Abstract
BackgroundThere is extensive documentation on skeletal muscle protein depletion during the initial phase of critical illness. However, for intensive care unit (ICU) long-stayers, objective data are very limited. In this study, we examined skeletal muscle protein and amino acid turnover in patients with a prolonged ICU stay.MethodsPatients (n = 20) were studied serially every 8–12 days between days 10 and 40 of their ICU stay as long as patients stayed in the ICU. Leg muscle protein turnover was assessed by measurements of phenylalanine kinetics, for which we employed a stable isotope-labeled phenylalanine together with two-pool and three-pool models for calculations, and results were expressed per 100 ml of leg volume. In addition, leg muscle amino acid flux was studied.ResultsThe negative leg muscle protein net balance seen on days 10–20 of the ICU stay disappeared by days 30–40 (p = 0.012). This was attributable mainly to an increase in the de novo protein synthesis rate (p = 0.007). It was accompanied by an attenuated efflux of free amino acids from the leg. Leg muscle protein breakdown rates stayed unaltered (p = 0.48), as did the efflux of 3-methylhistidine. The arterial plasma concentrations of free amino acids did not change over the course of the study.ConclusionsIn critically ill patients with sustained organ failure and in need of a prolonged ICU stay, the initial high rate of skeletal muscle protein depletion was attenuated over time. The distinction between the acute phase and a more prolonged and more stable phase concerning skeletal muscle protein turnover must be considered in study protocols as well as in clinical practice.Trial registrationAustralian New Zealand Trial Registry, ACTRN12616001012460. Retrospectively registered on 1 August 2016.
Highlights
There is extensive documentation on skeletal muscle protein depletion during the initial phase of critical illness
The protocol contained a measurement of skeletal muscle protein turnover as outlined below every tenth day (8–12 days) of the intensive care unit (ICU) stay, as long as the patient was in the ICU and the inclusion criteria were still met, leading to patients being studied serially one (n = 10), two (n = 9), or three (n = 1) times
In total, 30 measurements were performed in 20 patients with sustained multiple organ failure on days 10–40 of their ICU stay, with patients studied 1 (n = 10), 2 (n = 9), or 3 (n = 1) times
Summary
There is extensive documentation on skeletal muscle protein depletion during the initial phase of critical illness. Loss of muscle mass is a well-known phenomenon in critical illness. The loss of muscle mass and function is attributed to a combination of general inflammation, anabolic resistance, Several therapies are suggested and practiced to attenuate the loss of muscle mass and function, embracing the hypothesis that preserving this will smoothen recovery and improve outcomes. Nutritional interventions, on their own or in combination with general mobilization, bed exercise, electric stimulation, and pharmacologic interventions, are all examples of suggested treatment modalities [4]. The heterogeneity of diagnoses, comorbidities, and levels of fluid retention add to the complexity of studying muscle loss in critical illness
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