Muscles - Anatomy & Physiology

BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY

Introduction

• Skeletal muscle includes muscles of:
  • Posture
  • Movement
  • Respiration

• Two basic types of skeletal myofibre:
  • Type I
    • Grossly red
    • High myoglobin level
    • Slow rate of contraction
    • High oxidative activity
    • Function - postural
  • Type II
    • Grossly white
    • Low myoglobin level
    • Fast rate of contraction
    • High glycolytic activity
    • Function - exercise

• Each muscle is composed of multiple fascicles
  • Each fascicle is composed of multiple polygonal myofibres

Regeneration

Muscle regeneration (Image sourced from Bristol Biomed Image Archive with permission)

• Skeletal muscle myofibres have substantial regenerative ability
• Success depends on:
  • An intact sarcolemmal tube - to act as a support and guide
  • Availability of satellite cells - to act as progenitor cells for new sarcoplasm production
  • Macrophages to clear up cell debris
  • If these conditions are not met (e.g. severe thermal damage) fibrosis will occur
• Stages:

1. Nuclei in necrotic segement disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or mineralise
2. Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury)
3. Satellite cells move to centre
4. Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina
5. Satellite cells -> myoblasts (contain myosin) -> fuse forming myotubes with row of central nuclei; cytoplasmic processes fusing
6. Growing and differentiating fibre, striations appear - formation of sarcomeres
7. Nuclei move to peripheral position (2-3 weeks after initial injury)

• Regeneration by budding
  • When conditions are not optimal, disrupted sacrolemma
  • E.g. injection of irritating substance, trauma, infarction
  • Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells
• Monophasic lesions - all at same phase above
  • Damage occured at one time, e.g. trauma or one toxin exposure
• Multiphasic lesions - different stages as described above
  • Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin

Rigor Mortis

• Muscles remain biochemically active after the death of an animal
• Following a period of relaxation, contraction and stiffening occurs
• Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke
• Onset faster in ATP deprived animals (starvation, hunting, tetanus...)
• May be absent in cachetic animals
• Disappears due to autolysis or putrefaction
• See general pathology

BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY