During the initial shock or 'ebb' phase of injury, body glucose (serum glucose concentration X glucose space) is significantly increased but mass flow to peripheral tissue is only slightly altered. During the 'flow' or hypermetabolic phase of injury, mass flow of glucose is markedly increased, related to the extent of injury and directed primarily by increased sympathetic nervous system activity. Increased hepatic gluconeogenesis provides glucose which is converted to three-carbon precursors in the periphery and returns to the liver for reconversion to new glucose, utilising the Cori and alanine cycles. Increased ureagenesis is a consequence of skeletal muscle amino acids contributing to this cycle system. This energy shuttle system produces heat, and the rate of six- to three-carbon cycling correlates closely with the increased oxygen consumption of the injured patient. The glucose cycle may be altered by hormonal administration, food intake, exercise, weight loss, pharmacological manipulation and infection, but the basic reset in hepatic glucose production and energy demands in the injured patient appears essential for the inflammatory response and tissue repair.