In patients with nonhypercapnic acute hypoxemic respiratory failure, treatment with high-flow oxygen, standard oxygen, or noninvasive ventilation did not result in significantly different intubation rates. There was a significant difference in favor of high-flow oxygen in 90-day mortality. (Funded by the Programme Hospitalier de Recherche Clinique Interrégional 2010 of the French Ministry of Health; FLORALI ClinicalTrials.gov number, NCT01320384.).

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Substantial evidence supports the increased consumption of high-quality protein to achieve optimal health outcomes. A growing body of research indicates that protein intakes well above the current Recommended Dietary Allowance help to promote healthy aging, appetite regulation, weight management, and goals aligned with athletic performance. Higher protein intakes may help prevent age-related sarcopenia, the loss of muscle mass, and strength that predisposes older adults to frailty, disability, and loss of autonomy. Higher protein diets also improve satiety and lead to greater reductions in body weight and fat mass compared with standard protein diets, and may therefore serve as a successful strategy to help prevent and/or treat obesity. Athletes can also benefit from higher protein intakes to maximize athletic performance given the critical role protein plays in stimulating muscle protein remodelling after exercise. Protein quality, per meal dose, and timing of ingestion are also important considerations. Despite persistent beliefs to the contrary, we can find no evidence-based link between higher protein diets and renal disease or adverse bone health. This brief synopsis highlights recent learnings based on presentations at the 2015 Canadian Nutrition Society conference, Advances in Protein Nutrition across the Lifespan. Current evidence indicates intakes in the range of at least 1.2 to 1.6 g/(kg·day) of high-quality protein is a more ideal target for achieving optimal health outcomes in adults.Key words: protein, protein recommendations, protein quality, sarcopenia, elderly, weight management, obesity, muscle, athletes, exercise, satiety.Résumé : Beaucoup d'études probantes appuient la thèse selon laquelle l'augmentation de la consommation de protéines de haute qualité améliore la santé. De plus en plus d'études rapportent qu'une consommation de protéines bien supérieure aux rations alimentaires recommandées favorise le vieillissement en santé, la régulation de l'appétit, le contrôle du poids et les objectifs en matière de performance sportive. Une plus grande consommation de protéines pourrait prévenir la sarcopénie associée à l'âge, la perte de masse musculaire et de force musculaire qui prédispose les personnes âgées à la fragilité, l'incapacité et la perte de l'autonomie. Un régime alimentaire riche en protéines améliore la satiété et favorise une plus grande diminution de la masse corporelle et graisseuse comparativement aux régimes protéiques standards et pourrait constituer une stratégie gagnante pour la prévention et le traitement de l'obésité. Les athlètes ont aussi à gagner en consommant plus de protéines afin de maximiser leur performance sportive compte tenu du rôle essentiel des protéines dans la stimulation du remodelage des protéines musculaires à la suite de l'exercice physique. La qualité des protéines, la dose par repas et le moment de la consommation sont aussi à prendre en compte. Malgré les croyances ancrées du contraire, on ne trouve aucune donnée probante présentant une associa...

Fibromyalgia (FM) is a prevalent syndrome, characterised by chronic widespread pain, fatigue, and impaired sleep, that is challenging to diagnose and difficult to treat. The microbiomes of 77 women with FM and that of 79 control participants were compared using 16S rRNA gene amplification and whole-genome sequencing. When comparing FM patients with unrelated controls using differential abundance analysis, significant differences were revealed in several bacterial taxa. Variance in the composition of the microbiomes was explained by FM-related variables more than by any other innate or environmental variable and correlated with clinical indices of FM. In line with observed alteration in butyrate-metabolising species, targeted serum metabolite analysis verified differences in the serum levels of butyrate and propionate in FM patients. Using machine-learning algorithms, the microbiome composition alone allowed for the classification of patients and controls (receiver operating characteristic area under the curve 87.8%). To the best of our knowledge, this is the first demonstration of gut microbiome alteration in nonvisceral pain. This observation paves the way for further studies, elucidating the pathophysiology of FM, developing diagnostic aids and possibly allowing for new treatment modalities to be explored.

OBJECTIVE-We previously demonstrated that 1) obesity impairs and 2) sex influences insulin sensitivity of protein metabolism, while 3) poor glycemic control in type 2 diabetes accelerates protein turnover in daily fed-fasted states. We hypothesized that type 2 diabetes alters the insulin sensitivity of protein metabolism and that sex modulates it. RESEARCH DESIGN AND METHODS-Hyperinsulinemic(ϳ570 pmol/l), euglycemic (5.5 mmol/l), and isoaminoacidemic (kept at postabsorptive concentrations) clamps were performed in 17 hyperglycemic type 2 diabetic subjects and 23 subjects without diabetes matched for age and body composition, after 7 days on a inpatient, protein-controlled, isoenergetic diet. Glucose and leucine kinetics were determined using tracers.RESULTS-In type 2 diabetes, postabsorptive (baseline) glycemia was 8 -9 mmol/l, glucose production (R a ) and disposal (R d ) were elevated, and once clamped, endogenous glucose R a remained greater and R d was less (P Ͻ 0.05) than in control subjects. Baseline leucine kinetics did not differ despite higher insulin levels. The latter was an independent predictor of leucine flux within each sex. With clamp, total flux increased less (P ϭ 0.016) in type 2 diabetic men, although protein breakdown decreased equally (ϳ20%) in male groups but less in female groups. Whereas protein synthesis increased in male control subjects and in both female groups, it did not in male subjects with type 2 diabetes. In men, homeostasis model assessment of insulin resistance predicted 44%, and, in women, waist-to-hip ratio predicted 40% of the change in synthesis. T here is clear evidence for altered protein metabolism in type 1 diabetes (1-5), but in type 2 diabetes, results have been inconsistent. That protein metabolism in type 2 diabetes has been reported to be both unaffected and altered may stem from differences in study design: tracer method, adiposity, and sex of subjects; prevailing glycemia; normalization of data; and types of statistical analyses. We reported accelerated integrated fed-fasted kinetics of whole-body protein metabolism (using [ 15 N]glycine) in obese type 2 diabetic subjects with hyperglycemia (6 -9) compared with obese control subjects (6,7). Such studies required adjusting data for fat-free mass (FFM), sex, and age (6,8,9) and had precise control of protein and energy intake. When glycemic control was normalized with insulin (7), improved with oral antihyperglycemic agents (6), or normalized with oral agents and energy restriction (6), protein turnover was either improved or not different from that of obese control subjects. CONCLUSIONS-DuringMost reports showing no alterations in type 2 diabetes (10 -14) assessed postabsorptive and postinsulin states using amino acid tracers. However, one reported elevated postabsorptive catabolism in hyperglycemic type 2 diabetic patients, not corrected by prior insulin treatment (15). Another showed elevated rates of leucine transamination that decreased with better glycemic control, without altering leucine oxidation (16)....

