We investigated whether altered peripheral and/or corticospinal excitatory output and voluntary activation are implicated in hypohydration-induced reductions in muscle isometric and isokinetic (90°.s−1) strength. Nine male athletes completed two trials (hypohydrated, euhydrated) comprising 90 min cycling at 40°C, with body weight losses replaced in euhydrated trial. Peripheral nerve and transcranial magnetic stimulations were applied during voluntary contractions pre- and 40 min post-exercise to quantify voluntary activation and peripheral (M-wave) and corticospinal (motor evoked potential) evoked responses in m. vastus medialis. Both maximum isometric (−15.3±3.1 vs −5.4±3.5%) and isokinetic eccentric (−24.8±4.6 vs −7.3±7.2%) torque decreased to a greater extent in hypohydrated than euhydrated trials (p

Blastocystis is a unicellular eukaryote found in the gastrointestinal tract of both human and other animal hosts. The clinical significance of colonic Blastocystis colonization remains obscure. In this study, we used metabarcoding and bioinformatics analyses to identify differences in stool microbiota diversity between Blastocystis-positive and Blastocystis-negative individuals (n = 1285). Alpha diversity was significantly higher in Blastocystis carriers. At phylum level, Firmicutes and Bacteroidetes were enriched in carriers, while Proteobacteria were enriched in non-carriers. The genera Prevotella, Faecalibacterium, Flavonifracter, Clostridium, Succinivibrio, and Oscillibacter were enriched in carriers, whereas Escherichia, Bacteroides, Klebsiella, and Pseudomonas were enriched in non-carriers. No difference in beta diversity was observed. Individuals with Blastocystis-positive stools appear to have gut microbiomes associated with eubiosis unlike those with Blastocystisnegative stools, whose gut microbiomes are similar to those associated with dysbiosis. The role of Blastocystis as an indicator organism and potential modulator of the gut microbiota warrants further scrutiny.

INTRODUCTION: Montmorency cherry concentrate (MCC) supplementation enhances functional recovery from exercise, potentially due to antioxidant and anti-inflammatory effects. However, to date, supporting empirical evidence for these mechanistic hypotheses is reliant on indirect blood biomarkers. This study is the first to investigate functional recovery from exercise alongside molecular changes within the exercised muscle after MCC supplementation. METHODS: Ten participants completed two maximal unilateral eccentric knee extension trials after MCC or placebo (PLA) supplementation for 7 d before and 48 h after exercise. Knee extension maximum voluntary contractions, maximal isokinetic contractions, single leg jumps, and soreness measures were assessed before, immediately, 24 h, and 48 h after exercise. Venous blood and vastus lateralis muscle samples were collected at each time point. Plasma concentrations of interleukin-6, tumor necrosis factor alpha, C-reactive protein, creatine kinase, and phenolic acids were quantified. Intramuscular mRNA expressions of superoxide dismutase 1 (SOD1), SOD3, glutathione peroxidase 1 (GPX1), GPX3, GPX4, GPX7, catalase, and nuclear factor erythroid 2-related factor 2 and relative intramuscular protein expressions of SOD1, catalase, and GPX3 were quantified. RESULTS: MCC supplementation enhanced the recovery of normalized maximum voluntary contraction 1-s average compared with PLA (postexercise PLA, 59.5% ± 18.0%, vs MCC, 76.5% ± 13.9%; 24 h PLA, 69.8% ± 15.9%, vs MCC, 80.5% ± 15.3%; supplementation effect P = 0.024). MCC supplementation increased plasma hydroxybenzoic, hippuric, and vanillic acid concentrations (supplementation effect P = 0.028, P = 0.002, P = 0.003); SOD3, GPX3, GPX4, GPX7 (supplement effect P < 0.05), and GPX1 (interaction effect P = 0.017) gene expression; and GPX3 protein expression (supplementation effect P = 0.004) versus PLA. There were no significant differences between conditions for other outcome measures. CONCLUSIONS: MCC supplementation conserved isometric muscle strength and upregulated antioxidant gene and protein expression in parallel with increased phenolic acid concentrations.

Tart cherries (TC) are a rich source of polyphenols that elicit antioxidant and anti-inflammatory effects. As a consequence, the effects of TC derived supplements on markers of human health, exercise performance and sleep have been investigated. Supplementation protocols have been highly variable across studies and the dose of bioactive compounds used has often been poorly characterized. Specific and non-specific analytical methods were employed for measuring the total polyphenol and anthocyanin content in TC supplements. This review critically analyses the supplementation protocols and the analytical methods used for the characterization of TC supplements, culminating in recommendations for good practice in the analysis and reporting of the polyphenol content and profile of TC products. A literature search was conducted using PubMed/Medline and Web of Science up to May 4th, 2020, including studies published in all years prior. Only articles written in English that provided a TC dietary supplement as opposed to fresh whole TC were included in this review. Forty-three studies were identified as eligible and included for analysis in this review. The studies investigated the effects of TC supplementation on various aspects of human health, exercise recovery and performance and sleep. Twenty studies conducted an analysis of TC supplement and reported total polyphenol/anthocyanin content. Six studies did not report the polyphenol content of the TC supplement used. Seventeen studies reported the TC supplement polyphenol content but this was derived from previously published studies and presumably different supplement batches. The duration of the supplementation protocol ranged from acute supplementation to 84 days, meanwhile the total polyphenol and anthocyanin dose ranged from 143 to 2,140 mg/day and 15 to 547 mg/day, respectively. Due to the variety of specific and non-specific analytical methods used, the relative efficacy of different doses and polyphenol blends cannot reliably be extrapolated from critical analysis of the literature. Future studies should conduct an analysis of the study supplement batch. In addition to analysis and reporting of total polyphenol content, specific analytical methods such as HPLC UV/MS should be used to quantify total and individual anthocyanin contents.

Shatavari has long been used as an Ayurvedic herb for women’s health, but empirical evidence for its effectiveness has been lacking. Shatavari contains phytoestrogenic compounds that bind to the estradiol receptor. Postmenopausal estradiol deficiency contributes to sarcopenia and osteoporosis. In a randomised double-blind trial, 20 postmenopausal women (68.5 ± 6 years) ingested either placebo (N = 10) or shatavari (N = 10; 1000 mg/d, equivalent to 26,500 mg/d fresh weight shatavari) for 6 weeks. Handgrip and knee extensor strength were measured at baseline and at 6 weeks. Vastus lateralis (VL) biopsy samples were obtained. Data are presented as difference scores (Week 6—baseline, median ± interquartile range). Handgrip (but not knee extensor) strength was improved by shatavari supplementation (shatavari +0.7 ± 1.1 kg, placebo −0.4 ± 1.3 kg; p = 0.04). Myosin regulatory light chain phosphorylation, a known marker of improved myosin contractile function, was increased in VL following shatavari supplementation (immunoblotting; placebo −0.08 ± 0.5 a.u. shatavari +0.3 ± 1 arbitrary units (a.u.); p = 0.03). Shatavari increased the phosphorylation of Aktser473 (Aktser473 (placebo −0.6 ± 0.6 a.u. shatavari +0.2 ± 1.3 a.u.; p = 0.03) in VL. Shatavari supplementation did not alter plasma markers of bone turnover (P1NP, β-CTX) and stimulation of human osteoblasts with pooled sera (N = 8 per condition) from placebo and shatavari supplementation conditions did not alter cytokine or metabolic markers of osteoblast activity. Shatavari may improve muscle function and contractility via myosin conformational change and further investigation of its utility in conserving and enhancing musculoskeletal function, in larger and more diverse cohorts, is warranted.

