Soya–dairy protein blends can extend post-exercise muscle synthesis in young people more than whey protein control. Older adults differ metabolically from young people, and their ability to absorb amino acids from dietary protein is important for muscle function. The objective was to determine how protein source affects postprandial plasma amino acid response and/or metabolomic profile in older adults via a single-blind randomised crossover trial (n 16, males 50–70 years), using three nutritionally equivalent meal replacement drinks containing 30 g protein, from a 1:1 (mass ratio) soya:dairy blend, a 1:2 soya:dairy blend or whey protein. The outcome measures were plasma amino acid concentrations at 0–300 min postprandially and urine metabolomic fingerprint. Soya:dairy drinks gave similar amino acid response in plasma over time and similar urinary metabolite fingerprints. However, there were significant differences in plasma amino acid concentrations and AUC values for the soya:dairy drinks v. the whey protein drink. AUC for Leu, Trp and Lys was lower and AUC for Phe and Pro was higher for the soya:dairy drinks. Differences partly reflected the amino acid profiles of the drinks, but overall plasma amino acid response patterns were qualitatively unchanged. Plasma amino acid differences between the whey protein drink and the soya:dairy blends were reflected in urine metabolite patterns. In conclusion, postprandial plasma amino acid responses were broadly similar, irrespective of protein source (and soya:dairy ratio). There were significant differences for some plasma amino acid concentrations, reflecting different amino acid profiles of the protein source and influencing urine metabolite fingerprints.

Sarcopenia is a core contributor to several health consequences, including falls, fractures, physical limitations and disability. The pathophysiological processes of sarcopenia may be counteracted with the proper diet, delaying sarcopenia onset. Dietary pattern analysis is a whole diet approach used to investigate the relationship between diet and sarcopenia. Here, we aimed to investigate this relationship in an elderly Chinese population. A cross-sectional study with 2423 participants aged more than 60 years was performed. Sarcopenia was defined based on the guidelines of the Asian Working Group for Sarcopenia, composed of low muscle mass plus low grip strength and/or low gait speed. Dietary data were collected using a FFQ that included questions on 100 food items along with their specified serving sizes. Three dietary patterns were derived by factor analysis: sweet pattern, vegetable pattern and animal food pattern. The prevalence of sarcopenia was 16·1 %. The higher vegetable pattern score and animal food pattern score were related to lower prevalence of sarcopenia (Ptrend = 0·006 and < 0·001, respectively); the multivariate-adjusted OR of the prevalence of sarcopenia in the highest v. lowest quartiles were 0·54 (95 % CI 0·34, 0·86) and 0·50 (95 % CI 0·33, 0·74), separately. The sweet pattern score was not significantly related to the prevalence of sarcopenia. The present study showed that vegetable pattern and animal food pattern were related to a lower prevalence of sarcopenia in Chinese older adults. Further studies are required to clarify these findings.

The effect and the mechanism of high glucose on fish muscle cells are not fully understood. In the present study, muscle cells of olive flounder (Paralichthys olivaceus) were treated with high glucose (33 mM) in vitro. Cells were incubated in three kinds of medium containing 5 mM glucose, 5 mM glucose and 28 mM mannitol (as an isotonic contrast) or 33 mM glucose named the Control group, the Mannitol group and the high glucose (HG) group, respectively. Results showed that high glucose increased the ADP:ATP ratio and the reactive oxygen species (ROS) level, decreased mitochondrial membrane potential (MMP), induced the release of cytochrome C (CytC) and cell apoptosis. High glucose also led to cell glycogen accumulation by increasing the glucose uptake ability and affecting the mRNA expressions of glycogen synthase and glycogen phosphorylase. Meanwhile, it activated AMP-activated protein kinase (AMPK), inhibited the activity of mammalian target of rapamycin (mTOR) signalling pathway and the expressions of myogenic regulatory factors (MRF). The expressions of myostatin-1 (mstn-1) and E3 ubiquitin ligases including muscle RING-finger protein 1 (murf-1) and muscle atrophy F-box protein (mafbx) were also increased by the high glucose treatment. No difference was found between the Mannitol group and the Control group. These results demonstrate that high glucose has the effects of inducing apoptosis, increasing glycogen accumulation and inhibiting protein synthesis on muscle cells of olive flounder. The mitochondria-mediated apoptotic signalling pathway, AMPK and mTOR pathways participated in these biological effects.

