Date of Award:


Document Type:


Degree Name:

Master of Science (MS)


Nutrition, Dietetics, and Food Sciences

Committee Chair(s)

Sulaiman K. Matarneh


Sulaiman K. Matarneh


Kara J. Thornton-Kurth


Silvana Martini


The rate at which the muscle acidifies after an animal is harvested has a profound effect on the quality of the resulting pork. When acidification increases gradually, desirable pork quality characteristics are developed. In contrast, rapid acidification deteriorates pork quality, exemplified by the pale, soft, and exudative (PSE) pork defect. The rate of acidification is determined by the rate of anaerobic metabolism in postmortem muscle. Yet the processes controlling postmortem anaerobic metabolism are not well understood. Recent research suggests that mitochondria, the powerhouse of the cell, may influence this process by competing for substrate (pyruvate) with anaerobic metabolism, thereby reducing its rate. This study aimed to examine the role of mitochondria in post-harvest acidification of pork. We hypothesized that inhibiting mitochondrial ability to uptake pyruvate would increase the rate of acidification. To test this hypothesis, CPI-613 and Avidin, inhibitors of pyruvate dehydrogenase (PDH) and pyruvate carboxylase (PC), respectively, were used in lab settings mimicking postmortem muscle metabolism. Four treatments were tested: control, CPI-613, Avidin, and CPI-613 + Avidin. A similar follow-up study incorporated a tracer to track pyruvate's fate. The results showed that inhibition of PDH with CPI-613 increased anaerobic metabolism and decreased mitochondrial metabolite enrichment, evidenced by an increased rate of acidification and anaerobic metabolism compared to the control. No effect was observed in the PC-inhibited samples. These findings suggest that mitochondria could have a regulatory role on the rate of post-harvest metabolism. Overall, the data support our hypothesis that inhibiting mitochondrial ability to uptake pyruvate increases the rate of acidification.



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