Tart cherry (TC) supplementation can improve exercise recovery and performance; and may also improve sleep duration and quality. This study investigated the use and knowledge of TC supplementation by athletes of all competitive levels. Eighty participants (52.5% elite (international, national, professional), 47.5% sub-elite (semi-professional, state/regional, county level, club level, recreational)) completed an online questionnaire investigating their attitudes towards and use of TC supplementation. Overall, 22.6% of participants were using or had previously used TC supplements, and 12.5% of participants planned to used TC supplements. Improved recovery (71.4%), sleep (32.1%) and immunity and general health (32.1%) were the most frequently indicated goals by respondents using TC supplements. In total, 32.1% of respondents were supplemented with TC chronically, 39.3% acutely and 28.6% used a combination of chronic and acute supplementation. The majority of those employing TC supplementation chronically used TC either over 2-3 days (37.0%) or continuously (37.0%). The most popular TC pre- and post-loading period was one day (34.3% and 41.5%, respectively). There were no significant differences between elite and sub-elite athletes in any parameters assessed (p > 0.05). TC supplementation is not widely used by the athletes surveyed, and athletes using TC supplements showed poor awareness of an evidence-led dosing strategy, regardless of competitive level.

PURPOSE: This study tested the hypothesis that a novel, audio-visual-directed, home-based exercise training intervention would be effective at improving cardiometabolic health and mental well-being in inactive premenopausal women. METHODS: Twenty-four inactive premenopausal women (39 ± 10 years) were randomly assigned to an audio-visual-directed exercise training group (DVD; n = 12) or control group (CON; n = 12). During the 12-week intervention period, the DVD group performed thrice-weekly training sessions of 15 min. Training sessions comprised varying-intensity movements involving multiplanar whole-body accelerations and decelerations (average heart rate (HR) = 76 ± 3% HRmax). CON continued their habitual lifestyle with no physical exercise. A series of health markers were assessed prior to and following the intervention. RESULTS: Following the DVD intervention, HDL cholesterol (pre: 1.83 ± 0.45, post: 1.94 ± 0.46 mmol/L) and mental well-being, assessed via the Warwick Edinburgh Mental Well-Being Scale, improved (P  0.05). There were no pre-post intervention changes in any of the outcome variables in the CON group (P > 0.05). CONCLUSION: the present study suggests that a novel, audio-visual-directed exercise training intervention, consisting of varied-intensity movements interspersed with spinal and lower limb mobility and balance tasks, can improve [HDL cholesterol] and mental well-being in premenopausal women. Therefore, home-based, audio-visual-directed exercise training (45 min/week) appears to be a useful tool to initiate physical activity and improve aspects of health in previously inactive premenopausal women.

Tart cherry (TC) supplementation has been shown to accelerate post-exercise recovery, enhance endurance performance and improve sleep duration and quality. This study aimed to identify the use, practices and attitudes of sports nutrition and strength and conditioning practitioners towards tart cherry supplementation. Thirty-five practitioners anonymously completed an online survey investigating their use, practices and attitudes towards tart cherry supplements. Forty-six percent of the responders were currently recommending TC supplements, 11% had previously recommended TC supplements and 26% have not previously recommended TC supplements but were planning on doing so in the future. of those recommending TC, 50% recommended or were planning on recommending TC supplements to enhance exercise recovery and 26% to improve sleep duration and quality. Acute supplementation and daily use during multi-day competition or demanding training blocks with a 2–3-day pre-load were the most reported supplementation recommendations (28% and 18%, respectively). Fifty-two percent of responders indicated uncertainty about the daily polyphenol dose to recommend as part of a TC supplementation protocol. Despite the high use and interest from sports nutrition and strength and conditioning practitioners in TC supplements, their practices did not align with the protocols found to be effective within the literature.

Acute acetaminophen (ACT) ingestion has been shown to enhance cycling time-trial performance. The purpose of this study was to assess whether ACT ingestion enhances muscle activation and critical power (CP) during maximal cycling exercise. Sixteen active male participants completed two 3-min all-out tests against a fixed resistance on an electronically braked cycle ergometer 60 min after ingestion of 1 g of ACT or placebo (maltodextrin, PL). CP was estimated as the mean power output over the final 30 s of the test and W' (the curvature constant of the power-duration relationship) was estimated as the work done above CP. The femoral nerve was stimulated every 30 s to measure membrane excitability (M-wave) and surface electromyography (EMGRMS) was recorded continuously to infer muscle activation. Compared with PL, ACT ingestion increased CP (ACT: 297 ± 32 W vs. PL: 288 ± 31 W, P < 0.001) and total work done (ACT: 66.4 ± 6.5 kJ vs. PL: 65.4 ± 6.4 kJ, P = 0.03) without impacting W' (ACT: 13.1 ± 2.9 kJ vs. PL: 13.6 ± 2.4 kJ, P = 0.19) or the M-wave amplitude (P = 0.66) during the 3-min all-out cycling test. Normalised EMGRMS amplitude declined throughout the 3-min protocol in both PL and ACT conditions; however, the decline in EMGRMS amplitude was attenuated in the ACT condition, such that the EMGRMS amplitude was greater in ACT compared with PL over the last 60 s of the test (P = 0.04). These findings indicate that acute ACT ingestion might increase performance and CP during maximal cycling exercise by enhancing muscle activation.

Recent research suggests that acute consumption of pharmacological analgesics can improve exercise performance, but the ergogenic potential of ibuprofen (IBP) administration is poorly understood. This study tested the hypothesis that IBP administration would enhance maximal exercise performance. In one study, 13 physically active males completed 60 × 3-s maximal voluntary contractions (MVCs) of the knee extensors interspersed with 2-s passive recovery periods, on 2 occasions, with the critical torque (CT) estimated as the mean torque over the last 12 contractions (part A). In another study, 16 active males completed two 3-min all-out tests against a fixed resistance on an electronically braked cycle ergometer, with the critical power estimated from the mean power output over the final 30 s of the test (part B). All tests were completed 60 min after ingestion of maltodextrin (placebo, PL) or 400 mg of IBP. Peripheral nerve stimulation was administered at regular intervals and electromyography was measured throughout. For part A, mean torque (IBP: 60% ± 13% of pre-exercise MVC; PL: 58% ± 14% of pre-exercise MVC) and CT (IBP: 41% ± 16% of pre-exercise MVC; PL: 40% ± 15% of pre-exercise MVC) were not different between conditions (P > 0.05). For part B, end-test power output (IBP: 292 ± 28 W; PL: 288 ± 31 W) and work done (IBP: 65.9 ± 5.9 kJ; PL: 65.4 ± 6.4 kJ) during the 3-min all-out cycling tests were not different between conditions (all P > 0.05). For both studies, neuromuscular fatigue declined at a similar rate in both conditions (P > 0.05). In conclusion, acute ingestion of 400 mg of IBP does not improve single-leg or maximal cycling performance in healthy humans.