A moderate surplus of the one carbon (1C) nutrients methionine, folic acid, vitamin B6 and B12 above dietary recommendations for Atlantic salmon has shown to improve growth and reduce hepatosomatic index in the on-growing saltwater period when fed throughout smoltification. Metabolic properties and molecular mechanisms determining the improved growth are unexplored. Here, we investigate metabolic and transcriptional signatures in skeletal muscle taken before and after smoltification to acquire deeper insight into pathways and possible nutrient–gene interactions. A control feed (Ctrl) or 1C nutrient surplus feed (1C+) were fed to Atlantic salmon 6 weeks prior to smoltification until 3 months after saltwater transfer. Both metabolic and gene expression signatures revealed significant 1C nutrient-dependent changes already at pre-smolt, but differences intensified when analysing post-smolt muscle. Transcriptional differences revealed lower expression of genes related to translation, growth and amino acid metabolisation in post-smolt muscle when fed additional 1C nutrients. The 1C+ group showed less free amino acid and putrescine levels, and higher methionine and glutathione amounts in muscle. For Ctrl muscle, the overall metabolic profile suggests a lower amino acid utilisation for protein synthesis, and increased methionine metabolisation in polyamine and redox homoeostasis, whereas transcription changes are indicative of compensatory growth regulation at local tissue level. These findings point to fine-tuned nutrient–gene interactions fundamental for improved growth capacity through better amino acid utilisation for protein accretion when salmon was fed additional 1C nutrients throughout smoltification. It also highlights potential nutritional programming strategies on improved post-smolt growth through 1C+ supplementation before and throughout smoltification.

Sarcopenia, a skeletal muscle disorder that is characterised by loss of muscle strength and mass, is common in older populations and associated with poorer health outcomes. Although the individual and economic costs of sarcopenia are widely recognised, current understanding of its pathophysiology is incomplete, limiting efforts to translate research evidence into effective preventive and treatment strategies. While nutrition is a key field of sarcopenia research, the role of differences in habitual diets, and the effectiveness of dietary change as a prevention or treatment strategy, is uncertain. There is a growing evidence base that links low micronutrient intakes to sarcopenia risk and/or its components (low muscle strength and mass, impaired physical performance), although there remain many gaps in understanding. There is some consistency in findings across studies highlighting potential roles for antioxidant nutrients, B vitamins and magnesium; however, the evidence is largely observational and from cross-sectional studies, often describing associations with different muscle outcomes. As low intakes of some micronutrients are common in older populations, there is a need for new research, particularly from well-characterised prospective cohorts, to improve the understanding of their role and importance in the aetiology of sarcopenia and to generate the evidence needed to inform dietary guidelines to promote muscle health.

Ageing is associated with reduced muscle mass, strength, flexibility and balance, resulting in a poor quality of life (QOL). Past studies have occurred in highly controlled laboratory settings which provide strong support to determine whether similar gains can be made in community programmes. Twenty participants were enrolled in an eight-week community-based resistance training programme (mean age = 61.3 (standard error (SE) = 0.9) years); Body Mass Index = 32.0 (SE = 1.3) kg/m2). All participants completed surveys to assess outcomes associated with QOL. Given the relationship between muscle function and nerve health, nerve conduction studies (NCS) were also conducted in a separate group of participants (mean age = 64.9 (SE = 2.0) years; Body Mass Index = 32.6 (SE = 1.9) kg/m2). This community-based training programme significantly improved QOL measures in older adults (p < 0.001). Although weight loss was not the primary outcome of the study, participants reduced their body weights (p < 0.001), by primarily reducing fat mass (p = 0.007) while maintaining muscle mass. Significant improvements were observed in muscle strength (2.2%), flexibility and balance (3.2–464.2%, p ⩽ 0.05 for all). Improvements were also observed in plasma glucose (p = 0.05), haemoglobin A1C (p = 0.06) and aldolase enzyme levels (p < 0.001). Scores for surveys on memory and sleep improved (p < 0.05). Improved QOL was associated with increased lean mass (r = −0.714, p = 0.002), decreased fat mass (r = −0.702, p = 0.003) and improved flexibility and balance (r = −0.627, p = 0.008). An eight-week, community-based resistance training programme significantly improved QOL in older adults. Influence on the lipid profile and NCS still needs further investigation.

