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The benefits of high exogenous glucose availability for endurance exercise performance are well-established. Exogenous glucose oxidation rates are thought to be limited by intestinal glucose transport. Extracellular calcium in rodent intestine increases the translocation of the intestinal glucose transporter GLUT2 which, if translated to humans, could increase the capacity for exogenous glucose availability during exercise. Therefore, this pilot study aimed to explore the effect of calcium co-ingestion during endurance exercise on exogenous glucose oxidation in healthy men. Eight healthy men cycled for 2 h at 50% peak power output, ingesting either 1.2 g min−1 dextrose alone (GLU) or with the addition of 2000 mg calcium (GLU + CAL), in a randomised crossover design. Expired breath samples were collected to determine whole-body and exogenous glucose oxidation. Peak exogenous glucose oxidation during GLU was 0.83 ± 0.15 g min−1, and was not enhanced during GLU + CAL (0.88 ± 0.11 g min−1, p = 0.541). The relative contributions of exogenous carbohydrate (19 ± 3% vs. 20 ± 2%, p = 0.434), endogenous carbohydrate (65 ± 3% vs. 65 ± 3%, p = 0.822) and fat (16 ± 3% vs. 15 ± 3%, p = 0.677) to total substrate utilisation did not differ between trials. These results suggest the addition of calcium to glucose ingestion, at saturating glucose ingestion rates, does not appear to alter exogenous glucose oxidation during endurance exercise in healthy men. [ABSTRACT FROM AUTHOR]

Unaccustomed eccentric exercise using large muscle groups elicits soreness, decrements in physical function and impairs markers of whole-body insulin sensitivity; although these effects are attenuated with a repeated exposure. Eccentric exercise of a small muscle group (elbow flexors) displays similar soreness and damage profiles in response to repeated exposure. However, it is unknown whether damage to small muscle groups impacts upon whole-body insulin sensitivity. This pilot investigation aimed to characterize whole-body insulin sensitivity in response to repeated bouts of eccentric exercise of the elbow flexors. Nine healthy males completed two bouts of eccentric exercise separated by 2 weeks. Insulin resistance (updated homeostasis model of insulin resistance, HOMA2-IR) and muscle damage profiles (soreness and physical function) were assessed before, and 48 h after exercise. Matsuda insulin sensitivity indices (ISIMatsuda) were also determined in 6 participants at the same time points as HOMA2-IR. Soreness was elevated, and physical function impaired, by both bouts of exercise (both p < .05) but to a lesser extent following bout 2 (time x bout interaction, p < .05). Eccentric exercise decreased ISIMatsuda after the first but not the second bout of eccentric exercise (time x bout interaction p < .05). Eccentric exercise performed with an isolated upper limb impairs whole-body insulin sensitivity after the first, but not the second, bout. [ABSTRACT FROM AUTHOR]

Poor post-prandial glucose control is a risk factor for multiple health conditions. The second-meal effect refers to the progressively improved glycaemic control with repeated feedings, an effect which is achievable with protein ingestion at the initial eating occasion. The most pronounced glycaemic response each day therefore typically occurs following breakfast, so the present study investigated whether ingesting protein during the night could improve glucose control at the first meal of the day. In a randomised crossover design, fifteen adults (seven males, eight females; age, 22 (sd 3) years; BMI, 24·0 (sd 2·8) kg/m2; fasting blood glucose, 4·9 (sd 0·5) mmol/l) woke at 04.00 (sd 1) hours to ingest 300 ml water with or without 63 g whey protein. Participants then completed a mixed-macronutrient meal tolerance test (1 g carbohydrate/kg body mass, 2356 (sd 435) kJ), 5 h 39 min following the nocturnal feeding. Nocturnal protein ingestion increased the glycaemic response (incremental AUC) to breakfast by 43·5 (sd 55·5) mmol × 120 min/l (P = 0·009, d = 0·94). Consistent with this effect, individual peak blood glucose concentrations were 0·6 (sd 1·0) mmol/l higher following breakfast when protein had been ingested (P = 0·049, d = 0·50). Immediately prior to breakfast, rates of lipid oxidation were 0·02 (sd 0·03) g/min higher (P = 0·045) in the protein condition, followed by an elevated post-prandial energy expenditure (0·38 (sd 0·50) kJ/min, P = 0·018). Post-prandial appetite and energy intake were similar between conditions. The present study reveals a paradoxical second-meal phenomenon whereby nocturnal whey protein feeding impaired subsequent glucose tolerance, whilst increasing post-prandial energy expenditure. [ABSTRACT FROM AUTHOR]

