An exercise-inducible metabolite that suppresses feeding and obesity.

Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases1-5. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear6. Here we show that exercise stimulates the production of N-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity. The biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2+ cells, including macrophages, monocytes and other immune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure. Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training. Last, large activity-inducible increases in circulating Lac-Phe are also observed in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species. These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.

Postexercise muscle glycogen synthesis with glucose, galactose, and combined galactose-glucose ingestion.

Ingested galactose can enhance postexercise liver glycogen repletion when combined with glucose but effects on muscle glycogen synthesis are unknown. In this double-blind randomized study participants [7 men and 2 women; V̇o2max: 51.1 (8.7) mL·kg-1·min-1] completed three trials of exhaustive cycling exercise followed by a 4-h recovery period, during which carbohydrates were ingested at the rate of 1.2 g·kg-1·h-1 comprising glucose (GLU), galactose (GAL) or galactose + glucose (GAL + GLU; 1:2 ratio). The increase in vastus lateralis skeletal-muscle glycogen concentration during recovery was higher with GLU relative to GAL + GLU [contrast: +50 mmol·(kg DM)-1; 95%CL 10, 89; P = 0.021] and GAL [+46 mmol·(kg DM)-1; 95%CL 8, 84; P = 0.024] with no difference between GAL + GLU and GAL [-3 mmol·(kg DM)-1; 95%CL -44, 37; P = 0.843]. Plasma glucose concentration in GLU was not significantly different vs. GAL + GLU (+ 0.41 mmol·L-1; 95%CL 0.13, 0.94) but was significantly lower than GAL (-0.75 mmol·L-1; 95%CL -1.34, -0.17) and also lower in GAL vs. GAL + GLU (-1.16 mmol·-1; 95%CL -1.80, -0.53). Plasma insulin was higher in GLU + GAL and GLU compared with GAL but not different between GLU + GAL and GLU. Plasma galactose concentration was higher in GAL compared with GLU (3.35 mmol·L-1; 95%CL 3.07, 3.63) and GAL + GLU (3.22 mmol·L-1; 95%CL 3.54, 2.90) with no difference between GLU + GAL (0.13 mmol·L-1; 95%CL -0.11, 0.37) and GLU. Compared with galactose or a galactose + glucose blend, glucose feeding was more effective in postexercise muscle glycogen synthesis. Comparable muscle glycogen synthesis was observed with galactose-glucose coingestion and exclusive galactose-only ingestion.NEW & NOTEWORTHY Postexercise galactose-glucose coingestion or exclusive galactose-only ingestion resulted in a lower rate of skeletal-muscle glycogen replenishment compared with exclusive glucose-only ingestion. Comparable muscle glycogen synthesis was observed with galactose-glucose coingestion and exclusive galactose-only ingestion.

Co-Ingestion of Branched-Chain Amino Acids and Carbohydrate Stimulates Myofibrillar Protein Synthesis Following Resistance Exercise in Trained Young Men.

Branched-chain amino acids (BCAA) and carbohydrate (CHO) are commonly recommended postexercise supplements. However, no study has examined the interaction of CHO and BCAA ingestion on myofibrillar protein synthesis (MyoPS) rates following exercise. We aimed to determine the response of MyoPS to the co-ingestion of BCAA and CHO following an acute bout of resistance exercise. Ten resistance-trained young men completed two trials in counterbalanced order, ingesting isocaloric drinks containing either 30.6-g CHO plus 5.6-g BCAA (B + C) or 34.7-g CHO alone following a bout of unilateral, leg resistance exercise. MyoPS was measured postexercise with a primed, constant infusion of L-[ring13C6] phenylalanine and collection of muscle biopsies pre- and 4 hr postdrink ingestion. Blood samples were collected at time points before and after drink ingestion. Serum insulin concentrations increased to a similar extent in both trials (p > .05), peaking at 30 min postdrink ingestion. Plasma leucine (514 ± 34 nmol/L), isoleucine (282 ± 23 nmol/L), and valine (687 ± 33 nmol/L) concentrations peaked at 0.5 hr postdrink in B + C and remained elevated for 3 hr during exercise recovery. MyoPS was ∼15% greater (95% confidence interval [-0.002, 0.028], p = .039, Cohen's d = 0.63) in B + C (0.128%/hr ± 0.011%/hr) than CHO alone (0.115%/hr ± 0.011%/hr) over the 4 hr postexercise period. Co-ingestion of BCAA and CHO augments the acute response of MyoPS to resistance exercise in trained young males.