Se, an essential biological trace element, is required for fish growth. However, the underlying mechanisms remain unclear. Protein deposition in muscle is an important determinant for fish growth. This study was conducted on juvenile rainbow trout (Oncorhynchus mykiss) to explore the nutritional effects of Se on protein deposition in fish muscle by analysing the postprandial dynamics of both protein synthesis and protein degradation. Trout were fed a basal diet supplemented with or without 4 mg/kg Se (as Se yeast), which has been previously demonstrated as the optimal supplemental level for rainbow trout growth. After 6 weeks of feeding, dietary Se supplementation exerted no influence on fish feed intake, whereas it increased fish growth rate, feed efficiency, protein retention rate and muscle protein content. Results of postprandial dynamics (within 24 h after feeding) of protein synthesis and degradation in trout muscle showed that dietary Se supplementation led to a persistently hyperactivated target of rapamycin complex 1 pathway and the suppressive expression of numerous genes related to the ubiquitin–proteasome system and the autophagy–lysosome system after the feeding. However, the ubiquitinated proteins and microtubule-associated light chain 3B (LC3)-II:LC3-I ratio, biomarkers for ubiquitination and autophagy activities, respectively, exhibited no significant differences among the fish fed different experimental diets throughout the whole postprandial period. Overall, this study demonstrated a promoting effect of nutritional level of dietary Se on protein deposition in fish muscle by accelerating postprandial protein synthesis. These results provide important insights about the regulatory role of dietary Se in fish growth.

Obesity is a major public health issue with prevalence increasing worldwide. Obesity is a well-established risk factor for CVD and mortality in adult populations. However, the impact of being overweight or obese in the elderly on CVD and mortality is controversial. Some studies even suggest that overweight and obesity, measured by BMI, are apparently associated with a decreased mortality risk (known as the obesity paradox). Ageing is associated with an increase in visceral fat and a progressive loss of muscle mass. Fat mass is positively associated and lean mass is negatively associated with risk of mortality. Therefore, in older adults BMI is not a good indicator of obesity. Sarcopenia has been defined as the degenerative loss of muscle mass, quality and strength with age and is of major concern in ageing populations. Sarcopenia has previously been associated with increased risks of metabolic impairment, cardiovascular risk factors, physical disability and mortality. It is possible for sarcopenia to co-exist with obesity, and sarcopenic obesity is a new class of obesity in older adults who have high adiposity levels together with low muscle mass, quality or strength. Therefore, sarcopenia with obesity may act together to increase their effect on metabolic disorders, CVD and mortality. This review will discuss the available evidence for the health implications of sarcopenic obesity on CVD and mortality in older adults.

A 32-year-old male presents with diffuse myalgias, weakness, and dark urine for 1 day. The patient states he recently started a new exercise program. He is hemodynamically stable, and his physical examination reveals diffuse muscle tenderness. His creatine kinase (CK) returns at 8,000 international units per liter (IU/L), and his urinalysis reveals blood but only three red blood cells (RBCs) on microscopy.

Lamb live weight is one of the key drivers of profitability on sheep farms. Previous studies in Ireland have estimated genetic parameters for live weight and carcass composition traits using a multi-breed population rather than on an individual breed basis. The objective of the present study was to undertake genetic analyses of three lamb live weight and two carcass composition traits pertaining to purebred Texel, Suffolk and Charollais lambs born in the Republic of Ireland between 2010 and 2017, inclusive. Traits (with lamb age range in parenthesis) considered in the analyses were: pre-weaning weight (20 to 65 days), weaning weight (66 to 120 days), post-weaning weight (121 to 180 days), muscle depth (121 to 180 days) and fat depth (121 to 180 days). After data edits, 137 402 records from 50 372 lambs across 416 flocks were analysed. Variance components were derived using animal linear mixed models separately for each breed. Fixed effects included for all traits were contemporary group, age at first lambing of the dam, parity of the dam, a gender by age of the lamb interaction and a birth type by rearing type of the lamb interaction. Random effects investigated in the pre-weaning and weaning weight analyses included animal direct additive genetic, dam maternal genetic, litter common environment, dam permanent environment and residual variances. The model of analysis for post-weaning, muscle and fat depth included an animal direct additive genetic and litter common environment effect only. Significant direct additive genetic variation existed in all cases. Direct heritability for pre-weaning weight ranged from 0.14 to 0.30 across the three breeds. Weaning weight had a direct heritability ranging from 0.17 to 0.27 and post-weaning weight had a direct heritability ranging from 0.15 to 0.27. Muscle and fat depth heritability estimates ranged from 0.21 to 0.31 and 0.15 to 0.20, respectively. Positive direct correlations were evident for all traits. Results revealed ample genetic variation among animals for the studied traits and significant differences between breeds to suggest that genetic evaluations could be conducted on a per-breed basis.

