muscular sys 2

• Skeletal muscle


  Striated, larger fibers, more actin than myosin, multiple nuclei
• Cardiac muscle


  Striated, branched, single central nucleus
• Smooth muscle


  Not striated, spindle-shaped, single central nucleus, more actin than myosin
• Skeletal muscle contractions are controlled by the nervous system through action potentials
• Resting membrane potential


  Membrane voltage difference across membranes, inside cell more negative due to accumulation of large protein molecules, more K+ on inside than outside, K+ leaks out but not completely because negative proteins hold some back, outside cell more positive and more Na+ on outside than inside, Na+/K+ pump maintains this situation
• Muscle contraction energy sources

  1. Conversion of two ADP to one ATP and AMP (adenylate kinase)

  2. Transfer of phosphate from creatine kinase to ADP to form ATP

  3. Anaerobic respiration (breakdown of glucose to yield ATP and lactic acid)

  4. Aerobic respiration (breakdown of glucose to produce ATP, carbon dioxide and water)
• Neuromuscular junction


  Points of contact between motor neuron and muscle fiber, consisting of presynaptic terminal (axon terminal with synaptic vesicles containing neurotransmitter acetylcholine), synaptic cleft, and postsynaptic membrane (motor end-plate)
• Neuromuscular junction function


  1. Action potential arrives at presynaptic terminal, voltage-gated Ca2+ channels open, Ca2+ enters and initiates release of acetylcholine from synaptic vesicles by exocytosis

  2. Acetylcholine diffuses across synaptic cleft and binds to ligand-gated Na+ channels on postsynaptic membrane

  3. Na+ enters postsynaptic cell, causing depolarization and action potential generation

  4. Acetylcholinesterase breaks down acetylcholine in synaptic cleft, choline recycled to presynaptic terminal to reform acetylcholine
• Muscle contraction


  1. Action potential propagated along sarcolemma and T tubules

  2. Depolarization of T tubule causes Ca2+ release from sarcoplasmic reticulum

  3. Ca2+ binds to troponin, exposing actin binding sites

  4. Myosin heads bind to actin, forming cross-bridges
• Muscle relaxation


  1. Ca2+ pumped back into sarcoplasmic reticulum

  2. Ca2+ moves away from troponin-tropomyosin complex

  3. Complex re-establishes position and blocks myosin binding sites
• T tubules


  Continuous extensions of sarcolemma that transmit electrical impulse deep within cell structure
• Sarcoplasmic reticulum


  Elaborate smooth endoplasmic reticulum that surrounds each myofibril, stores and releases calcium to regulate contraction
• Excitation-contraction coupling


  Links electrical and mechanical components of contraction, action potential propagated into T tubules causes calcium release from sarcoplasmic reticulum, calcium binds to troponin to initiate contraction
• Role of calcium


  Calcium binds to troponin, causing troponin and tropomyosin to move and expose myosin binding sites on actin
• Smooth muscle contraction


  Hormone or depolarization causes Ca2+ influx, Ca2+ binds to calmodulin which activates myosin kinase, myosin phosphorylation initiates cross-bridge cycling and contraction, relaxation occurs when myosin phosphatase removes phosphate from myosin
• Muscle energy metabolism


  • Glycolysis produces ATP from glucose and glycogen
  • Oxidative phosphorylation produces ATP aerobically
  • Anaerobic glycolysis produces lactic acid
• Muscle fibre types


  • Fast twitch (type II) - short term, fast contraction, anaerobic ATP production
  • Slow twitch (type I) - endurance, aerobic ATP production, more mitochondria
• Muscle fibre type composition is genetically determined
• Glycolytic/anaerobic muscles fatigue faster due to lactic acid buildup
• Endurance muscles with high slow twitch fibres maintain constant energy supply through aerobic metabolism
• Muscle adaptation to training

  1. Endurance training increases aerobic capacity, mitochondria and capillaries

  2. Strength training increases fibre diameter and nuclear content
• Muscle fibre numbers do not increase with training, only structure and function are enhanced
• Muscle atrophy


  Muscle wasting due to lack of exercise, disease or old age
• Rigor mortis


  Muscular stiffness that occurs after death, caused by calcium leaking into sarcoplasm and forming cross-bridges between actin and myosin
• Differences between muscle types

  • Skeletal - striated, larger fibers, more actin than myosin, multiple nuclei
  • Cardiac - striated, branched, single central nucleus
  • Smooth - not striated, spindle-shaped, single central nucleus, more actin than myosin
• Skeletal muscle contractions are controlled by the nervous system, cardiac muscle contractions are involuntary, and smooth muscle contractions are controlled by hormones and local factors