close and K+ channels open. The cell is in a refractory period and cannot be stimulated again until it returns to a polarized state (-70mv).

E-C COUPLING: Action potential transmission leading to myofilament sliding.

  1. The action potential is propagated along the sarcolemma and down the T-tubule system of the muscle fiber.

  2. The sarcoplasmic reticulum releases Ca++ into the sarcoplasm. Ca++ is now available to the myofilaments.

  3. The Ca++ signal is short-lived. An ATP-driven calcium pump moves Ca++ back into the SR.

SLIDING FILAMENT: Myofilaments slide and overlap causing muscle cell shortening/contraction.

  1. Ca++ in sarcoplasm binds to troponin complex on the thin filament. A conformational change occurs, moving tropomyosin from the myosin-binding site on actin.

  2. Myosin heads of thick filament bind to the actin and form cross-bridges. High energy state.

  3. ADP (adenosine diphosphate) and Pi (inorganic phosphate) are released from the myosin heads. The myosin heads bend (power stroke) pulling on the attached thin filament, sliding it towards the center of the sarcomere, decreasing the H-zone.

  4. ATP (adenosine triphosphate) binds to bent myosin heads and cross-bridges are detached. Low energy state.

  5. Hydrolysis of ATP by ATPase on myosin heads provides energy required to “re-cock” myosin heads.

  6. Back to the start: if Ca++ signal exists, then the active sites are exposed on the thin filaments and myosin can attach and form cross-bridges.