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ANSC 2340 (44)

Conversion of Muscle to Meat.docx

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University of Guelph
Animal Science
ANSC 2340
Ira Mandell

Conversion of Muscle to Meat AFTER EXSANGUINATION -exsanguination – the primary mode of death Changes in Tissue Function  Blood is lost from the circulatory system o Loss of transportation:  Nutrients to muscles  Removal of waste products and metabolites  Delivery of O2  Myoglobin (stores O2) o Supply of O2 in muscle depends on amount of myoglobin and muscle fiber type  Loss of the two methods of heat – through lungs and skin (heat transported via blood) Changes to Muscle Fiber  Anaerobic metabolism post mortem o Glycogen in glycolysis used  Homeostatic mechanism  Less efficient use of ATP  Continues until glycogen is depleted or lactic acid accumulates  Glycogen stores vary depending on the animal was handled, and other stress factors o Glycogen generally makes up 1% of muscle  Build up of lactic acid = protein denaturation o Lactic acid remains in cell – cannot be removed  Build up of lactic acid  Lowers pH  inactivates glycolytic enzymes o Anaerobic metabolism stopped, production of ATP stopped  Causes protein denaturation o Affects muscle’s ability to hold water  Impacts eating quality of meat  Too much or too lactate can be produced  Influenced by glycogen levels at slaughter and rate of lactic acid production  Problem with autolysis – enzymatic machinery start degrading things  When O2 available (in live animal): o Aerobic metabolism can continue  Efficient generation of ATP via nutrient metabolism and battery charging  ADP + phosphocreatine converted to ATP and creatine  When O2 runs out (in live animal) o Anaerobic metabolism  Inefficient generation of ATP  Produces lactic acid  heart or liver Changes to Animal  Rise in body temp (due to heat accumulation) soon after exsanguination affected by: o Some slaughter processes add heat (eg: burning off pig hair – “stinging”) o Rate of heat glycolysis impacts carcass temp increase o Size and location of muscles (deep vs close to surface) o Amount of fat insulation – fat = thermal insulator o Fiber type – red vs white  More glycolytic/anaerobic activity in white  Body temp impacts chilling of carcass o Chill carcass rapidly and efficiently to prevent microbial growth CONVERSION OF MUSCLE TO MEAT  Affected by: o Fast (red) vs slow (white) vs switch hitters (intermediate) contracting fibers Acidification process in the conversion of muscle to meat  The acidification process and what happens during it are responsible for the conversion of muscle to meat  Anaerobic glycolysis produces lactate o Too little lactate produced when low amount of glycogen when animal is killed  DFD (Dark, Firm, Dry) meat o Too much lactate produced when high amount of glycogen in animal at death  rapid rates of glycolysis)  PSE (Pale, Soft, exucative)  Increased heat production = delay chilling  Protein denaturation caused by rapid rates of glycogen and heat production  Time for completion of acidification process: o Pigs – 4 – 8 hr (faster rate of pH decline than cattle) o Sheep – 15 – 24 hr o Cattle 15 – 36 hr o Turkey breast – 15 min -more glycogen in muscle at death = lower ultimate pH b/c more glycogen to produce glucose which produces lactic acid -more lactate (lactic acid produced) = lower pH b/c lactic acid remains in muscle fiber Conversion of Muscle to Meat is Complete When:  Muscles are depleted of energy reserves OR  Muscles have lost the ability to utilize remaining energy reserves RIGOR MORTIS – stiffness of death  Muscles become stiff, not extensible o Muscle will rip if stretched o Relaxation is impossible – cannot get rid of Ca (No ATP to pump Ca out of sarcoplasm into sarcoplasmic reticulum) o Muscles attached to skeleton shorten less than unrestrained muscles o Amount of ATP is directly related to the extensibility of a muscle fiber  Rigor Mortis – latin for stiffness of death  An individual fiber can go into rigor quickly, but there is extensive variability among muscle fibers o Rigor develops gradually in the whole animal (carcass gets progressively stiffer) Role of ATP in Muscle Contraction  Without ATP, head cannot detach from actin after ATP binding o Formation of permanent cross bridges  In resting muscle o ATP forms complex with Mg2+ - this complex binds to myosin head and prevents formation of actomyosin  Ca+2 is not released from the sarc reticulum  Delay phase of Rigor Mortis: o Immediately after exsanguination, muscle very extensible and elastic o A load an be added to stretch it  Natural elasticity allows muscle to return to original length (resting length) when load removed  Slow loss of extensibility o ATP being synthesized  Previously, phosphocreatine + ADP  ATP + creatine  When phosphocreatine is no longer available, glycogen stores are used to phosphorylate ADP  Only a finite amount of ATP gets synthesized o Glycogen stores vary depending on animal and handling prior to slaughter o Actomyosin bridges form  Onset phase o Rapid loss of extensibility – dependent on ATP availability o Ca may leak from sarcoplasmic reticulum to stimulate muscle
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