The following sections 3.5.1 to 3.5.3.2, which previously read.

BACKGROUND: Muscle strength loss following immobilisation has been predominantly attributed to rapid muscle atrophy. However, this cannot fully explain the magnitude of muscle strength loss, so changes in neuromuscular function (NMF) may be involved. OBJECTIVES: We systematically reviewed literature that quantified changes in muscle strength, size and NMF following periods of limb immobilisation in vivo in humans. METHODS: Studies were identified following systematic searches, assessed for inclusion, data extracted and quality appraised by two reviewers. Data were tabulated and reported narratively. RESULTS: Forty eligible studies were included, 22 immobilised lower and 18 immobilised upper limbs. Limb immobilisation ranged from 12 h to 56 days. Isometric muscle strength and muscle size declined following immobilisation; however, change magnitude was greater for strength than size. Evoked resting twitch force decreased for lower but increased for upper limbs. Rate of force development either remained unchanged or slowed for lower and typically slowed for upper limbs. Twitch relaxation rate slowed for both lower and upper limbs. Central motor drive typically decreased for both locations, while electromyography amplitude during maximum voluntary contractions decreased for the lower and presented mixed findings for the upper limbs. Trends imply faster rates of NMF loss relative to size earlier in immobilisation periods for all outcomes. CONCLUSIONS: Limb immobilisation results in non-uniform loss of isometric muscle strength, size and NMF over time. Different outcomes between upper and lower limbs could be attributed to higher degrees of central neural control of upper limb musculature. Future research should focus on muscle function losses and mechanisms following acute immobilisation. REGISTRATION: PROSPERO reference: CRD42016033692.

Polyphenols are characterised structurally by two or more hydroxyl groups attached to one or more benzene rings, and provide the taste and colour characteristics of fruits and vegetables. They are radical scavengers and metal chelators, but due to their low concentration in biological fluids in vivo their antioxidant properties seem to be related to enhanced endogenous antioxidant capacity induced via signalling through the Nrf2 pathway. Polyphenols also seem to possess anti-inflammatory properties and have been shown to enhance vascular function via nitric oxide-mediated mechanisms. As a consequence, there is a rationale for supplementation with fruit-derived polyphenols both to enhance exercise performance, since excess reactive oxygen species generation has been implicated in fatigue development, and to enhance recovery from muscle damage induced by intensive exercise due to the involvement of inflammation and oxidative damage within muscle. Current evidence would suggest that acute supplementation with ~ 300 mg polyphenols 1-2 h prior to exercise may enhance exercise capacity and/or performance during endurance and repeated sprint exercise via antioxidant and vascular mechanisms. However, only a small number of studies have been performed to date, some with methodological limitations, and more research is needed to confirm these findings. A larger body of evidence suggests that supplementation with > 1000 mg polyphenols per day for 3 or more days prior to and following exercise will enhance recovery following muscle damage via antioxidant and anti-inflammatory mechanisms. The many remaining unanswered questions within the field of polyphenol research and exercise performance and recovery are highlighted within this review article.

Limited evidence suggests that the consumption of polyphenols may improve glycaemic control and insulin sensitivity. The gut microbiome produces phenolic metabolites and increases their bioavailability. A handful of studies have suggested that polyphenol consumption alters gut microbiome composition. There are no data available investigating such effects in polyphenol-rich Montmorency cherry (MC) supplementation. A total of 28 participants (aged 40-60 years) were randomized to receive daily MC or glucose and energy-matched placebo supplementation for 4 wk. Faecal and blood samples were obtained at baseline and at 4 wk. There was no clear effect of supplementation on glucose handling (Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and Gutt indices), although the Matsuda index decreased significantly in the MC group post-supplementation, reflecting an increase in serum insulin concentration. Contrastingly, placebo, but not MC supplementation induced a 6% increase in the Oral Glucose Insulin Sensitivity (OGIS) estimate of glucose clearance. Serum IL-6 and C reactive protein were unaltered by either supplement. The faecal bacterial microbiome was sequenced; species richness and diversity were unchanged by MC or placebo and no significant correlation existed between changes in Bacteroides and Faecalibacterium abundance and any index of insulin sensitivity. Therefore, 4 weeks of MC supplementation did not alter the gut microbiome, glycaemic control or systemic concentrations of IL-6 and CRP in a middle-aged population.

AIM: Acetaminophen is a commonly used medicine for pain relief and emerging evidence suggests that it may improve endurance exercise performance. This study investigated some of the physiological mechanisms by which acute acetaminophen ingestion might blunt muscle fatigue development. METHODS: Thirteen active males completed 60 × 3 s maximum voluntary contractions (MVC) of the knee extensors with each contraction separated by a 2 s passive recovery period. This protocol was completed 60 min after ingesting 1 g of maltodextrin (placebo) or 1 g of acetaminophen on two separate visits. Peripheral nerve stimulation was administered every 6th contraction for assessment of neuromuscular fatigue development, with the critical torque (CT), which reflects the maximal sustainable rate of oxidative metabolism, taken as the mean torque over the last 12 contractions. Surface electromyography was recorded continuously as a measure of muscle activation. RESULTS: Mean torque (61 ± 11 vs. 58 ± 14% pre-exercise MVC) and CT (44 ± 13 vs. 40 ± 15% pre-exercise MVC) were greater in the acetaminophen trial compared to placebo (both P  0.05). However, the decline in electromyography amplitude was attenuated in the acetaminophen trial, with electromyography amplitude being greater compared to placebo from 210 s onwards (P 

(1) Background: Mucilage within cacao pods contains high levels of polyphenols. We investigated whether consumption of cacao juice enhances the recovery of muscle function following intensive knee extension exercise. (2) Methods: Ten recreationally active males completed two trials of 10 sets of 10 single leg knee extensions at ~80% one repetition maximum. Participants consumed each supplement (ZumoCacao® juice, CJ or a dextrose drink, PL) for 7 days prior to and 48 h post exercise. Knee extension maximum voluntary contraction (MVC) and a counter movement jump (CMJ) were performed at baseline, immediately, 24 h, and 48 h post-exercise. Venous blood samples were collected at each time point and analyzed for indices of inflammation, oxidative damage, and muscle damage. (3) Results: CMJ height recovered faster with CJ at 24 h and 48 h post-exercise (p < 0.05), but there was no effect of CJ on recovery of MVC (both p > 0.05). There was also no effect of the trial on any blood markers (all p > 0.05). (4) Conclusions: Supplementation with CJ for 7 days prior to and 2 days after intensive knee extensor exercise improved functional recovery as shown by an improved recovery of CMJ up to 48 h post-exercise. However, the precise mechanism of action is unclear and requires further investigation.

