Metabolic stress

Metabolic stress is a burden on the metabolism (metabolism) caused by exogenous factors (injury and / or illness). Hypermetabolism (increased metabolism) and (injury-related) catabolism characterize the metabolic changes as a result of a stress reaction. Metabolic stress affects all body systems in different ways: it inhibits the ability of the immune system to protect the body against intruders, it slows down wound healing and can reduce muscle strength. The healing possibilities are increased if the patient receives adequate medical and nutritional care to prevent sepsis and organ failure. As a response to stress, cells of the body's own defense ( monocytes , macrophages , neutrophils ), hormones , cytokines and messenger substances are increasingly formed.

Metabolic Factors

Among other

metabolism

The metabolism is divided into protein, carbohydrate and fat metabolism:

Protein metabolism

The proteins consist of amino acids . Some of these consist of nitrogen . In the stress metabolism, the total protein turnover is increased (i.e. the energy expenditure increases), but the synthesis (regeneration) rate is increased to a lesser extent than the breakdown rate. Muscle mass is preferentially broken down: Increased cortisol and catecholamine levels lead to increased protein breakdown. The insulin plays a special role in the regulation of protein metabolism under stress conditions. You can roughly compare insulin as an “ anabolic hormone ” (build-up of fat, glycogen, protein is promoted, nitrogen balance becomes positive) and “ catabolic hormones ” (stress hormones = “anti-insulin factors”). The most important stress hormones are catecholamines, glucagon and cortisol.

Carbohydrate metabolism

Carbohydrates are the most important substrate for energy production. Humans only have limited carbohydrate reserves in the form of glycogen , which can be used for a few hours. It is characteristic of the stress metabolism that glucose is broken down preferentially anaerobically to lactate and pyruvate. Insulin and corticosteroids ( cortisol ) behave antagonistically (cortisol ↑ - insulin ↓).

In the stress metabolism, the relative insulin deficiency and the phenomenon of insulin resistance create a metabolic situation that is similar to that of type 2 diabetes mellitus. This leads to a glucose utilization disorder and thus to a lack of energy in the cells. This in turn leads to a reduction in the availability of transmitters. The regulation of metabolic processes can be improved by stopping normoglycemia.

Fat metabolism

In the human organism, fatty acids are mainly stored as triglycerides . The turnover of triglycerides and fatty acids is increased in the stress metabolism. Almost all tissues can meet their energy needs by burning fatty acids.

Stages of metabolic stress

Ebb phase	Onset of metabolic stress; Energy is conserved immediately after the injury
Acute flow phase	The energy requirements are increasing, in some cases significantly
Adaptive flow phase	Beginning of the healing process

Local answer

The “local” response after trauma occurs quickly and leads to the disruption of cellular vitality in the injury zone. This early tissue reaction is mainly caused by vascular changes, which are characterized by increased vascular permeability. The functions of the stomach and intestines are also severely restricted by stress and medication.

Systemic response

A trauma also induces a hyperinflammatory (overinflammatory) reaction of the organism, which leads to generalized immunosuppression ( immune deficiency).

In addition, the hormones cortisol, catecholamines (adrenaline), prostaglandins and interleukins lead to a weakening of the cell-mediated immune response. The risk of infection and blood clotting disorders increase. The systemic inflammatory processes are in principle useful in overcoming the trauma. Immediately after a trauma, all metabolic processes are rearranged in such a way that quickly available energy sources are made available. These energy sources are mainly glucose and free fatty acids (FFS: non-membrane-forming lipids). Lipolysis is stimulated in adipose tissue, while proteolysis and the release of amino acids are stimulated in muscles. The uptake of glucose is inhibited in both tissues, mainly due to the lack of insulin-induced expression of the GLUT4 transporter. The glycogen synthesis in hepatocytes is increased. The breakdown of amino acids leads to increased urea synthesis and excretion.

literature

Elisabet Rytter et al .: Glycaemic status in relation to oxidative stress and inflammation in well-controlled type 2 diabetes subjects. In: British Journal of Nutrition. Vol. 101, Issue 10 (May 2009), pp. 1423-1426, PMID 19459227 .
Hugo Van Aken (Ed.): Intensive Care Medicine. 2nd, revised edition. Thieme, Stuttgart / New York 2007, ISBN 978-3-13-114872-8 .
Hans-Konrad Biesalski et al. (Ed.): Nutritional medicine. 3rd, expanded edition. Thieme, Stuttgart / New York 2004, ISBN 3-13-100293-X .
Rudolf Deiml: Selected Topics on Operative Intensive Care Medicine. 5th, revised edition. Self-published, Hamburg 2007, ISBN 978-3-00-020074-8 .
Johann Michael Hackl: Determination of the nutritional status. In: Jürgen Stein, Karl-Walter Jauch (Hrsg.): Praxishandbuch clinical nutrition and infusion therapy. Springer, Berlin / Heidelberg 2003, ISBN 978-3-540-41925-9 , pp. 3–20 ( PDF; 587 kB ).
Kurt Mosetter: Chronic stress on the level of molecular biology and neurobiochemistry. In: Gottfried Fischer, Peter Schay (ed.): Psychodynamic psycho- and trauma therapy. Verlag für Sozialwissenschaften, Wiesbaden 2008, ISBN 978-3-531-16129-7 , pp. 77-98.