Desk based prompts to replace workplace sitting with stair climbing; a pilot study of acceptability, effects on behaviour and disease risk factors.

BACKGROUND: Prolonged sitting is associated with increased risk of obesity, type 2 diabetes and cardiovascular disease. Occupational sitting accounts for up to 50 h/week for employees. This pilot study assessed the acceptability of stair climbing as an interruption to sitting throughout working hours, and provided preliminary data of the effects on glucose and lipid profiles. METHODS: A quasi-experimental design was conducted involving 16 sedentary office workers (five females and 11 males) for intervention (n = 8) and control groups (n = 8) with mean age of 36.38 (5.58). For the eight-week intervention, a continuous four-floor stair climb and descent was performed eight times/day spread evenly over the working day. A prompt to climb was presented on the participant's computer eight times/day. Participants in the experimental group recorded daily floors climbed and steps (measured using pedometers) in a weekly log sheet. Blood samples were collected pre and post intervention to test effects on fasting glucose and 2 h plasma glucose, triglycerides, and total (TC), LDL and HDL cholesterol. Experimental participants were interviewed at the end of the study. The Wilcoxon signed rank test was used to compare the median changes (pre-post) of the dependent variables. RESULTS: On average, the experimental group climbed 121 floors/week when prompted. There were significant reductions in fasting blood glucose, TC and LDL, as well as the derived measures of 'bad' cholesterol and the TC/HDL ratio in the experimental group. Post-experimental interviews indicated that the interruption to sitting was well tolerated. CONCLUSION: Prompted stair climbing activity had impacts on health outcomes and was found acceptable to employees at work. TRIAL REGISTRATION: Ethics for this study was approved by Science, Technology, Engineering and Mathematics Ethical Review Committee, University of Birmingham with ethics reference number ERN_15_0491.

Increased exogenous but unaltered endogenous carbohydrate oxidation with combined fructose-maltodextrin ingested at 120 g h-1 versus 90 g h-1 at different ratios.

PURPOSE: This study aimed to investigate whether carbohydrate ingestion during 3 h long endurance exercise in highly trained cyclists at a rate of 120 g h-1 in 0.8:1 ratio between fructose and glucose-based carbohydrates would result in higher exogenous and lower endogenous carbohydrate oxidation rates as compared to ingestion of 90 g h-1 in 1:2 ratio, which is the currently recommended approach for exercise of this duration. METHODS: Eleven male participants (V̇O2peak 62.6 ± 7 mL kg-1 min-1, gas exchange threshold (GET) 270 ± 17 W and Respiratory compensation point 328 ± 32 W) completed the study involving 4 experimental visits consisting of 3 h cycling commencing after an overnight fast at an intensity equivalent to 95% GET. During the trials they received carbohydrates at an average rate of 120 or 90 g h-1 in 0.8:1 or 1:2 fructose-maltodextrin ratio, respectively. Carbohydrates were naturally high or low in 13C stable isotopes enabling subsequent calculations of exogenous and endogenous carbohydrate oxidation rates. RESULTS: Exogenous carbohydrate oxidation rates were higher in the 120 g h-1 condition (120-180 min: 1.51 ± 0.22 g min-1) as compared to the 90 g h-1 condition (1.29 ± 0.16 g min-1; p = 0.026). Endogenous carbohydrate oxidation rates did not differ between conditions (2.15 ± 0.30 and 2.20 ± 0.33 g min-1 for 120 and 90 g h-1 conditions, respectively; p = 0.786). CONCLUSIONS: The results suggest that carbohydrate ingestion at 120 g h-1 in 0.8:1 fructose-maltodextrin ratio as compared with 90 g h-1 in 1:2 ratio offers higher exogenous carbohydrate oxidation rates but no additional sparing of endogenous carbohydrates. Further studies should investigate potential performance effects of such carbohydrate ingestion strategies.

Peak fat oxidation is positively associated with vastus lateralis CD36 content, fed-state exercise fat oxidation, and endurance performance in trained males.

