L9.3 Muscle injury

Question 1

Contusion?

Answer 1

• Contusion = impact on muscles

Question 2

Process of injury to repair

Answer 2

• Degenerate → inflammatory response → regeneration (nuclei centralised & overtime migrates to periphery in human muscles) → Fibrosis (Connective tissue infiltrates area where muscles are, may compromise successful muscle repair)

Question 3

Types of muscle injuries

Answer 3

• ONLY muscle fibres
  
  • e.g. from myotoxic damage
  • COMPLETELY restoration
• Crush/laceration → ECM compromised
  
  • Impaired functional restoration
  • Extensive fibrosis

Question 4

What happens to unsuccessful muscle repairs?

Answer 4

• Prone to re-injury
• Loss/long term disability
• ↓quality of life, health care burden
• Implications for muscle diseases (MD) → susceptible to injury (Duchenne’s → ↓relative force compared to healthy)

Question 5

What actions causes muscle injury?

Answer 5

Eccentric (Pliometric) → force 2x higher during stretch

Question 6

Measures of muscle injury

Answer 6

• Levels of CK (creatine kinase) released from muscles
• Delayed, ↑variable inflammatory response
• ↑Ca2+ influx
• ↓Max force (in absence of fatigue) → Most valid measure of TOTALITY of injury
• Muscle soreness

Question 7

CK levels

Answer 7

• ↑↑after eccentric exercise
• ↓ with repeated bouts
  
  • Protection develops (even after 1st bout)
• Can’t tell how much muscles have been damaged

Question 8

Sarcomere inhomogeneirty hypothesis

Answer 8

• Injury initiated → weak sarcomeres stretched by stronger sarcomeres
  
  • Weakest ones are randomly distributed on the descending limb of length-tension relationship
  • Stretched → popped → misalignment → sarcomere remains at lengthened portion

Question 9

Initial injury

Answer 9

• Mechanical event
• Sarcomeres stretched excessively → causing mechanical traumas to t-tubules (located at the overlap of thin&thick filaments)
  
  • ↑Ca2+ → sarcolemma leaking Ca2+
  • ↑Na2+ → ↑activity of Na+
  • Disrupts t-systems → ↓AP conduction
• Loss of sarcomere architect → function/force compromised

Question 10

Secondary injury

Answer 10

• 1-3 days after injury → release CK→ delayed muscle pain
• Due to loss of Ca2+ homeostasis
  
  • Elevated Ca2+ at site of damage, if SR unable to control levels → injury proceeds to this phase
    
    • Ca2+ mediates many cell damage process → destruction of muscle fibres
• Need ↑protease & phospholipase activities → initiate regeneration (phagocytic pathway)

Question 11

Inflammatory response following injury

Answer 11

• Inflammatory response necessary for repair (autolysis)
  
  • 1) Localised neutrophils
    
    • Release degradation enzymes
    • Destroy debris
    • Stimulate release of monocytes
    • Stimulate sat cells
  • 2) Macrophages released
    
    • Phagocytosis of debris & neutrophils
    • Stimulate & activates sat cells

Question 12

Differences b/w major & minor muscle damage?

Answer 12

• Minor damage:
  
  • Limited intracellular disruption
  • Minor damage to cell membranes
  • Able to buffer Ca2+, no degeneration → membrane resealed
• Major damage:
  
  • No buffer, irreplaceable intracellular disruption
  • Compromise cell membrane
  • Cell degeneration, fibre replacement via regeneration

Question 13

Muscle protection

Answer 13

• Repeat bout → muscles buffer better
• Eccentric conditioning → prevent muscle strains
• Trained → ↑ sarcomere homogeneity → less likely to pull on sarcomere
• Overtrained → lose protection