Copyright © 2019 the American Physiological Society. Flavonoid supplementation improves brachial artery flow-mediated dilation (FMD), but it is not known whether flavonoids protect against vascular dysfunction induced by ischemia-reperfusion (IR) injury and associated respiratory burst. In a randomized, double-blind, placebo-controlled, crossover study, we investigated whether 4 wk supplementation with freeze-dried Montmorency cherry (MC) attenuated suppression of FMD after IR induced by prolonged forearm occlusion. Twelve physically inactive overweight, middle-aged men (52.8 5.8 yr, BMI: 28.1 5.3 kg/m 2 ) consumed MC (235 mg/day anthocyanins) or placebo capsules for 4 wk, with supplementation blocks separated by 4 wk washout. Before and after each supplementation block, FMD responses and plasma nitrate and nitrite ([NO 2 ]) concentrations were measured at baseline and 15, 30, and 45 min after prolonged (20 min) forearm occlusion. FMD response was significantly depressed by the prolonged occlusion (P 0.001). After a 45-min reperfusion, FMD was restored to baseline levels after MC (FMD presupplementation: 30.5 8.4%, postsupplementation: 0.6 9.5%) but not placebo supplementation (FMD presupplementation: 11.6 10.6, postsupplementation: 25.4 4.0%; condition supplement interaction: P 0.038). Plasma [NO 2 ] decreased after prolonged occlusion but recovered faster after MC compared with placebo (45 min to baseline; MC: presupplementation: 15.3 9.6, postsupplementation: 6.2 8.1; Placebo: presupplementation: 16.3 5.9, postsupplementation: 27.7 11.1 nmol/l; condition supplement time interaction: P 0.033). Plasma peroxiredoxin concentration ([Prx2]) was significantly higher after MC (presupplementation: 22.8 1.4, postsupplementation: 28.0 2.4 ng/ml, P 0.029) but not after placebo supplementation (presupplementation: 22.1 2.2, postsupplementation: 23.7 1.5 ng/ml). In conclusion, 4 wk MC supplementation enhanced recovery of endothelium-dependent vasodilatation after IR, in parallel with faster recovery of plasma [NO 2 ], suggesting NO dependency. These protective effects seem to be related to increased plasma [Prx2], presumably conferring protection against the respiratory burst during reperfusion.

Purpose: Repeated cycles of endothelial ischemia–reperfusion injury and the resulting respiratory burst contribute to the irreversible pathophysiology of vascular diseases, and yet, the effects of ischemia reperfusion on vascular function, oxidative stress, and nitric oxide (NO) bioavailability have not been assessed simultaneously. Therefore, this study sought to examine the effects of prolonged forearm occlusion and subsequent reperfusion on NO-dependent brachial artery endothelial function. Methods: Flow-mediated dilatation was measured at baseline and 15, 30, and 45 min after 20-min forearm occlusion in 14 healthy, but physically inactive middle-aged men (53.7 ± 1.2 years, BMI: 28.1 ± 0.1 kg m−2). Venous blood samples collected from the occluded arm were analyzed for NO metabolites and markers of oxidative stress. Results: FMD was significantly depressed after the prolonged occlusion compared to baseline, with a significant reduction 15-min post-occlusion (6.6 ± 0.7 to 2.9 ± 0.4%, p < 0.001); FMD remained depressed after 30 min (4.1 ± 0.6%, p = 0.001), but was not significantly different to baseline after 45-min recovery (5.4 ± 0.7%, p = 0.079). Plasma nitrate (main time effect: p = 0.015) and nitrite (main time effect: p = 0.034) concentrations were significantly reduced after prolonged occlusion. Plasma catalase activity was significantly elevated at 4- (p = 0.016) and 45-min (p = 0.001) post-occlusion, but plasma peroxiredoxin 2 and protein carbonyl content did not change. Conclusions: Prolonged forearm occlusion resulted in acute impairment of endothelium-dependent vasodilatation of the brachial artery for at least 30 min after reperfusion. We demonstrate that this vascular dysfunction is associated with oxidative stress and reduced NO bioavailability following reperfusion.

BACKGROUND: Oxidative stress and inflammation may contribute to anabolic resistance in response to protein and exercise in older adults. We investigated whether consumption of montmorency cherry concentrate (MCC) increased anabolic sensitivity to protein ingestion and resistance exercise in healthy older men. METHODS: Sixteen healthy older men were randomized to receive MCC (60 mL·d-1) or placebo (PLA) for two weeks, after baseline measures in week 1. During week 3, participants consumed 10 g whey protein·d-1 and completed three bouts of unilateral leg resistance exercise (4 × 8-10 repetitions at 80% 1RM). Participants consumed a bolus (150 mL) and weekly (50 mL) doses of deuterated water. Body water 2H enrichment was measured in saliva and vastus lateralis biopsies were taken from the non-exercised leg after weeks 1, 2 and 3, and the exercised leg after week 3, to measure tracer incorporation at rest, in response to protein and protein + exercise. RESULTS: Myofibrillar protein synthesis increased in response to exercise + protein compared to rest (p 

© 2017, Canadian Science Publishing. All rights reserved. Blueberries are rich in flavonoids, which possess antioxidant and anti-inflammatory properties. High flavonoid intakes attenuate age-related cognitive decline, but data from human intervention studies are sparse. We investigated whether 12 weeks of blueberry concentrate supplementation improved brain perfusion, task-related activation, and cognitive function in healthy older adults. Participants were randomised to consume either 30 mL blueberry concentrate providing 387 mg anthocyanidins (5 female, 7 male; age 67.5 ± 3.0 y; body mass index, 25.9 ± 3.3 kg·m −2 ) or isoenergetic placebo (8 female, 6 male; age 69.0 ± 3.3 y; body mass index, 27.1 ± 4.0 kg·m −2 ). Pre-and postsupplementation, participants undertook a battery of cognitive function tests and a numerical Stroop test within a 1.5T magnetic resonance imaging scanner while functional magnetic resonance images were continuously acquired. Quantitative resting brain perfusion was determined using an arterial spin labelling technique, and blood biomarkers of inflammation and oxidative stress were measured. Significant increases in brain activity were observed in response to blueberry supplementation relative to the placebo group within Brodmann areas 4/6/10/ 21/40/44/45, precuneus, anterior cingulate, and insula/thalamus (p. <. 0.001) as well as significant improvements in grey matter perfusion in the parietal (5.0 ± 1.8 vs-2.9 ± 2.4%, p = 0.013) and occipital (8.0 ± 2.6 vs-0.7 ± 3.2%, p = 0.031) lobes. There was also evidence suggesting improvement in working memory (2-back test) after blueberry versus placebo supplementation (p = 0.05). Supplementation with an anthocyanin-rich blueberry concentrate improved brain perfusion and activation in brain areas associated with cognitive function in healthy older adults.

Lactate or gas exchange threshold (GET) and critical power (CP) are closely associated with human exercise performance. We tested the hypothesis that the limit of tolerance (Tlim) during cycle exercise performed within the exercise intensity domains demarcated by GET and CP is linked to discrete muscle metabolic and neuromuscular responses. Eleven men performed a ramp incremental exercise test, 4-5 severe-intensity (SEV; >CP) constant-work-rate (CWR) tests until Tlim, a heavy-intensity (HVY; GET) CWR test until Tlim, and a moderate-intensity (MOD;. 0.05) muscle metabolic milieu (i.e. low pH and [PCr] and high [lactate]) was attained at Tlim (approximately 2-14 min) for all SEV exercise bouts. The muscle metabolic perturbation was greater at Tlim following SEV compared with HVY, and also following SEV and HVY compared with MOD (all P < 0.05). The normalized M-wave amplitude for the vastus lateralis (VL) muscle decreased to a similar extent following SEV (-38 ± 15%), HVY (-68 ± 24%), and MOD (-53 ± 29%), (P > 0.05). Neural drive to the VL increased during SEV (4 ± 4%; P < 0.05) but did not change during HVY or MOD (P > 0.05). During SEV and HVY, but not MOD, the rates of change in M-wave amplitude and neural drive were correlated with changes in muscle metabolic ([PCr], [lactate]) and blood ionic/acid-base status ([lactate], [K+]) (P < 0.05). The results of this study indicate that the metabolic and neuromuscular determinants of fatigue development differ according to the intensity domain in which the exercise is performed.NEW & NOTEWORTHY the gas exchange threshold and the critical power demarcate discrete exercise intensity domains. For the first time, we show that the limit of tolerance during whole-body exercise within these domains is characterized by distinct metabolic and neuromuscular responses. Fatigue development during exercise greater than critical power is associated with the attainment of consistent "limiting" values of muscle metabolites, whereas substrate availability and limitations to muscle activation may constrain performance at lower intensities.

