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  1. Primary myogenesis
    Conception to 3.5 months, when # of primary myotubules are established
  2. Secondary myogenesis
    From 3 months to 7.75 months, creating primary and secondary myotubules
  3. Muscle fiber hypertrophy
    From 5.5 months on, the increase in muscle mass
  4. Myogensis
    • Occurs primarily during prenatal (embryonic & fetal)
    • Somatic growth during prenatal period involved myogenesis (muscle development), adipogenesis and fibrogenesis
  5. Embryonic stage
    • (~1st trimester of pregnancy):
    • Paraxial mesodermal cells differentiate into dermomyotome which gives rise to the early muscle (myotome) and skeletal muscle progenitor cells (mesenchymal stem cells).
    • Progenitor cells form satellite cells ad embryonic & fetal myoblasts.
    • Primary myogenesis: Embryonic myoblasts -> proliferate, elongate, fuse -> myotubes -> 1st wave of primary fibers
  6. Fetal stage
    • (~2 triester of pregnancy)
    • Secondary myogenesis: Foetal myoblasts -> proliferate, elongate, fuse -> myotubes -> 2nd wave of secondary fibers (majority of skeletal muscle fibers formed)
    • No: of fibers is fixed at end of 2nd trimester of gestation.
    • Fiber hypertrophy in the last trimester.
    • Nutrient restriction -> decrease muscle fiber # and muscle mass
  7. Postnatal
    • Hypertrophy: by proliferation & fusion of satelitte cells to muscle fibers
    • Nutrient restriction -> decrease muscle mass
  8. Muscle hypertrophy
    • Double muscling: myostatin: member of TGFbeta superfamily - expression limited to skeletal muscle-important for inhibiting muscle cell hypertrophy & hyperplasia
    • Mutations in myostatin - muscle mass increased - "double muscling"
    • Cattle (belgian blue & Piedmontese:
  9. Muscle atrophy
    • Neurogenic: denervation -> Lysosomal protein degradation -> decrease 50% muscle mass + EMG abnormalities (Sweeney" in horses)
    • Myogenic: Malnutrition, cachexia (weight loss secondary to other diseases), corticosteroid excess
    • Slow progression, normal EMG, atrophy only to type 2 fibers
  10. Muscle necrosis or Rhabdomyolysis
    • Tying up/Monday morning sickness/Azoturia. May affect fiber or subgroup of sarcomeres within a fiber - loss of striations
    • Clinical features: muscle pain, contracture, increased respiratory rate & sweating: increase Creatine Kinase & aspartate transaminase in serum; myoglobinuria
    • Causes: Nutrition: deficiency of Vitamin E and Selenium (anti-oxidants) "white muscle disease" - degenerative disease of skeletal and cardiac muscle: hypokalemia; Toxins (ionophores)
    • Infectious (clostridial, viral, toxoplasmosis, sarcocysts)
    • Immune mediated (masticatory muscle myositis - dogs)
    • Metabolic (Glycogenoses, Lipid storage disorders)
  11. Muscular dsystrophy
    • Inherited - progressive degeneration of skeletal muscle in small animals
    • Duchenne's muscular dystrophy- human. Dogs - German short hair pointers, Golden retrieves: puppies - stunted growth, elbow abduction, bunny hop-like gait; adult- "plantigrade stance"
    • Deficiency of "dystrophin" - a protein that anchors sarcolemma to actin of cytoskeleton - sarcolemma leakage - fiber damage
  12. Altered electrical conduction
    • Altered motor neuron firing: hypocalcemia
    • Altered motor end plate depolarization: Myasthenia gravis, congenital deficiency of Ach receptors#, acquired - autoantibodies to Ach receptor and Botulism: clostridium botulinum toxin
    • Altered sarcolemma excitability: myotonia - muscle hypertrophy, stiffness, rigidity, prolonged muscle contraction and Goats: autosomal dominant mutation in Cl- channel
Card Set
Last lecture on muscles
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