BackgroundICU patients lose muscle mass rapidly and maintenance of muscle mass may contribute to improved survival rates and quality of life. Protein provision may be beneficial for preservation of muscle mass and other clinical outcomes, including survival. Current protein recommendations are expert-based and range from 1.2 to 2.0 g/kg. Thus, we performed a systematic review and meta-analysis on protein provision and all clinically relevant outcomes recorded in the available literature.MethodsWe conducted a systematic review and meta-analyses, including studies of all designs except case control and case studies, with patients aged ≥18 years with an ICU stay of ≥2 days and a mean protein provision group of ≥1.2 g/kg as compared to <1.2 g/kg with a difference of ≥0.2 g/kg between protein provision groups. All clinically relevant outcomes were studied. Meta-analyses were performed for all clinically relevant outcomes that were recorded in ≥3 included studies.ResultsA total of 29 studies published between 2012 and 2022 were included. Outcomes reported in the included studies were ICU, hospital, 28-day, 30-day, 42-day, 60-day, 90-day and 6-month mortality, ICU and hospital length of stay, duration of mechanical ventilation, vomiting, diarrhea, gastric residual volume, pneumonia, overall infections, nitrogen balance, changes in muscle mass, destination at hospital discharge, physical performance and psychological status. Meta-analyses showed differences between groups in favour of high protein provision for 60-day mortality, nitrogen balance and changes in muscle mass.ConclusionHigh protein provision of more than 1.2 g/kg in critically ill patients seemed to improve nitrogen balance and changes in muscle mass on the short-term and likely 60-day mortality. Data on long-term effects on quality of life are urgently needed.
MULTIFILE
Background: Lipoedema is a chronic disorder of adipose tissue typically involving an abnormal build-up of fat cells in the legs, thighs and buttocks. Occurring almost exclusively in women, it often co-exists with obesity. Due to an absence of clear objective diagnostic criteria, lipoedema is frequently misdiagnosed as obesity, lymphoedema or a combination of both. The purpose of this observational study was to compare muscle strength and exercise capacity in patients with lipoedema and obesity, and to use the findings to help distinguish between lipoedema and obesity. Design: This cross-sectional, comparative pilot study performed in the Dutch Expertise Centre of Lymphovascular Medicine, Drachten, a secondary-care facility, included 44 women aged 18 years or older with lipoedema and obesity. Twenty-two women with lipoedema (diagnosed according the criteria of Wold et al, 1951) and 22 women with body mass index ≥30kg/m2 (obesity) were include in the study. No interventions were undertaken as part of the study. Results: Muscle strength of the quadriceps was measured with the MicroFET™, and functional exercise capacity was measured with the 6-minute walk test. The group with lipoedema had, for both legs, significantly lower muscle strength (left: 259.9 Newtons [N]; right: 269.7 N; p < 0.001) than the group with obesity. The group with lipoedema had a non-significant, but clinically relevant lower exercise-endurance capacity (494.1±116.0 metres) than the group with obesity (523.9±62.9 metres; p=0.296). Conclusions: Patients with lipoedema exhibit muscle weakness in the quadriceps. This finding provides a potential new criterion for differentiating lipoedema from obesity. We recommend adding measuring of muscle strength and physical endurance to create an extra diagnostic parameter when assessing for lipoedema.
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Insulin sensitivity and metabolic flexibility decrease in response to bed rest, but the temporal and causal adaptations in human skeletal muscle metabolism are not fully defined. Here, we use an integrative approach to assess human skeletal muscle metabolism during bed rest and provide a multi-system analysis of how skeletal muscle and the circulatory system adapt to short- and long-term bed rest (German Clinical Trials: DRKS00015677). We uncover that intracellular glycogen accumulation after short-term bed rest accompanies a rapid reduction in systemic insulin sensitivity and less GLUT4 localization at the muscle cell membrane, preventing further intracellular glycogen deposition after long-term bed rest. We provide evidence of a temporal link between the accumulation of intracellular triglycerides, lipotoxic ceramides, and sphingomyelins and an altered skeletal muscle mitochondrial structure and function after long-term bed rest. An intracellular nutrient overload therefore represents a crucial determinant for rapid skeletal muscle insulin insensitivity and mitochondrial alterations after prolonged bed rest.