The experiment was conducted to investigate the effects of dietary threonine (Thr) on growth performance and muscle growth, protein synthesis and antioxidant-related signalling pathways of hybrid catfish Pelteobagrus vachelli♀ × Leiocassis longirostris♂. A total of 1200 fish (14·19 (se 0·13) g) were randomly distributed into six groups with four replicates each, fed six diets with graded level of Thr (9·5, 11·5, 13·5, 15·4, 17·4 and 19·3 g/kg diets) for 56 d. Results showed (P < 0·05) that dietary Thr (1) increased percentage weight gain, specific growth rate, feed efficiency and protein efficiency ratio; (2) up-regulated growth hormone (GH), insulin-like growth factor 1 (IGF-1), proliferating cell nuclear antigen, myogenic regulation factors (MyoD, Myf5, MyoG and Mrf4) and myosin heavy chain (MyHC) mRNA levels; (3) increased muscle protein content via regulating the protein kinase B/target of rapamycin signalling pathway and (4) decreased malondialdehyde and protein carbonyl contents, increased catalase, glutathione-S-transferase, glutathione reductase and GSH activities, up-regulated mRNA levels of antioxidant enzymes related to NFE2-related factor 2 and γ-glutamylcysteine ligase catalytic subunit. These results suggest that Thr has a potential role to improve muscle growth and protein synthesis, which might be due to the regulation of GH-IGF system, muscle growth-related gene, antioxidative capacity and protein synthesis-related signalling pathways. Based on the quadratic regression analysis of specific growth rate, the Thr requirement of hybrid catfish (14·19–25·77 g) was estimated to be 13·77 g/kg of the diet (33·40 g/kg of dietary protein).

Meat and dairy products derived from grassland carry premium values and sensory and nutritional qualities that aroused much interest for authentication methods to guarantee grassland origin claims. This article reviews the current state of knowledge on the authentication of meat and dairy of grassland origin from food analysis in both cattle and sheep. A range of methods alone or combined, involving analysis of elemental or molecular constituents of food product and fingerprinting profiling combined with chemometrics, have been developed and proved useful to differentiate contrasted feeding regimes and authenticate grass-fed meat and dairy. Their robustness and discriminatory reliability in more complex feeding conditions, such as in the case of dietary switches or when grass only makes up part of the animal’s diet, are under active investigation. Our review highlights the possibilities and limitations of these methods, the latter being chiefly posed by variations in the quantity, characteristics and composition of grassland feedstuffs consumed by animals, which are nevertheless inherent to grassland-based production systems, variations in animal responses within and across breeds, and difficulties in detecting the consumption of non-grass feedstuffs by the animal. It also highlights a number of issues for consideration, points of caution and caveats in applying these methods. Scientists agree that much of the research carried out so far has been a ‘proof of concept’ type and that efforts should be made in the future to develop more databases to help gain genericity and robustness.

Vitamin D receptor expression and associated function have been reported in various muscle models, including C2C12, L6 cell lines and primary human skeletal muscle cells. It is believed that 1,25-hydroxyvitamin D3 (1,25(OH)2D3), the active form of vitamin D, has a direct regulatory role in skeletal muscle function, where it participates in myogenesis, cell proliferation, differentiation, regulation of protein synthesis and mitochondrial metabolism through activation of various cellular signalling cascades, including the mitogen-activated protein kinase pathway(s). It has also been suggested that 1,25(OH)2D3 and its associated receptor have genomic targets, resulting in regulation of gene expression, as well as non-genomic functions that can alter cellular behaviour through binding and modification of targets not directly associated with transcriptional regulation. The molecular mechanisms of vitamin D signalling, however, have not been fully clarified. Vitamin D inadequacy or deficiency is associated with muscle fibre atrophy, increased risk of chronic musculoskeletal pain, sarcopenia and associated falls, and may also decrease RMR. The main purpose of the present review is to describe the molecular role of vitamin D in skeletal muscle tissue function and metabolism, specifically in relation to proliferation, differentiation and protein synthesis processes. In addition, the present review also includes discussion of possible genomic and non-genomic pathways of vitamin D action.