Sires from Duroc, Berkshire, Yorkshire and Pietrain breeds were used to produce crossbred progeny, free of the HAL-1843TM gene, that exhibit pork quality differences. Loin muscle temperature, color, firmness/wetness, marbling, and water-holding capacity were determined for sixteen progeny within each sire group (n=64 total). Rapid energy (ATP) consumption in muscle is associated with rapid breakdown of glycogen (glycolysis) and accumulation of hydrogen ions, which cause muscle acidification (pH decline). Rapid muscle acidification early postmortem, while the muscle temperature is still relatively high, causes protein denaturation and reduced protein solubility, which leads to production of pale, soft and exudative products. To better understand the regulation of postmortem energy utilization, muscle acidification and the consequences of these events, estimates of ATP utilization were made, and the capacities of enzymes that regulate energy utilization and production were quantified. Additionally, the ability of muscle to buffer the effects of acidification and the relationship between denaturation of specific proteins and pork quality was determined. Our results confirm that inferior pork water-holding capacity is caused by accelerated ATP utilization and pH decline that leads to denaturation of both contractile and soluble proteins. However, accelerated ATP utilization does not appear to be associated with an increased quantity of ATP-utilizing enzymes or an insufficient quantity of ATP-generating enzymes. Additionally, pork loin muscles with high buffering capacity exhibited a higher degree of fluid loss than those with lower buffering capacity. The latter suggests that elevated buffering capacity may be an adaptation to more frequent or severe acidification of living muscle in some pigs, which also corresponds to production of inferior pork from these animals. Physical or psychological stressors may trigger elevated ATP utilization, or rapid ATP utilization may result from a metabolic disorder similar to that created by the Hal-1843 mutation, which results in abnormal calcium homeostasis. Further elucidation of these mechanisms will lead to strategies that enable consistent production of high quality pork.