PURPOSE: Whole-body fat oxidation during exercise can be measured non-invasively during athlete profiling. Gaps in understanding exist in the relationships between fat oxidation during incremental fasted exercise and skeletal muscle parameters, endurance performance, and fat oxidation during prolonged fed-state exercise. METHODS: Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to assess peak whole-body fat oxidation (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 30-min maximal-effort cycling time-trial preceded by 2-h of fed-state moderate-intensity cycling to assess endurance performance and fed-state metabolism on separate occasions within one week. RESULTS: PFO (0.58 ± 0.28 g.min-1) was associated with vastus lateralis citrate synthase activity (69.2 ± 26.0 µmol.min-1.g-1 muscle protein, r = 0.84, 95% CI 0.58, 0.95, P < 0.001), CD36 abundance (16.8 ± 12.6 µg.g-1 muscle protein, rs = 0.68, 95% CI 0.31, 1.10, P = 0.01), pre-loaded 30-min time-trial performance (251 ± 51 W, r = 0.76, 95% CI 0.40, 0.91, P = 0.001; 3.2 ± 0.6 W.kg-1, r = 0.62, 95% CI 0.16, 0.86, P = 0.01), and fat oxidation during prolonged fed-state cycling (r = 0.83, 95% CI 0.57, 0.94, P < 0.001). Addition of PFO to a traditional model of endurance (peak oxygen uptake, power at 4 mmol.L-1 blood lactate concentration, and gross efficiency) explained an additional ~ 2.6% of variation in 30-min time-trial performance (adjusted R2 = 0.903 vs. 0.877). CONCLUSION: These associations suggest non-invasive measures of whole-body fat oxidation during exercise may be useful in the physiological profiling of endurance athletes.

Nicotinamide riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise.

KEY POINTS: Acute nicotinamide riboside (NR) supplementation does not alter substrate metabolism at rest, during or in recovery from endurance exercise. NR does not alter NAD+ -sensitive signalling pathways in human skeletal muscle. NR supplementation and acute exercise influence the NAD+ metabolome. ABSTRACT: Oral supplementation of the NAD+ precursor nicotinamide riboside (NR) has been reported to alter metabolism alongside increasing sirtuin (SIRT) signalling and mitochondrial biogenesis in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study assessed the effect of 7-day NR supplementation on whole-body metabolism and exercise-induced mitochondrial biogenic signalling in skeletal muscle. Eight male participants (age: 23 ± 4 years, V̇O2peak 46.5 ± 4.4 ml kg-1  min-1 ) received 1 week of NR or cellulose placebo (PLA) supplementation (1000 mg day-1 ). Muscle biopsies were collected from the medial vastus lateralis prior to supplementation and pre-, immediately post- and 3 h post-exercise (1 h of 60% Wmax cycling) performed following the supplementation period. There was no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Global acetylation, auto-PARylation of poly ADP-ribose polymerase 1 (PARP1), acetylation of Tumour protein 53 (p53)Lys382 and Manganese superoxide dismutase (MnSOD)Lys122 were also unaffected by NR supplementation or exercise. NR supplementation did not increase skeletal muscle NAD+ concentration, but it did increase the concentration of deaminated NAD+ precursors nicotinic acid riboside (NAR) and nicotinic acid mononucleotide (NAM) and methylated nicotinamide breakdown products (Me2PY and Me4PY), demonstrating the skeletal muscle bioavailability of NR supplementation. In summary, 1 week of NR supplementation does not alter whole-body metabolism or skeletal muscle signal transduction pathways implicated in the mitochondrial adaptation to endurance exercise.

Carb-conscious: the role of carbohydrate intake in recovery from exercise.

PURPOSE OF REVIEW: The present review summarized evidence on the role of carbohydrates in recovery from exercise within the context of acute and chronic effects on metabolism and performance. RECENT FINDINGS: Recent studies demonstrate that, in contrast to recovery of muscle glycogen stores, the recovery of liver glycogen stores can be accelerated by the co-ingestion of fructose with glucose-based carbohydrates. Three recent studies suggest this can extend time-to-exhaustion during endurance exercise tests. However, periodically restricting carbohydrate intakes during recovery from some training sessions to slow the recovery of liver and muscle glycogen stores may, over time, result in a modest increase in the ability to oxidize fat during exercise in a fasted state. Whether this periodized strategy translates into a performance advantage in the fed state remains to be clearly demonstrated. SUMMARY: To maximize recovery of glycogen stores and the capacity to perform in subsequent endurance exercise, athletes should consider ingesting at least 1.2 g carbohydrate per kilogram body mass per hour - for the first few hours of recovery - as a mixture of fructose and glucose-based carbohydrates. However, if a goal is increased capacity for fat oxidation, athletes should consider restricting carbohydrate intakes during recovery from some key training sessions. VIDEO ABSTRACT: http://links.lww.com/COCN/A15.