Purpose: To examine whether calcium type and co-ingestion with protein alter gut hormone availability. Methods: Healthy adults aged 26 ± 7 years (mean ± SD) completed three randomized, double-blind, crossover studies. In all studies, arterialized blood was sampled postprandially over 120 min to determine GLP-1, GIP and PYY responses, alongside appetite ratings, energy expenditure and blood pressure. In study 1 (n = 20), three treatments matched for total calcium content (1058 mg) were compared: calcium citrate (CALCITR); milk minerals rich in calcium (MILK MINERALS); and milk minerals rich in calcium plus co-ingestion of 50 g whey protein hydrolysate (MILK MINERALS + PROTEIN). In study 2 (n = 6), 50 g whey protein hydrolysate (PROTEIN) was compared to MILK MINERALS + PROTEIN. In study 3 (n = 6), MILK MINERALS was compared to the vehicle of ingestion (water plus sucralose; CONTROL). Results: MILK MINERALS + PROTEIN increased GLP-1 incremental area under the curve (iAUC) by ~ ninefold (43.7 ± 11.1 pmol L−1 120 min; p < 0.001) versus both CALCITR and MILK MINERALS, with no difference detected between CALCITR (6.6 ± 3.7 pmol L−1 120 min) and MILK MINERALS (5.3 ± 3.5 pmol L−1 120 min; p > 0.999). MILK MINERALS + PROTEIN produced a GLP-1 iAUC ~ 25% greater than PROTEIN (p = 0.024; mean difference: 9.1 ± 6.9 pmol L−1 120 min), whereas the difference between MILK MINERALS versus CONTROL was small and non-significant (p = 0.098; mean difference: 4.2 ± 5.1 pmol L−1 120 min). Conclusions: When ingested alone, milk minerals rich in calcium do not increase GLP-1 secretion compared to calcium citrate. Co-ingesting high-dose whey protein hydrolysate with milk minerals rich in calcium increases postprandial GLP-1 concentrations to some of the highest physiological levels ever reported. Registered at ClinicalTrials.gov: NCT03232034, NCT03370484, NCT03370497. [ABSTRACT FROM AUTHOR]

Purpose: Prior studies exploring the reliability of peak fat oxidation (PFO) and the intensity that elicits PFO (FATMAX) are often limited by small samples. This study characterised the reliability of PFO and FATMAX in a large cohort of healthy men and women.Methods: Ninety-nine adults [49 women; age: 35 (11) years; [Formula: see text]O2peak: 42.2 (10.3) mL·kg BM-1·min-1; mean (SD)] completed two identical exercise tests (7-28 days apart) to determine PFO (g·min-1) and FATMAX (%[Formula: see text]O2peak) by indirect calorimetry. Systematic bias and the absolute and relative reliability of PFO and FATMAX were explored in the whole sample and sub-categories of: cardiorespiratory fitness, biological sex, objectively measured physical activity levels, fat mass index (derived by dual-energy X-ray absorptiometry) and menstrual cycle status.Results: No systematic bias in PFO or FATMAX was found between exercise tests in the entire sample (- 0.01 g·min-1 and 0%[Formula: see text]O2peak, respectively; p > 0.05). Absolute reliability was poor [within-subject coefficient of variation: 21% and 26%; typical errors: ± 0.06 g·min-1 and × / ÷ 1.26%[Formula: see text]O2peak; 95% limits of agreement: ± 0.17 g·min-1 and × / ÷ 1.90%[Formula: see text]O2peak, respectively), despite high (r = 0.75) and moderate (r = 0.45) relative reliability for PFO and FATMAX, respectively. These findings were consistent across all sub-groups.Conclusion: Repeated assessments are required to more accurately determine PFO and FATMAX. [ABSTRACT FROM AUTHOR]

