Transcript Slide 1

Early post
mortem
events
Buenos Aires
Sept 2008
Outline
• Consequences of circulatory failure.
• Muscle metabolism post slaughter.
• Effect on pH.
• Biochemistry of rigor mortis.
Circulatory failure
Muscle continues
using energy (ATP)
Localised oxygen
consumed (ie in blood)
Aerobic
metabolism stops
ATP conc. falls stimulating
anaerobic metabolism
Ultimate pH (pHu) 5.5
stops metabolism
Rigor mortis
pH declines due to
lactic acid build up
Glycogen catabolised as
fuel producing lactic acid
Muscle Metabolism
• Two sources of energy
(ATP)
- Creatine Phosphate
- glucose
Creatine Phosphate
• Short term energy supply (intense exercise).
• ATP drops when Creatine Phosphate used
up.
ATP breaks actin/myosin
linkages
• enables muscles to relax
again.
- no ATP… rigor mortis!
Glycolysis
Aerobic
Anaerobic
Glucose
Glycolysis
Glycolysis
Glucose
ADP
ATP
ADP
ATP
Heat
Some
ATP
Pyruvate
O2
TCA
Pyruvate
Heat
CO2
H2O
ATP
Lactic acid
Mitochondrial Wall
Changes in metabolite
conc. post mortem
pH decline
• To rapid – heat shortening, or
PSE (pale soft exudative
meat).
• To slow – cold shortening.
• pHu (5.5) not reached – dark cutting meat
(DFD meat).
Factors affecting rate
of pH decline
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•
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Muscle type (ie red/white)
Species (horse>pig>cow)
Temperature
Stimulation
Rigor Mortis: Definition
• Biochemical – ATP insufficient to
break actin/myosin linkages.
• Chemical – post mortem muscle
pH is lower than 6.0
• Practical – muscle has “set”.
Stiff to the touch.
Rigor: biochemical scenario
Slaughter
Onset of rigor
CP depleted
Actin/myosin links increase
Glycogen
pH
Lactate
Ca2+ leaks
ATP conc. drops
ATP breaks links
Actin/myosin links
(contraction)
Conclusions
• Circulatory failure
• Post Mortem muscle metabolism
- Glycolysis
- Creatine Phosphate
• Factors affecting pH decline
- Species
- Muscle type
- Temperature
• Biochemistry of Rigor Mortis