Excitation-Contraction Coupling & Neuromuscular Junction

Excitation-Contraction Coupling

• Describes the process where a muscle fiber action potential leads to muscle contraction.
• Steps include:
  • A motor nerve action potential travels to its endings on muscle fibers.
  • The nerve endings secrete acetylcholine.
  • Acetylcholine depolarizes the muscle fiber membrane, initiating an action potential.
  • The action potential travels along the muscle fiber membrane.
  • The action potential depolarizes the T tubules.
  • Sarcoplasmic reticulum releases stored calcium ions due to T tubule depolarization.
  • Attractive forces between actin and myosin filaments are initiated by calcium ions, causing sliding and contraction.
  • Calcium ions are pumped back into the sarcoplasmic reticulum by a Ca++ membrane pump, ceasing contraction until another action potential arrives.

Neuromuscular Junction

• The site of contact between a motor neuron and a muscle fiber.
• Signal Transmission:
  • An action potential arrives at the motor neuron's axon terminal.
  • Voltage-gated calcium channels open, allowing calcium ions into the axon terminal.
  • Vesicles containing acetylcholine (ACh) fuse with the presynaptic membrane due to calcium influx, releasing ACh into the synaptic cleft.
  • ACh diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the muscle fiber's motor endplate.
  • nAChRs are ligand-gated ion channels; ACh binding opens these channels, allowing sodium ions (Na+) influx and causing a localized depolarization known as an endplate potential (EPP).
  • An action potential is initiated if the EPP reaches threshold, propagating along the muscle fiber membrane and leading to contraction.
  • Acetylcholinesterase (AChE) in the synaptic cleft rapidly hydrolyzes ACh into acetate and choline to prevent prolonged muscle fiber depolarization.
  • Choline is reabsorbed by the presynaptic terminal for new acetylcholine synthesis.

Metabolism In Muscle Contraction

• Energy Sources:

  • ATP (Adenosine Triphosphate) powers muscle contraction, needed for: Myosin ATPase activity (cross-bridge cycling), Pumping calcium ions back into the sarcoplasmic reticulum, and Maintaining sodium and potassium ion gradients across the muscle fiber membrane.
  • Creatine Phosphate: Quick ATP regeneration during initial muscle contraction stages occurs as it donates a phosphate group to ADP (adenosine diphosphate).
  • Glycogen: Storage form of glucose in muscle cells that is broken down into glucose, metabolized through glycolysis to produce ATP and pyruvic acid.
  • Oxidative Metabolism: Primary energy source during prolonged muscle activity; glucose, fatty acids, and amino acids are broken down in the presence of oxygen to produce ATP, water, and carbon dioxide, occurring in the mitochondria.

• Metabolic Pathways:

  • ATP-Creatine Phosphate System: Immediate energy for short bursts of high-intensity activity.
  • Glycolysis: Anaerobic glucose breakdown producing ATP and pyruvic acid; during intense activity, pyruvic acid is converted to lactic acid.
  • Oxidative Metabolism (Aerobic): The primary energy source for prolonged, low-to-moderate intensity activity, occurring in the mitochondria.

• Muscle Fatigue:

  • Defined as the inability of a muscle to maintain its force of contraction after prolonged activity.
  • Factors contributing to muscle fatigue include: Depletion of energy reserves (ATP, creatine phosphate, glycogen), Accumulation of metabolic byproducts (lactic acid, ADP, phosphate), Failure of the neuromuscular junction, and Central fatigue (reduced drive from the central nervous system).

Explanation of how a muscle fiber action potential leads to muscle contraction. It details the role of acetylcholine, T tubules, and calcium ions. Covers neuromuscular junction and signal transmission.