Social media use informing behaviours related to physical activity, diet and quality of life during COVID-19: a mixed methods study.

BACKGROUND: This mixed methods study explored how social media use informed physical activity and diet-related behaviours, and self-perceived Quality of Life (QoL) during COVID-19, and assessed the contextual factors that drive social media use for health-related behaviour change in diverse groups. During the COVID-19 lockdown periods there were reported changes to social media use and health behaviours, and this gave an opportunity to investigate potential relationships. METHODS: An explanatory sequential research design of two parts was used: (1) An online survey that assessed social media use in relation to physical activity levels, diet quality and QoL (n = 786; Mage 45.1 ± 19.1 (range 16-88) years; Female =69%); (2) 20 purposive focus groups (n = 69; Mage = 52.88 ± 18.45 years, Female n = 68%) to understand the contextual factors that drive social media use for health-related behaviour change. Descriptive and thematic analysis were conducted. RESULTS: Participants in this study reported that social media facilitated the self-management of behaviours related to physical activity, diet and QoL, through access to information to inform workouts and dietary quality, and the opportunities for interaction with peers, family members and within social groups. Contextual factors including work, home and lifestyle arrangements, pre-existing health-related knowledge and behaviours, and the perceived value of social media for health influenced the relationship between social media use and self-reported outcomes. Social media influencers, peers/family members, and official organisations influenced the application of health-related information accessed via social media. CONCLUSIONS: The evidence shows that participants were critical users of social media and were able to use social media to derive benefit for their health and wellbeing. Detailed guidance for those who use social media, as well as those who recommend and endorse social media content is required to maximise the potential of social media to support health behaviours. Future public health strategies and social media interventions should acknowledge diversity in contextual factors driving social media use for health behaviour change.

Daily Myofibrillar Protein Synthesis Rates in Response to Low- and High-Frequency Resistance Exercise Training in Healthy, Young Men.

The impact of resistance exercise frequency on muscle protein synthesis rates remains unknown. The aim of this study was to compare daily myofibrillar protein synthesis rates over a 7-day period of low-frequency (LF) versus high-frequency (HF) resistance exercise training. Nine young men (21 ± 2 years) completed a 7-day period of habitual physical activity (BASAL). This was followed by a 7-day exercise period of volume-matched, LF (10 × 10 repetitions at 70% one-repetition maximum, once per week) or HF (2 × 10 repetitions at ∼70% one-repetition maximum, five times per week) resistance exercise training. The participants had one leg randomly allocated to LF and the other to HF. Skeletal muscle biopsies and daily saliva samples were collected to determine myofibrillar protein synthesis rates using 2H2O, with intracellular signaling determined using Western blotting. The myofibrillar protein synthesis rates did not differ between the LF (1.46 ± 0.26%/day) and HF (1.48 ± 0.33%/day) conditions over the 7-day exercise training period (p > .05). There were no significant differences between the LF and HF conditions over the first 2 days (1.45 ± 0.41%/day vs. 1.25 ± 0.46%/day) or last 5 days (1.47 ± 0.30%/day vs. 1.50 ± 0.41%/day) of the exercise training period (p > .05). Daily myofibrillar protein synthesis rates were not different from BASAL at any time point during LF or HF (p > .05). The phosphorylation status and total protein content of selected proteins implicated in skeletal muscle ribosomal biogenesis were not different between conditions (p > .05). Under the conditions of the present study, resistance exercise training frequency did not modulate daily myofibrillar protein synthesis rates in young men.

Dietary supplementation with inulin-propionate ester or inulin improves insulin sensitivity in adults with overweight and obesity with distinct effects on the gut microbiota, plasma metabolome and systemic inflammatory responses: a randomised cross-over trial.

