Muscle function in critically ill patients

Endotoxemia and inflammation (cytokines) lead to an acute decrease of the muscle resting membrane potential, loss of the sodium-potassium gradient and to an increase in cytosolic Ca2+in critically ill intensive care unit patients. As a consequence, muscle (and nerve) contractility is reduced. As a consequence also, amino acid gradients are reduced, proteolysis is increased, the mitochondrial density is reduced to levels as low as 10% of normal within 2–3 days and cellular substrate metabolism is impaired. The author of this paper proposes that treatment modalities in clinical nutrition should primarily aim at improving muscle function and restoring muscle membrane potential and that these variables should be used as the primary outcome variables of clinical trials. Attempts to modify these measurements such that they can be used routinely in the ICU setting are ongoing in our group. Muscle protein and substrate metabolism can only be normalized when these primary variables have successfully been restored. The use of muscle relaxants may lead to a functional denervation of the muscle, to changes in the molecular structure of the myofibrils and may postpone a successfull recovery. Learning objectives:• Causes of muscle weakness and loss of contractility in ICU patients;• Relation between loss of contractility and impairments in muscle metabolism;• Muscle function as an endpoint variable for clinical nutrition interventions.