The anabolic potential of a dietary protein is determined by its ability to elicit postprandial rises in circulating essential amino acids and insulin. Minimal data exist regarding the bioavailability and insulinotropic effects of non-animal-derived protein sources. Mycoprotein is a sustainable and rich source of non-animal-derived dietary protein. We investigated the impact of mycoprotein ingestion, in a dose-response manner, on acute postprandial hyperaminoacidaemia and hyperinsulinaemia. In all, twelve healthy young men completed five experimental trials in a randomised, single-blind, cross-over design. During each trial, volunteers consumed a test drink containing either 20 g milk protein (MLK20) or a mass matched (not protein matched due to the fibre content) bolus of mycoprotein (20 g; MYC20), a protein matched bolus of mycoprotein (40 g; MYC40), 60 g (MYC60) or 80 g (MYC80) mycoprotein. Circulating amino acid, insulin and uric acid concentrations, and clinical chemistry profiles, were assessed in arterialised venous blood samples during a 4-h postprandial period. Mycoprotein ingestion resulted in slower but more sustained hyperinsulinaemia and hyperaminoacidaemia compared with milk when protein matched, with overall bioavailability equivalent between conditions (P>0·05). Increasing the dose of mycoprotein amplified these effects, with some evidence of a plateau at 60-80 g. Peak postprandial leucine concentrations were 201 (sem 24) (30 min), 118 (sem 10) (90 min), 150 (sem 14) (90 min), 173 (sem 23) (45 min) and 201 (sem 21 (90 min) µmol/l for MLK20, MYC20, MYC40, MYC60 and MYC80, respectively. Mycoprotein represents a bioavailable and insulinotropic dietary protein source. Consequently, mycoprotein may be a useful source of dietary protein to stimulate muscle protein synthesis rates.

© 2016 J. L. Bowtell et al. We aimed to study whether short-duration vibration exercise or football sessions of two different durations acutely changed plasma markers of bone turnover and muscle strain. Inactive premenopausal women (n=56) were randomized to complete a single bout of short (FG15) or long duration (FG60) small sided football or low magnitude whole body vibration training (VIB). Procollagen type 1 amino-terminal propeptide (P1NP) was increased during exercise for FG15 (51.6±23.0 to 56.5±22.5 μg·L -1 , mean ± SD, P < 0.05) and FG60 (42.6±11.8 to 50.2±12.8 μg·L -1 , P < 0.05) but not for VIB (38.8±15.1 to 36.6±14.7 μg·L -1 , P > 0.05). An increase in osteocalcin was observed 48 h after exercise (P < 0.05), which did not differ between exercise groups. C-terminal telopeptide of type 1 collagen was not affected by exercise. Blood lactate concentration increased during exercise for FG15 (0.6±0.2 to 3.4±1.2 mM) and FG60 (0.6±0.2 to 3.3±2.0 mM), but not for VIB (0.6±0.2 to 0.8±0.4 mM) (P < 0.05). Plasma creatine kinase increased by 55±63% and 137±119% 48 h after FG15 and FG60 (P < 0.05), but not after VIB (26±54%, NS). In contrast to the minor elevation in osteocalcin in response to a single session of vibration exercise, both short and lo nger durations of small sided football acutely increased plasma P1NP, osteocalcin, and creatine kinase. This may contribute to favorable effects of chronic training on musculoskeletal health.

Objectives: Our aim was to determine the effects of different inspired oxygen fractions on repeated sprint performance and cardiorespiratory and neuromuscular responses, to construct a hypoxic dose response. Design: Nine male well-trained multi-sport athletes completed 10×6s all-out running sprints with 30s recovery in 5 conditions with different inspired oxygen fraction (FIO2: 12%, 13%, 14%, 15%, 21%). Methods: Peak running speed was measured in each sprint and electromyography data were recorded from m. vastus lateralis in parallel with heart rate and blood oxygen saturation. Cardiorespiratory response was assessed via breath by breath expired air analysis and muscle oxygenation status was evaluated via near infrared spectroscopy. Results: in parallel with the higher heart rate, minute ventilation, blood lactate concentration, and muscle deoxygenation; lower blood oxygen saturation, pulmonary oxygen uptake and integrated EMG (all p < 0.05) were registered in all hypoxic conditions, with the greatest changes from baseline observed during the 13% trial. However, fatigue index and speed decrement were significantly greater only during the 12% vs 21% trial (p < 0.05). Conclusions: Physiological responses associated with performing 10×6s sprints interspersed with 30s passive recovery was incrementally greater as FIO2 decreased to 13%, yet fatigue development was significantly exacerbated relative to normoxia (FIO2: 21%) only at the 12% FIO2. © 2013 Sports Medicine Australia.

Purpose: the present study investigated the effects of 16 weeks of small-volume, small-sided soccer training soccer group (SG, n=13) and oscillating whole-body vibration training vibration group (VG, n=17) on body composition, aerobic fitness, and muscle PCr kinetics in healthy inactive premenopausal women in comparison with an inactive control group (CO, n=14). Methods: Training for SG and VG consisted of twice-weekly 15-min sessions with average heart rates (HRs) of ~155 and 90bpm respectively. Pre- and post-measurements of body composition (DXA), phosphocreatine (PCr) on- and off-kinetics, and HR measurements during standardised submaximal exercise were performed. Results: After 16 weeks of training in SG, fat percentage was lowered (p=0.03) by 1.7%±2.4% from 37.5%±6.9% to 35.8%±6.2% and the PCr decrease in the quadriceps during knee-extension ramp exercise was attenuated (4%±8%, p=0.04), with no changes in VG or CO (time-group effect: p=0.03 and p=0.03). Submaximal exercise HR was also reduced in SG after 16 weeks of training (6%±5% of HRmax, p=0.01). Conclusion: Short duration soccer training for 16 weeks appears to be sufficient to induce favourable changes in body composition and indicators of aerobic fitness and muscle oxidative capacity in untrained premenopausal women.

