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mct
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Primary myogenesis
Conception to 3.5 months, when # of primary myotubules are established
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Secondary myogenesis
From 3 months to 7.75 months, creating primary and secondary myotubules
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Muscle fiber hypertrophy
From 5.5 months on, the increase in muscle mass
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Myogensis
- Occurs primarily during prenatal (embryonic & fetal)
- Somatic growth during prenatal period involved myogenesis (muscle development), adipogenesis and fibrogenesis
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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
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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
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Postnatal
- Hypertrophy: by proliferation & fusion of satelitte cells to muscle fibers
- Nutrient restriction -> decrease muscle mass
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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:
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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
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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)
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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
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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
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