Exploring individual responses to exercise training is a growing area of interest. Understanding reasons behind true observed inter-individual responses may help personalise exercise training to maximise the benefits received. While numerous factors have been explored, an often underappreciated consideration in the sport and exercise science field is the influence intra-individual variation, both in a single measurement and in response to an intervention, may have on training outcomes. Several study designs and statistical approaches are available to incorporate intra-individual variation into interventions and accordingly provide information on whether 'true' inter-individual responses are present or if they are an artefact of intra-individual variation. However, such approaches are sparingly applied. Moreover, intra-individual variation may also be important when true inter-individual response differences are present. In this perspective piece, the concept of intra-individual variation is described before briefly summarising study designs and statistical practices to account for intra-individual variation. We then outline two examples of physiological practices (stratified randomisation and prescribing exercise programmes upon training parameters) to demonstrate why sport and exercise scientists should acknowledge intra-individual variation prior to the implementation of an intervention, which potentially offers an additional explanation behind observed true inter-individual responses to training. Repeated testing pre-implementation of exercise training would conceptually provide more confident estimates of training parameters, which if utilised in a study design will help attenuate biases that may dictate inter-individual differences. Moreover, the incorporation of intra-individual differences will facilitate insights into alternative factors that may predict and/or explain true observed individual responses to an exercise training programme. [ABSTRACT FROM AUTHOR]

Obesity remains a major public health concern and intermittent fasting is a popular strategy for weight loss, which may present independent health benefits. However, the number of diet books advising how fasting can be incorporated into our daily lives is several orders of magnitude greater than the number of trials examining whether fasting should be encouraged at all. This review will consider the state of current understanding regarding various forms of intermittent fasting (e.g. 5:2, time-restricted feeding and alternate-day fasting). The efficacy of these temporally defined approaches appears broadly equivalent to that of standard daily energy restriction, although many of these models of intermittent fasting do not involve fed-fasted cycles every other 24 h sleep-wake cycle and/or permit some limited energy intake outside of prescribed feeding times. Accordingly, the intervention period therefore may not regularly alternate, may not span all or even most of any given day, and may not even involve absolute fasting. This is important because potentially advantageous physiological mechanisms may only be initiated if a post-absorptive state is sustained by uninterrupted fasting for a more prolonged duration than applied in many trials. Indeed, promising effects on fat mass and insulin sensitivity have been reported when fasting duration is routinely extended beyond sixteen consecutive hours. Further progress will require such models to be tested with appropriate controls to isolate whether any possible health effects of intermittent fasting are primarily attributable to regularly protracted post-absorptive periods, or simply to the net negative energy balance indirectly elicited by any form of dietary restriction. [ABSTRACT FROM AUTHOR]

The objective of this review paper is to evaluate the impact of undertaking aerobic exercise in the overnight-fasted v. fed-state, in the context of optimising the health benefits of regular physical activity. Conducting a single bout of aerobic exercise in the overnight-fasted v. fed-state can differentially modulate the aspects of metabolism and energy balance behaviours. This includes, but is not limited to, increased utilisation of fat as a fuel source, improved plasma lipid profiles, enhanced activation of molecular signalling pathways related to fuel metabolism in skeletal muscle and adipose tissue, and reductions in energy intake over the course of a day. The impact of a single bout of overnight-fasted v. fed-state exercise on short-term glycaemic control is variable, being affected by the experimental conditions, the time frame of measurement and possibly the subject population studied. The health response to undertaking overnight-fasted v. fed-state exercise for a sustained period of time in the form of exercise training is less clear, due to a limited number of studies. From the extant literature, there is evidence that overnight-fasted exercise in young, healthy men can enhance training-induced adaptations in skeletal muscle metabolic profile, and mitigate against the negative consequences of short-term excess energy intake on glucose tolerance compared with exercising in the fed-state. Nonetheless, further long-term studies are required, particularly in populations at-risk or living with cardio-metabolic disease to elucidate if feeding status prior to exercise modulates metabolism or energy balance behaviours to an extent that could impact upon the health or therapeutic benefits of exercise. [ABSTRACT FROM AUTHOR]

Exposure to hypoxia appears to depress appetite and energy intake, however the mechanisms are not fully understood. The aim of this review was to determine the magnitude of changes in hunger and energy intake in hypoxic compared with normoxic environments, and establish any alterations in appetite-related hormone concentrations. PubMed and The Cochrane Library as well as MEDLINE, SPORTDiscus, PsycINFO and CINAHL, via EBSCOhost, were searched through 1st April 2017 for studies that evaluated hunger, energy intake and/or appetite-related hormones in normoxia and during hypoxic exposure in a within-measures design. A total of 28 studies (comprising 54 fasted and 22 postprandial comparisons) were included. A random-effects meta-analysis was performed to establish standardised mean difference (SMD) with 95% confidence intervals. Hypoxic exposure resulted in a trivial but significant decrease in postprandial hunger scores (SMD: -0.15, 95% CI: -0.29 to -0.01; n = 14; p = 0.043) and a moderate decrease in energy intake (SMD: -0.50, 95% CI: -0.85 to -0.15; n = 8; p = 0.006). Hypoxic exposure resulted in a decrease (albeit trivial) in postprandial acylated ghrelin concentrations (SMD: -0.16, 95% CI: -0.25 to -0.08; n = 7; p < 0.0005), and a moderate increase in fasted insulin concentrations (SMD: 0.41, 95% CI: 0.17 to 0.65; n = 34; p = 0.001). Meta-regression revealed a decrease in postprandial acylated ghrelin concentrations (p = 0.010) and an increase in fasted insulin concentrations (p = 0.020) as hypoxic severity increased. Hypoxic exposure reduces hunger and energy intake, which may be mediated by decreased circulating concentrations of acylated ghrelin and elevated insulin concentrations. PROSPERO registration number: CRD42015017231. [ABSTRACT FROM AUTHOR]