OBJECTIVE: To investigate the underlying mechanisms behind changes in glucose homeostasis with delivery of propionate to the human colon by comprehensive and coordinated analysis of gut bacterial composition, plasma metabolome and immune responses. DESIGN: Twelve non-diabetic adults with overweight and obesity received 20 g/day of inulin-propionate ester (IPE), designed to selectively deliver propionate to the colon, a high-fermentable fibre control (inulin) and a low-fermentable fibre control (cellulose) in a randomised, double-blind, placebo-controlled, cross-over design. Outcome measurements of metabolic responses, inflammatory markers and gut bacterial composition were analysed at the end of each 42-day supplementation period. RESULTS: Both IPE and inulin supplementation improved insulin resistance compared with cellulose supplementation, measured by homeostatic model assessment 2 (mean±SEM 1.23±0.17 IPE vs 1.59±0.17 cellulose, p=0.001; 1.17±0.15 inulin vs 1.59±0.17 cellulose, p=0.009), with no differences between IPE and inulin (p=0.272). Fasting insulin was only associated positively with plasma tyrosine and negatively with plasma glycine following inulin supplementation. IPE supplementation decreased proinflammatory interleukin-8 levels compared with cellulose, while inulin had no impact on the systemic inflammatory markers studied. Inulin promoted changes in gut bacterial populations at the class level (increased Actinobacteria and decreased Clostridia) and order level (decreased Clostridiales) compared with cellulose, with small differences at the species level observed between IPE and cellulose. CONCLUSION: These data demonstrate a distinctive physiological impact of raising colonic propionate delivery in humans, as improvements in insulin sensitivity promoted by IPE and inulin were accompanied with different effects on the plasma metabolome, gut bacterial populations and markers of systemic inflammation.

Skipping Breakfast Before Exercise Creates a More Negative 24-hour Energy Balance: A Randomized Controlled Trial in Healthy Physically Active Young Men.

BACKGROUND: At rest, omission of breakfast lowers daily energy intake, but also lowers energy expenditure, attenuating any effect on energy balance. The effect of breakfast omission on energy balance when exercise is prescribed is unclear. OBJECTIVES: The aim of this study was to assess the effect on 24-h energy balance of omitting compared with consuming breakfast prior to exercise. METHODS: Twelve healthy physically active young men (age 23 ± 3 y, body mass index 23.6 ± 2.0 kg/m2) completed 3 trials in a randomized order (separated by >1 week): a breakfast of oats and milk (431 kcal; 65 g carbohydrate, 11 g fat, 19 g protein) followed by rest (BR); breakfast before exercise (BE; 60 min cycling at 50 % peak power output); and overnight fasting before exercise (FE). The 24-h energy intake was calculated based on the food consumed for breakfast, followed by an ad libitum lunch, snacks, and dinner. Indirect calorimetry with heart-rate accelerometry was used to measure substrate utilization and 24-h energy expenditure. A [6,6-2H2]glucose infusion was used to investigate tissue-specific carbohydrate utilization. RESULTS: The 24-h energy balance was -400 kcal (normalized 95% CI: -230, -571 kcal) for the FE trial; this was significantly lower than both the BR trial (492 kcal; normalized 95% CI: 332, 652 kcal) and the BE trial (7 kcal; normalized 95% CI: -153, 177 kcal; both P < 0.01 compared with FE). Plasma glucose utilization in FE (mainly representing liver glucose utilization) was positively correlated with energy intake compensation at lunch (r = 0.62, P = 0.03), suggesting liver carbohydrate plays a role in postexercise energy-balance regulation. CONCLUSIONS: Neither exercise energy expenditure nor restricted energy intake via breakfast omission were completely compensated for postexercise. In healthy men, pre-exercise breakfast omission creates a more negative daily energy balance and could therefore be a useful strategy to induce a short-term energy deficit. This trial was registered at clinicaltrials.gov as NCT02258399.

Preexercise breakfast ingestion versus extended overnight fasting increases postprandial glucose flux after exercise in healthy men.