BACKGROUND: Foods with low glycaemic index (LGI) are reported to suppress appetite mainly in overweight population but have not been investigated in athletic adults. OBJECTIVE: the aim of this study was to compare the short-term effects of LGI and high GI (HGI) meals over a day on subsequent subjective appetite sensation, energy intake, energy expenditure, energy balance and resting metabolic rate in physically active males. METHODS: This cross-sectional randomized crossover study included 14 active males (mean ± SD; age 34.5 ± 8.9 years, body mass index 22.8 ± 2.1 kg m(-2)) to consume LGI and HGI meals on two separate days. On each trial day, participants consumed a breakfast in the laboratory and then left with a packed lunch, dinner and snacks. Appetite scores, energy intake and expenditure were assessed. RESULTS: the area under the curve for appetite scores of the HGI trial was significantly smaller than that of the LGI trial during the laboratory period (p = 0.027) and throughout the day (p = 0.009). No significant differences in energy intake, energy expenditure, energy balance and resting metabolic rate were found between groups, between the trial days and between the corresponding post-trial days. CONCLUSIONS: These results show that frequent ingestion of the HGI meals, contrary to the previous reports, suppresses appetite more than that of LGI meals, but did not affect energy balance in physically active normal-weight males.

Increased muscle activation during whole-body vibration (WBV) is mainly ascribed to a complex spinal and supraspinal neurophysiological mechanism termed the tonic vibration reflex (TVR). However, TVR has not been experimentally demonstrated during low-frequency WBV, therefore this investigation aimed to determine the expression of TVR during WBV. Whilst seated, eight healthy males were exposed to either vertical WBV applied to the leg via the plantar-surface of the foot, or Achilles tendon vibration (ATV) at 25 Hz and 50 Hz for 70s. Ankle plantar-flexion force, tri-axial accelerations at the shank and vibration source, and surface EMG activity of m. soleus (SOL) and m. tibialis anterior (TA) were recorded from the unloaded and passively loaded leg to simulate body mass supported during standing. Plantar flexion force was similarly augmented by WBV and ATV and increased over time in a load- and frequency dependent fashion. SOL and TA EMG amplitudes increased over time in all conditions independently of vibration mode. 50 Hz WBV and ATV resulted in greater muscle activation than 25 Hz in SOL when the shank was loaded and in TA when the shank was unloaded despite the greater transmission of vertical acceleration from source to shank with 25 Hz and WBV, especially during loading. Low-amplitude WBV of the unloaded and passively loaded leg produced slow tonic muscle contraction and plantar-flexion force increase of similar magnitudes to those induced by Achilles tendon vibration at the same frequencies. This study provides the first experimental evidence supporting the TVR as a plausible mechanism underlying the neuromuscular response to whole-body vibration.

Repeated sprint ability (RSA) is a critical success factor for intermittent sport performance. Repeated sprint training has been shown to improve RSA, we hypothesised that hypoxia would augment these training adaptations. Thirty male well-trained academy rugby union and rugby league players (18.4 ± 1.5 years, 1.83 ± 0.07 m, 88.1 ± 8.9 kg) participated in this single-blind repeated sprint training study. Participants completed 12 sessions of repeated sprint training (10 × 6 s, 30 s recovery) over 4 weeks in either hypoxia (13% FiO₂) or normoxia (21% FiO₂). Pretraining and post-training, participants completed sports specific endurance and sprint field tests and a 10 × 6 s RSA test on a non-motorised treadmill while measuring speed, heart rate, capillary blood lactate, muscle and cerebral deoxygenation and respiratory measures. Yo-Yo Intermittent Recovery Level 1 test performance improved after RS training in both groups, but gains were significantly greater in the hypoxic (33 ± 12%) than the normoxic group (14 ± 10%, p

In upper limb muscles, altered corticospinal excitability and reduction in neural drive are observed in parallel with peripheral fatigue during prolonged and/or repeated contractions. However, the fatigue-induced adaptations of central and peripheral elements and their relative contribution to lower limb muscle performance are yet to be fully explored. In the present study, corticospinal excitability and peripheral contractility of ankle Xexor muscles were quantiWed before, during and after repeated brief unilateral maximal dorsiXexions to fatigue in eleven healthy volunteers. Transcranial magnetic stimulation of the motor cortex area related to lower limb muscles was performed, and the evoked twitch and EMG responses in tibialis anterior (TA) and soleus (SOL) were measured. The motor evoked potentials (MEPs) in fatigued TA during post-exercise maximal dorsiXexions were smaller (20 ± 6 %, p = 0.026) and remained depressed for at least 5 min. Postexercise MEPs in fatigued SOL and silent periods in TA and SOL were not diVerent compared to pre-exercise. These changes were accompanied by lower voluntary torque (8 3 %, p = 0.013), estimated resting twitch (36 ± 5 %, p = 0.003) and voluntary activation (17 9 %, p = 0.021) versus pre-exercise. During last versus Wrst maximal contraction in the fatiguing protocol lower voluntary torque (40 4 %, p = 0.003), higher MEP amplitudes (>+49 %, p < 0.021) and longer silent periods (>+24 %, p

PURPOSE: Montmorency cherries contain high levels of polyphenolic compounds including flavonoids and anthocyanins possessing antioxidant and anti-inflammatory effects. We investigated whether the effects of intensive unilateral leg exercise on oxidative damage and muscle function were attenuated by consumption of a Montmorency cherry juice concentrate using a crossover experimental design. METHODS: Ten well-trained male overnight-fasted athletes completed two trials of 10 sets of 10 single-leg knee extensions at 80% one-repetition maximum. Trials were separated by 2 wk, and alternate legs were used in each trial. Participants consumed each supplement (CherryActive® (CA) or isoenergetic fruit concentrate (FC)) for 7 d before and 48 h after exercise. Knee extension maximum voluntary contractions (MVC) were performed before, immediately after, and 24 and 48 h after the damaging exercise. Venous blood samples were collected at each time point, and serum was analyzed for creatine kinase (CK) activity, nitrotyrosine, high-sensitivity C-reactive protein, total antioxidant capacity, and protein carbonyls (PC). Two-way repeated-measures ANOVA were used for statistical analysis of the data. RESULTS: MVC force recovery was significantly faster (24 h: CA 90.9% ± 4.2% of initial MVC vs FC 84.9% ± 3.4% of initial MVC; 48 h: CA 92.9% ± 3.3% of initial MVC vs FC 88.5% ± 2.9% of initial MVC (mean ± SEM); P < 0.05) after CA than FC consumption. Only serum CK and PC increased significantly from baseline, peaking 24 h after exercise (P < 0.001). The exercise-induced increase in CK activity was not different between trials. However, both the percentage (24 h after: CA 23.8% ± 2.9% vs FC 82.7% ± 11.7%; P = 0.013) and absolute (24 h after: CA 0.31 ± 0.03 nmol·mg(-1) protein vs FC 0.60 ± 0.08 nmol·mg(-1) protein; P = 0.079) increase in PC was lower in CA than FC trials. CONCLUSIONS: Montmorency cherry juice consumption improved the recovery of isometric muscle strength after intensive exercise perhaps owing to the attenuation of the oxidative damage induced by the damaging exercise.