The importance of post-exercise recovery nutrition has been well described in recent years, leading to its incorporation as an integral part of training regimes in both athletes and active individuals. Muscle glycogen depletion during an initial prolonged exercise bout is a main factor in the onset of fatigue and so the replenishment of glycogen stores may be important for recovery of functional capacity. Nevertheless, nutritional considerations for optimal short-term (3-6 h) recovery remain incompletely elucidated, particularly surrounding the precise amount of specific types of nutrients required. Current nutritional guidelines to maximise muscle glycogen availability within limited recovery are provided under the assumption that similar fatigue mechanisms (i.e., muscle glycogen depletion) are involved during a repeated exercise bout. Indeed, recent data support the notion that muscle glycogen availability is a determinant of subsequent endurance capacity following limited recovery. Thus, carbohydrate ingestion can be utilised to influence the restoration of endurance capacity following exhaustive exercise. One strategy with the potential to accelerate muscle glycogen resynthesis and/or functional capacity beyond merely ingesting adequate carbohydrate is the co-ingestion of added protein. While numerous studies have been instigated, a consensus that is related to the influence of carbohydrate-protein ingestion in maximising muscle glycogen during short-term recovery and repeated exercise capacity has not been established. When considered collectively, carbohydrate intake during limited recovery appears to primarily determine muscle glycogen resynthesis and repeated exercise capacity. Thus, when the goal is to optimise repeated exercise capacity following short-term recovery, ingesting carbohydrate at an amount of ≥1.2 g kg body mass-1⋅h-1 can maximise muscle glycogen repletion. The addition of protein to carbohydrate during post-exercise recovery may be beneficial under circumstances when carbohydrate ingestion is sub-optimal (≤0.8 g kg body mass-1⋅h-1) for effective restoration of muscle glycogen and repeated exercise capacity. [ABSTRACT FROM AUTHOR]

The carbohydrate deficit induced by exercise is thought to play a key role in increased post-exercise insulin action. However, the effects of replacing carbohydrate utilized during exercise on postprandial glycaemia and insulin sensitivity are yet to be determined. This study therefore isolated the extent to which the insulin-sensitizing effects of exercise are dependent on the carbohydrate deficit induced by exercise, relative to other exercise-mediated mechanisms. Fourteen healthy adults performed a 90-min run at 70% ...O2max starting at 1600-1700 h before ingesting either a non-caloric artificially-sweetened placebo solution (CHO-DEFICIT) or a 15% carbohydrate solution (CHO-REPLACE; 221.4 ± 59.3 g maltodextrin) to precisely replace the measured quantity of carbohydrate oxidized during exercise. The alternate treatment was then applied one week later in a randomized, placebo-controlled, and double-blinded crossover design. A standardized low-carbohydrate evening meal was consumed in both trials before overnight recovery ahead of a two-hour oral glucose tolerance test (OGTT) the following morning to assess glycemic and insulinemic responses to feeding. Compared to the CHO-DEFICIT condition, CHO-REPLACE increased the incremental area under the plasma glucose curve by a mean difference of 68 mmol⋅L-1 (95% CI: 4 to 132 mmol⋅L-1; p = 0.040) and decreased the Matsuda insulin sensitivity index by a mean difference of -2 au (95% CI: -1 to -3 au; p = 0.001). This is the first study to demonstrate that post-exercise feeding to replaceme the carbohydrate expended during exercise can attenuate glucose tolerance and insulin sensitivity the following morning. The mechanism through which exercise improves insulin sensitivity is therefore (at least in part) dependent on carbohydrate availability and so the day-to-day metabolic health benefits of exercise might be best attained by maintaining a carbohydrate deficit overnight. [ABSTRACT FROM AUTHOR]