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Studies of extreme endurance have suggested that there is an alimentary limit to energy intake (EI) of ∼2.5 × resting metabolic rate (RMR). To gain further insight, this study aimed to simultaneously measure EI, total energy expenditure (TEE) body mass and muscle mass in a large cohort of males and females of varying ages during a transatlantic rowing race. Forty‐nine competitors (m = 32, f = 17; age 24–67 years; time at sea 46 ± 7 days) in the 2020 and 2021 Talisker Whisky Atlantic Challenge rowed 12–18 hday−1 for ∼3000 miles. TEE was assessed in the final week of the row using 2H218O doubly labelled water, and EI was analysed from daily ration packs over this period. Thickness of relatively active (vastus lateralis, intermedius, biceps brachaii and rectus abdominus) and inactive (gastrocnemius, soleus and triceps) muscles was measured pre (<7 days) and post (<24 h) row using ultrasound. Body mass was measured and used to calculate RMR from standard equations. There were no sex differences in males and females in EI (2.5 ± 0.5 and 2.3 ± 0.4 × RMR, respectively, P = 0.3050), TEE (2.5 ± 1.0 and 2.3 ± 0.4 × RMR, respectively, P = 0.5170), or body mass loss (10.2 ± 3.1% and 10.0 ± 3.0%, respectively, P = 0.8520), and no effect of age on EI (P = 0.5450) or TEE (P = 0.9344). Muscle loss occurred exclusively in the calf (15.7% ± 11.4% P < 0.0001), whilst other muscles remained unchanged. After 46 days of prolonged ultra‐endurance ocean rowing incurring 10% body mass loss, maximal sustainable EI of ∼2.5 × RMR was unable to meet total TEE suggesting that there is indeed a physiological capacity to EI. What is the central question of this study?During a prolonged endurance transatlantic ocean rowing race over ∼46 days, what changes occur in energy intake (EI), total energy expenditure (TEE) and body mass and are there differences between males and females or an effect of age?What is the main finding and its importance?During a ∼46 days, there appeared to be a maximal sustainable EI of ∼2.5 × resting metabolic rate (RMR), matching TEE of 2.5 × RMR, incurring a 10% body mass loss There were no sex differences, and minimal influence of age. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions High‐protein diets have been recognized as a potential strategy in the nutritional management of type 2 diabetes (T2D). Mycoprotein is a high‐fibre, high‐protein food ingredient previously shown to improve acute glycaemic control. We determined whether incorporating mycoprotein into a high‐protein vegan diet would improve glycaemic control to a greater extent than an isonitrogenous omnivorous diet in people with T2D.Seventeen adults (f = 5, age = 58.3 ± 8.3 years, BMI = 32.9 ± 4.7 kg∙m−2, HbA1c = 60 ± 15 mmol∙mol−1) with T2D were randomly allocated to a 5‐week eucaloric high‐protein (30% energy from protein) diet, either an omnivorous diet (OMNI; 70% protein from omnivorous sources) or an isonitrogenous, mycoprotein‐rich, vegan diet (VEG; 50% protein from mycoprotein). Glycaemic control was assessed using a two‐step hyperinsulinaemic‐euglycaemic clamp (HEC) with D‐[6,6‐2H2] glucose infusion, a mixed‐meal tolerance test (MMTT) and continuous glucose monitoring.The rate of glucose disappearance (RdT), glucose disposal rate and endogenous glucose production, as well as postprandial time‐course of blood glucose, serum insulin and C‐peptide were assessed during the HEC and MMTT, respectively. Both groups had improved peripheral insulin sensitivity (intervention effect, p = 0.006; increased RdT/Insulin of 1.0 ± 0.6 and 1.0 ± 0.3 mg kg−1 min−1 in OMNI and VEG, respectively), HbA1c (intervention; p = 0.001) and glycaemic variability (intervention; p = 0.040; increased time in‐range of 11.8 ± 9.3% and 23.3 ± 12.9% in OMNI and VEG). There were no improvements in hepatic insulin sensitivity or in postprandial blood glucose and serum C‐peptide (p > 0.05) during the MMTT.High‐protein diets, whether predicated on vegan or omnivorous proteins, can improve glycaemic control by increasing peripheral insulin sensitivity in people with T2D. [ABSTRACT FROM AUTHOR]

The article focuses on a research study which examined the roles of two muscle-specific ubiquitin ligases, MuRF1 and MAFbx, in muscle atrophy. It outlines the mechanisms responsible for the loss of muscle protein content. It observes the role of both MAFbx and MuRF1 in the loss of muscle mass following dexamethasone administration.