One of the hallmark metabolic responses to stress (i.e. injury, sepsis, surgery) is catabolism. Generally speaking, the degree of catabolism is proportional to the degree of stress. Catabolism is caused by increased breakdown of skeletal muscle. The subsequent release of amino acids provides some of the substrate for increased hepatic gluconeogenesis.
During periods of stress, the overall nitrogen balance is negative. However, there is conflicting data regarding the degree of skeletal muscle protein synthetic activity. Studies have reported reduced skeletal muscle protein synthesis after open cholecystectomy, decreased hepatic protein synthesis that becomes directly proportional to the duration of surgery, and a reduction in the protein synthesis within tissues that have rapidly replicating cells. Other studies postulate that the negative nitrogen balance is the result of protein breakdown that exceeds the increased protein synthetic rate.
Stress hormones like cortisol and cytokines such as TNF-a, IL-1, IL-6, and interferon-g mediate catabolic activity. The release of these cytokines stimulate increased hepatic synthesis of the acute-phase proteins such as fibrinogen, haptoglobin, complement, immunoglobulin’s, serum amyloid A, and CRP. The increase in acute-phase proteins lead to a greater ability to fight infection, promote wound healing, and improve hemostasis.
Overall, this promotes the body’s return to homeostasis.
Weissman, C. Nutrition and Metabolic Control. Chapter 95. Miller Anesthesia. 7th Edition. Saunders; 2007.