Our results suggest that greater protein intakes and a more even distribution across meals are modifiable factors associated with higher muscle mass in older adults but not with losses over 2 y. Interventional studies should determine longer-term effects on preserving LM with aging.

BackgroundThe exact impact of ageing on skeletal muscle phenotype and mitochondrial and lipid content remains controversial, probably because physical activity, which greatly influences muscle physiology, is rarely accounted for. The present study was therefore designed to investigate the effects of ageing, physical activity, and pre‐frailty on skeletal muscle phenotype, and mitochondrial and intramyocellular lipid content in men.MethodsRecreationally active young adult (20–30 yo; YA); active (ACT) and sedentary (SED) middle‐age (50–65 yo; MA‐ACT and MA‐SED); and older (65 + yo; 65 + ACT and 65 + SED) and pre‐frail older (65 + PF) men were recruited. Muscle biopsies from the vastus lateralis were collected to assess, on muscle cross sections, muscle phenotype (using myosin heavy chain isoforms immunolabelling), the fibre type‐specific content of mitochondria (by quantifying the succinate dehydrogenase stain intensity), and the fibre type‐specific lipid content (by quantifying the Oil Red O stain intensity).ResultsOnly 65 + SED and 65 + PF displayed significantly lower overall and type IIa fibre sizes vs. YA. 65 + SED displayed a lower type IIa fibre proportion vs. YA. MA‐SED and 65 + SED displayed a higher hybrid type IIa/IIx fibre proportion vs. YA. Sedentary and pre‐frail, but not active, men displayed lower mitochondrial content irrespective of fibre type vs. YA. 65 + SED, but not 65 + ACT, displayed a higher lipid content in type I fibres vs. YA. Finally, mitochondrial content, but not lipid content, was positively correlated with indices of muscle function, functional capacity, and insulin sensitivity across all subjects.ConclusionsTaken altogether, our results indicate that ageing in sedentary men is associated with (i) complex changes in muscle phenotype preferentially affecting type IIa fibres; (ii) a decline in mitochondrial content affecting all fibre types; and (iii) an increase in lipid content in type I fibres. They also indicate that physical activity partially protects from the effects of ageing on muscle phenotype, mitochondrial content, and lipid accumulation. No skeletal specific muscle phenotype of pre‐frailty was observed.

Elevations of plasma methylarginines in obesity and ageing are related to insulin sensitivity and rates of protein turnover Abstract Aims/hypothesis: Increased circulating methylarginines (MA) have been linked to the metabolic syndrome to explain endothelial dysfunction and cardiovascular disease risk. Proteins that contain MA are regulatory and release them during catabolism. We hypothesised that increased protein turnover in insulin-resistant states contributes to an increase in circulating MA. Materials and methods: We performed hyperinsulinaemic, euglycaemic, and isoaminoacidaemic experiments on 49 lean, obese and elderly subjects, with measurements of the kinetics of glucose and protein metabolism. Plasma MA, i.e. asymmetrical dimethylarginine (ADMA), symmetrical dimethylarginine (SDMA), and N G -monomethyl-L-arginine (NMMA), lipids and body composition were measured. Results: Insulin resistance of glucose and protein metabolism occurred in obese and elderly subjects. ADMA concentrations were 29 to 120% higher in obese and 34% higher in elderly than in lean subjects. SDMA were 34 and 20% higher in obese than in lean and than in elderly subjects, respectively. NMMA were 32% higher in obese than in lean subjects. ADMA differed by sex, being higher in men, namely by 1.75× in obese men and by 1.27× in elderly men. Postabsorptive ADMA (r=0.71), SDMA (r=0.46), and NMMA (r=0.31) correlated (all p<0.05) with rates of protein flux. All three MA correlated negatively with clamp glucose infusion rates and uptake (p<0.001). ADMA and SDMA correlated negatively with net protein synthesis and clamp amino acid infusion rates (p<0.05). All MA also correlated with adiposity indices and fasting insulin and triglycerides (p<0.05). Conclusions/ interpretation: Obesity, sex and ageing affect MA. Elevations of the three MA in obese, and of ADMA in elderly men, are related to increased protein turnover and to lesser insulin sensitivity of protein metabolism. These interrelationships might amplify insulin resistance and endothelial dysfunction.