The aim of this study was to characterize postprandial glucose flux after exercise in the fed versus overnight fasted state and to investigate the potential underlying mechanisms. In a randomized order, twelve men underwent breakfast-rest [(BR) 3 h semirecumbent], breakfast-exercise [(BE) 2 h semirecumbent before 60 min of cycling (50% peak power output)], and overnight fasted exercise [(FE) as per BE omitting breakfast] trials. An oral glucose tolerance test (OGTT) was completed after exercise (after rest on BR). Dual stable isotope tracers ([U-13C] glucose ingestion and [6,6-2H2] glucose infusion) and muscle biopsies were combined to assess postprandial plasma glucose kinetics and intramuscular signaling, respectively. Plasma intestinal fatty acid binding (I-FABP) concentrations were determined as a marker of intestinal damage. Breakfast before exercise increased postexercise plasma glucose disposal rates during the OGTT, from 44 g/120 min in FE {35 to 53 g/120 min [mean (normalized 95% confidence interval)] to 73 g/120 min in BE [55 to 90 g/120 min; P = 0.01]}. This higher plasma glucose disposal rate was, however, offset by increased plasma glucose appearance rates (principally OGTT-derived), resulting in a glycemic response that did not differ between BE and FE ( P = 0.11). Plasma I-FABP concentrations during exercise were 264 pg/ml (196 to 332 pg/ml) lower in BE versus FE ( P = 0.01). Breakfast before exercise increases postexercise postprandial plasma glucose disposal, which is offset (primarily) by increased appearance rates of orally ingested glucose. Therefore, metabolic responses to fed-state exercise cannot be readily inferred from studies conducted in a fasted state.

The diet-derived short chain fatty acid propionate improves beta-cell function in humans and stimulates insulin secretion from human islets in vitro.

AIMS: Diet-derived short chain fatty acids (SCFAs) improve glucose homeostasis in vivo, but the role of individual SCFAs and their mechanisms of action have not been defined. This study evaluated the effects of increasing colonic delivery of the SCFA propionate on ß-cell function in humans and the direct effects of propionate on isolated human islets in vitro. MATERIALS AND METHODS: For 24 weeks human subjects ingested an inulin-propionate ester that delivers propionate to the colon. Acute insulin, GLP-1 and non-esterified fatty acid (NEFA) levels were quantified pre- and post-supplementation in response to a mixed meal test. Expression of the SCFA receptor FFAR2 in human islets was determined by western blotting and immunohistochemistry. Dynamic insulin secretion from perifused human islets was quantified by radioimmunoassay and islet apoptosis was determined by quantification of caspase 3/7 activities. RESULTS: Colonic propionate delivery in vivo was associated with improved ß-cell function with increased insulin secretion that was independent of changes in GLP-1 levels. Human islet ß-cells expressed FFAR2 and propionate potentiated dynamic glucose-stimulated insulin secretion in vitro, an effect that was dependent on signalling via protein kinase C. Propionate also protected human islets from apoptosis induced by the NEFA sodium palmitate and inflammatory cytokines. CONCLUSIONS: Our results indicate that propionate has beneficial effects on ß-cell function in vivo, and in vitro analyses demonstrated that it has direct effects to potentiate glucose-stimulated insulin release and maintain ß-cell mass through inhibition of apoptosis. These observations support ingestion of propiogenic dietary fibres to maintain healthy glucose homeostasis.

No effect of acute L-arginine supplementation on O2 cost or exercise tolerance.

The extent to which dietary supplementation with the nitric oxide synthase (NOS) substrate, L-arginine (ARG), impacts on NO production and NO-mediated physiological responses is controversial. This randomised, double blinded, cross-over study investigated the effects of acute ARG supplementation on NO biomarkers, O2 cost of exercise and exercise tolerance in humans. In one experiment, 15 subjects completed moderate- and severe-intensity running bouts after acute supplementation with 6 g ARG or placebo (PLA). In another experiment, eight subjects completed moderate- and severe-intensity cycling bouts after acute supplementation with 6 g ARG plus 25 g of carbohydrate (ARG + CHO) or an energy-matched dose of carbohydrate alone (CHO). The plasma nitrite concentration was not different after ARG (Pre: 204 ± 79; Post: 241 ± 114 nM; P > 0.05) or ARG + CHO consumption (Pre: 304 ± 57; Post: 335 ± 116 nM; P > 0.05). During moderate-intensity exercise, the steady-state pulmonary VO2 was not different, relative to the respective placebo conditions, after ARG (PLA: 2,407 ± 318, ARG: 2,422 ± 333 mL min(-1)) or ARG + CHO (CHO: 1,695 ± 304, ARG + CHO: 1,712 ± 312 mL min(-1)) ingestion (P > 0.05). The tolerable duration of severe exercise was also not significantly different (P > 0.05) after ingesting ARG (PLA: 551 ± 140, ARG: 552 ± 150 s) or ARG + CHO (CHO: 457 ± 182, ARG + CHO: 441 ± 221 s). In conclusion, acute dietary supplementation with ARG or ARG + CHO did not alter biomarkers of NO synthesis, O2 cost of exercise or exercise tolerance in healthy subjects.