COPD patients have reduced muscle glutamate which may contribute to an impaired response of oxidative metabolism to exercise. We hypothesised that prior glutamine supplementation would enhance V(O2) peak, V(O2) at lactate threshold and speed pulmonary oxygen uptake kinetics in COPD. 13 patients (9 males, age 66±5 years, mean±SD) with severe COPD (mean FEV(1) 0.88±0.23l, 33±7% predicted) performed on separate days ramp cycle-ergometry (5-10 W min(-1)) to volitional exhaustion and subsequently square-wave transitions to 80% estimated lactate threshold (LT) following consumption of either placebo (CON) or 0.125 g kg bm(-1) of glutamine (GLN) in 5 ml kg bm(-1) placebo. Oral glutamine had no effect on peak or V(O2) at LT, {V(O2) peak: CON=0.70±0.1 l min(-1) vs. GLN=0.73±0.2 l min(-1); LT: CON=0.57±0.1 l min(-1) vs. GLN=0.54±0.1 lmin(-1)} or V(O2) kinetics {tau: CON=68±22 s vs. GLN=68±16 s}. Ingestion of glutamine before exercise did not improve indices of oxidative metabolism in this patient group.

The purpose of the present study was to quantify vibration transmissibility through the lower extremity during exercise on a whole-body vibration (WBV) platform. Six healthy adults completed 20 trials of 30-second static squat exercise at 30 or 40 degrees of knee flexion angle on a WBV platform working at combinations of 5 frequencies (VF: 20, 25, 30, 35, 40 Hz) and 2 amplitudes (VA: low, 1.5 mm or high, 3 mm). Accelerations induced by the platform were recorded simultaneously at the shank and the thigh using triaxial accelerometers positioned at the segmental center of mass. Root-mean-square (RMS) acceleration amplitude and transmission ratios between the platform and the leg segments were calculated and compared between the experimental conditions. An alpha level of 0.05 was set to establish significance. Shank vertical acceleration was greatest at the lower VF (p = 0.028), higher VA (p = 0.028), and deeper squat (p = 0.048). Thigh vertical acceleration was not affected by depth of squat (p = 0.25), but it was greatest at higher VA (p = 0.046) and lower VF (p = 0.028). Medial-lateral shank acceleration was greatest at higher VF and deeper squat (both p = 0.046) and at higher VA (p = 0.028). Medial-lateral thigh acceleration was positively related to both VF (p = 0.046) and VA (p = 0.028) but was not affected by knee angle (p = 0.46). Anterior-posterior shank acceleration was higher at deeper squat (p = 0.046) and at lower VF and higher VA (both p = 0.028). Anterior-posterior thigh acceleration was related positively to the VA (p = 0.028), inversely to the VF (p = 0.028), and not dependent on knee angle (p = 0.75). Identification of specific vibration parameters and posture, which underpin WBV training efficacy, will enable coaches and athletes to design WBV training programs to specifically target shank or thigh muscles for enhanced performance.

This study was conducted to investigate whether the low-frequency (5-Hz) oscillatory vibration-like stimulus, purported to be delivered by exercising with Flexi-bar, acutely affects muscle activation and maximal voluntary contraction (MVC) force. Nine healthy men participated in 2 trials, separated by at least 1 week, during which 4 x 30-second sets of exercise were performed with either the Flexi bar or a Sham bar. Maximal voluntary contraction force for elbow flexion, elbow extension, and knee extension were measured before and after the exercise. Root-mean-square amplitude and median frequency of electromyography (EMG) signal were calculated for the first and last 10 seconds of each exercise set and during the MVCs from biceps brachii (BB), triceps brachii (TB), rectus femoris (RF), and vastus lateralis (VL) for each trial. Electromyography amplitude was significantly higher for all studied muscles during Flexi-bar than Sham-bar exercise (32-203%, p < 0.05). Median frequency of EMG power spectrum was significantly lower in arm (TB: -40 +/- 13%, p < 0.0001; BB: -32 +/- 25%, p = 0.015) but not in leg (RF: -12 +/- 18%; VL: +6 +/- 32%; p > 0.05) muscles during Flexi-bar compared with Sham-bar exercise. Knee extension MVC force significantly decreased after Flexi-bar exercise (-3 +/- 7%, p = 0.048) in parallel with reduced RF EMG amplitude (-8 +/- 5%, p = 0.04), but there were no acute residual effects on elbow flexion/extension MVC or arm and VL EMG muscle activity. Using Flexi bar during exercise provoked acute alterations in arm- and leg-muscle EMG parameters and maximum force-generating capacity, indicating greater fatigue development than when exercising with the Sham bar. The results of this study indicate that Flexi bar may therefore be used to impose a stronger training stimulus on the muscle during submaximal exercise.

The existence of an acetyl group deficit at or above 90% of maximal oxygen uptake (VO(2max)) has proved controversial, with contradictory results likely relating to limitations in previous research. The purpose of the present study was to determine whether the "acetyl group deficit" occurs at the start of exercise at 90%VO(2max) in a well-controlled study. Eight male participants (age: 33.6 +/- 2.0 years; VO(2max): 3.60 +/- 0.21 litres. min(-1)) completed two exercise bouts at 90%VO(2max) for 3 min following either 30 min of saline (control) or dichloroacetate (50 mg. kg(-1) body mass) infusion, ending 15 min before exercise. Muscle biopsies were obtained immediately before and after exercise while continuous non-invasive measures of pulmonary oxygen uptake and muscle deoxygenation were made. Muscle pyruvate dehydrogenase activity was significantly higher before exercise following dichloroacetate infusion (control: 2.67 +/- 0.98 vs. dichloroacetate: 17.9 +/- 1.1 mmol acetyl-CoA. min(-1). mg(-1) protein, P = 0.01) and resulted in higher pre- and post-exercise muscle acetylcarnitine (pre-exercise control: 3.3 +/- 0.95 vs. pre-exercise dichloroacetate: 8.0 +/- 0.88 vs. post-exercise control: 11.9 +/- 1.1 vs. post-exercise dichloroacetate: 17.2 +/- 1.1 mmol. kg(-1) dry muscle, P < 0.05). However, substrate-level phosphorylation (control: 125 +/- 20 vs. dichloroacetate: 113 +/- 13 mmol adenosine triphosphate. kg(-1) dry muscle) and VO(2) kinetics (control: 19.2 +/- 2.2 vs. dichloroacetate: 22.8 +/- 2.5 s), were unaltered. Furthermore, dichloroacetate infusion blunted the slow component of VO(2) and muscle deoxygenation and slowed muscle deoxygenation kinetics, possibly by enhancing oxygen delivery during exercise. These data support the hypothesis that the "acetyl group deficit" does not occur at or above 90%VO(2max).

The aim of this study was to differentiate between endurance and power athletes based on electromyographic (EMG) data analysed using new spectral indices. Nine endurance and six strength athletes were recruited to complete sets of knee extension repetitions (15 per set) until exhaustion, with each set followed by a maximal voluntary isometric knee extensor contraction. Peripheral muscle fatigue of the vastus lateralis, vastus medialis, and rectus femoris (bilaterally) was quantified by the changes in median frequency of the EMG power spectrum and a new spectral EMG fatigue index. Cluster analysis of the fatigue indices differentiated athletes into two groups: endurance (fatigue resistant) and strength (faster fatigue), whereas cluster analysis of the median EMG power spectrum frequency produced six indistinct groups. The average fatigue index for the quadriceps group increased across repetitions by 40 +/- 24% in the endurance group and by 184 +/- 12% in the strength group. The decrease in peak force and power across repetitions, and the rate of force decrease during maximal voluntary contraction per set, were significantly smaller for the endurance than for the strength group. The new spectral EMG indices effectively discriminated between strength and endurance athletes, thus providing a useful functional index that could be applied to track training adaptations as well as potentially talent identification.