Is there a specific role for sucrose in sports and exercise performance?

The consumption of carbohydrate before, during, and after exercise is a central feature of the athlete's diet, particularly those competing in endurance sports. Sucrose is a carbohydrate present within the diets of athletes. Whether sucrose, by virtue of its component monosaccharides glucose and fructose, exerts a meaningful advantage for athletes over other carbohydrate types or blends is unclear. This narrative reviews the literature on the influence of sucrose, relative to other carbohydrate types, on exercise performance or the metabolic factors that may underpin exercise performance. Inference from the research to date suggests that sucrose appears to be as effective as other highly metabolizable carbohydrates (e.g., glucose, glucose polymers) in providing an exogenous fuel source during endurance exercise, stimulating the synthesis of liver and muscle glycogen during exercise recovery and improving endurance exercise performance. Nonetheless, gaps exist in our understanding of the metabolic and performance consequences of sucrose ingestion before, during, and after exercise relative to other carbohydrate types or blends, particularly when more aggressive carbohydrate intake strategies are adopted. While further research is recommended and discussed in this review, based on the currently available scientific literature it would seem that sucrose should continue to be regarded as one of a variety of options available to help athletes achieve their specific carbohydrate-intake goals.

Measurement of Energy Intake Using the Principle of Energy Balance Overcomes a Critical Limitation in the Assessment of Energy Availability.

Prolonged low energy availability, which is the underpinning aetiology of the Relative Energy Deficiency in Sport and the Female and Male Athlete Triad frameworks, can have unfavourable impacts on both health and performance in athletes. Energy availability is calculated as energy intake minus exercise energy expenditure, expressed relative to fat free mass. The current measurement of energy intake is recognized as a major limitation for assessing energy availability due to its reliance on self-report methods, in addition to its short-term nature. This article introduces the application of the energy balance method for the measurement of energy intake, within the context of energy availability. The energy balance method requires quantification of the change in body energy stores over time, with concurrent measurement of total energy expenditure. This provides an objective calculation of energy intake, which can then be used for the assessment of energy availability. This approach, the Energy Availability - Energy Balance (EAEB) method, increases the reliance on objective measurements, provides an indication of energy availability status over longer periods and removes athlete burden to self-report energy intake. Implementation of the EAEB method could be used to objectively identify and detect low energy availability, with implications for the diagnosis and management of Relative Energy Deficiency in Sport and the Female and Male Athlete Triad.

New Horizons in Carbohydrate Research and Application for Endurance Athletes.

The importance of carbohydrate as a fuel source for exercise and athletic performance is well established. Equally well developed are dietary carbohydrate intake guidelines for endurance athletes seeking to optimize their performance. This narrative review provides a contemporary perspective on research into the role of, and application of, carbohydrate in the diet of endurance athletes. The review discusses how recommendations could become increasingly refined and what future research would further our understanding of how to optimize dietary carbohydrate intake to positively impact endurance performance. High carbohydrate availability for prolonged intense exercise and competition performance remains a priority. Recent advances have been made on the recommended type and quantity of carbohydrates to be ingested before, during and after intense exercise bouts. Whilst reducing carbohydrate availability around selected exercise bouts to augment metabolic adaptations to training is now widely recommended, a contemporary view of the so-called train-low approach based on the totality of the current evidence suggests limited utility for enhancing performance benefits from training. Nonetheless, such studies have focused importance on periodizing carbohydrate intake based on, among other factors, the goal and demand of training or competition. This calls for a much more personalized approach to carbohydrate recommendations that could be further supported through future research and technological innovation (e.g., continuous glucose monitoring). Despite more than a century of investigations into carbohydrate nutrition, exercise metabolism and endurance performance, there are numerous new important discoveries, both from an applied and mechanistic perspective, on the horizon.

Oxidation of independent and combined ingested galactose and glucose during exercise.

Coingestion of glucose and galactose has been shown to enhance splanchnic extraction and metabolism of ingested galactose at rest; effects during exercise are unknown. This study examined whether combined ingestion of galactose and glucose during exercise enhances exogenous galactose oxidation. Fourteen endurance-trained male and female participants [age, 27 (5) yr; V̇o2peak, 58.1 (7.0) mL·kg-1·min-1] performed cycle ergometry for 150 min at 50% peak power on four occasions, in a randomized counterbalanced manner. During exercise, they ingested beverages providing carbohydrates at rates of 0.4 g.min-1 galactose (GAL), 0.8 g.min-1 glucose (GLU), and on two occasions 0.8 g.min-1 total galactose-glucose (GAL + GLU; 1:1 ratio). Single-monosaccharide 13C-labeling (*) was used to calculate independent (GAL, GLU, GAL* + GLU, and GAL + GLU*) and combined (GAL* + GLU*, COMBINE) exogenous-monosaccharide oxidation between exercise. Plasma galactose concentrations with GAL + GLU [0.4 mmol.L; 95% confidence limits (CL): 0.1, 0.6] were lower (contrast: 0.5 mmol.L; 95% CL: 0.2, 0.8; P < 0.0001) than when GAL alone (0.9 mmol.L; 95% CL: 0.7, 1.2) was ingested. Exogenous carbohydrate oxidation with GAL alone (0.31 g·min-1; 95% CL: 0.28, 0.35) was marginally reduced (contrast: 0.05 g·min-1; 95% CL: -0.09, 0.00007; P = 0.01) when combined with glucose (GAL* + GLU 0.27 g·min-1; 0.24, 0.30). Total combined exogenous-carbohydrate oxidation (COMBINE: 0.57 g·min-1; 95% CL: 0.49, 0.64) was similar (contrast: 0.02 g·min-1; 95% CL: -0.05, 0.09; P = 0.63) when compared with isoenergetic GLU (0.55 g·min-1; 95% CL: 0.52, 0.58). In conclusion, coingestion of glucose and galactose did not enhance exogenous galactose oxidation during exercise. When combined, isoenergetic galactose-glucose ingestion elicited similar exogenous-carbohydrate oxidation to glucose suggesting galactose-glucose blends are a valid alternative for glucose as an exogenous-carbohydrate source during exercise.NEW & NOTEWORTHY Glucose and galactose coingestion blunted the galactosemia seen with galactose-only ingestion during exercise. Glucose and galactose coingestion did not enhance the oxidation of ingested galactose during exercise. Combined galactose-glucose (1:1 ratio) ingestion was oxidized to a similar extent as isoenergetic glucose-only ingestion during exercise. Galactose-glucose blends are a viable exogenous carbohydrate energy source for ingestion during exercise.

High rates of fat oxidation are maintained after the sleep low approach despite delayed carbohydrate feeding during exercise.

Training with low carbohydrate availability enhances endurance training adaptations but training volume may be compromised. We explored whole-body metabolism and performance with delayed carbohydrate feeding during exercise undertaken following acute sleep-low training. We hypothesised this strategy would not suppress fat oxidation and would maintain exercise performance. The study involved three experimental trials and included 9 men and 1 woman (⩒O2peak = 58.8 ± 5.5 mL kg-1 min-1). Each trial started in the afternoon with an exhaustive cycling protocol. The following morning 1-h of steady-state cycling (SS) was followed by a time trial (TT). Carbohydrates (CHO) were not ingested in recovery from exhaustive exercise or during next day exercise in the Placebo trial (PLA); CHO were not ingested during recovery but were fed (15 g every ∼15-min) from 30-min into SS and continued during the TT in the delayed feeding trial (DELAY); CHO were provided during recovery (1.2 g/kg/h for 7 h) and next day exercise (as in DELAY) in a third condition (CHO). Exercise metabolism was assessed using indirect calorimetry and blood sampling. Fat oxidation rates during SS were similar in PLA (0.83 ± 0.17 g/min) and DELAY (0.78 ± 0.14 g/min) (p > 0.05) and higher than CHO (0.57 ± 0.27 g/min) (p < 0.05). There were no significant differences in TT performance (49.1 ± 10.7, 43.4 ± 7.6, 41.0 ± 7.9 min in PLA, DELAY and CHO, respectively; p > 0.05). Delayed carbohydrate feeding could be a strategy to maintain high-fat oxidation rates typically associated with exercise undertaken after the sleep-low approach to training but the acute performance effects remain inconclusive.