The aim of this study was to determine whether low-frequency whole-body vibration (WBV) modulates the excitability of the corticospinal and intracortical pathways related to tibialis anterior (TA) muscle activity, thus contributing to the observed changes in neuromuscular function during and after WBV exercise. Motor-evoked potentials (MEPs) elicited in response to transcranial magnetic stimulation (TMS) of the leg area of the motor cortex were recorded in TA and soleus (SOL) muscles of seven healthy male subjects whilst performing 330 s continuous static squat exercise. Each subject completed two conditions: control (no WBV) and WBV (30 Hz, 1.5 mm vibration applied from 111 to 220 s). Five single suprathreshold and five paired TMS were delivered during each squat period lasting 110 s (pre-, during and post-WBV). Two interstimulus intervals (ISIs) between the conditioning and the testing stimuli were employed in order to study the effects of WBV on short-interval intracortical inhibition (SICI, ISI = 3 ms) and intracortical facilitation (ICF, ISI = 13 ms). During vibration relative to squat exercise alone, single-pulse TMS provoked significantly higher TA MEP amplitude (56 +/- 14%, P = 0.003) and total area (71 +/- 19%, P = 0.04), and paired TMS with ISI = 13 ms provoked smaller MEP amplitude (-21 +/- 4%, P = 0.01) but not in SOL. Paired-pulse TMS with ISI = 3 ms elicited significantly lower MEP amplitude (TA, -19 +/- 4%, P = 0.009; and SOL, -13 +/- 4%, P = 0.03) and total area (SOL, -17 +/- 6%, P = 0.02) during vibration relative to squat exercise alone in both muscles. Tibialis anterior MEP facilitation in response to single-pulse TMS suggests that WBV increased corticospinal pathway excitability. Increased TA and SOL SICI and decreased TA ICF in response to paired-pulse TMS during WBV indicate vibration-induced alteration of the intracortical processes as well.

A sharp intake of breath followed by a strong vocalisation is widely observed in response to acute pain although its function and mechanism is poorly understood. This study investigated the effect of percutaneous (overlying the tibial bone) electrical stimulation delivered early (20-30% of inspiratory time) during inspiration (INSP) or expiration (EXP) (20-30% of expiratory time) at sensory intensities at (100%), above (125%) and below (50% and 75%) the pre-determined pain threshold (PT), upon within-a-breath respiratory parameters (via pneumotachography). All INSP stimulation intensities provoked significant inspiratory time shortening thereby elevating mean inspiratory flow. Tidal volume, but not peak flow was increased in response to 100% PT and 125% PT stimulation (vs. PRE). Shortening and increased tidal volume combined to evoke significant mean inspiratory airflow increments. In contrast, EXP stimulation failed to evoke any effect. Thus, our study provides evidence of a within-a-breath inspiratory-specific, augmentory response to noxious stimulation.

OBJECTIVE: to investigate whether 10 breaths against a vibration stimulus elicits increments of spontaneous and maximal inspiratory mouth pressure (maxMP) and tidal mean inspiratory flow (iV(T)/T(I)) upon stimulus removal. METHODS: Twelve healthy subjects (8 female, 4 male; 22-50 years old), recruited from the University student body, completed 3 maximal inspirations before (pre) and after (post) 10 inspirations against resistive loading with a vibration-type stimulus (VIB; youbreathe, Exoscience Ltd. London, UK), pressure-matched resistive loading (RES) or resting breathing (CON; no load). The trials were presented in a random order. maxMP and involuntary tidal breathing were compared pre and post conditioning. RESULTS: Inspiratory neural drive increased only after VIB as evidenced by increased tidal and maxMP and mean inspiratory flow (iV(T)/T(I); p < 0.05). There was no effect of either resistance or control breathing on maximal maxMP or tidal responses. CONCLUSIONS: Ten conditioning breaths of VIB lead to increased maximal inspiratory mouth pressure and spontaneous mouth pressure and mean inspiratory flow possibly through a common mechanism of increased descending respiratory drive.

Glutamine enhances the exercise-induced expansion of the tricarboxylic acid intermediate pool. The aim of the present study was to determine whether oral glutamine, alone or in combination with hyperoxia, influenced oxidative metabolism and cycle time-trial performance. Eight participants consumed either placebo or 0.125 g kg body mass(-1) of glutamine in 5 ml kg body mass(-1) placebo 1 h before exercise in normoxic (control and glutamine respectively) or hyperoxic (FiO(2) = 50%; hyperoxia and hyperoxia + glutamine respectively) conditions. Participants then cycled for 6 min at 70% maximal oxygen uptake (VO(2max)) immediately before completing a brief high-intensity time-trial (approximately 4 min) during which a pre-determined volume of work was completed as fast as possible. The increment in pulmonary oxygen uptake during the performance test (DeltaVO(2max), P = 0.02) and exercise performance (control: 243 s, s(x) = 7; glutamine: 242 s, s(x) = 3; hyperoxia: 231 s, s(x) = 3; hyperoxia + glutamine: 228 s, s(x) = 5; P < 0.01) were significantly improved in hyperoxic conditions. There was some evidence that glutamine ingestion increased DeltaVO(2max) in normoxia, but not hyperoxia (interaction drink/FiO(2), P = 0.04), but there was no main effect or impact on performance. Overall, the data show no effect of glutamine ingestion either alone or in combination with hyperoxia, and thus no limiting effect of the tricarboxylic acid intermediate pool size, on oxidative metabolism and performance during maximal exercise.

The aim of the present study was to determine whether glutamine ingestion, which has been shown to enhance the exercise-induced increase in the tricarboxylic acid intermediate (TCAi) pool size, resulted in augmentation of the rate of increase in oxidative metabolism at the onset of exercise. In addition, the potential interaction with oxygen availability was investigated by completing exercise in both normoxic and hyperoxic conditions. Eight male cyclists cycled for 6 min at 70% VO2max following consumption of a drink (5 ml kg body mass(-1)) containing a placebo or 0.125 g kg body mass(-1) of glutamine in normoxic (CON and GLN respectively) and hyperoxic (HYP and HPG respectively) conditions. Breath-by-breath pulmonary oxygen uptake and continuous, non-invasive muscle deoxygenation (via near infrared spectroscopy: NIRS) data were collected throughout exercise. The time constant of the phase II component of pulmonary oxygen uptake kinetics was unchanged between trials (CON: 21.5 +/- 3.0 vs. GLN: 18.2 +/- 1.3 vs. HYP: 18.9 +/- 2.0 vs. HPG: 18.6 +/- 1.2 s). There was also no alteration of the kinetics of relative muscle deoxygenation as measured via NIRS (CON: 5.9 +/- 0.7 vs. GLN: 7.3 +/- 0.8 vs. HYP: 6.5 +/- 0.9 vs. HPG: 5.2 +/- 0.4 s). Conversely, the mean response time of pulmonary oxygen uptake kinetics was faster (CON: 33.4 +/- 1.2 vs. GLN: 29.8 +/- 2.3 vs. HYP: 33.2 +/- 2.6 vs. HPG: 31.6 +/- 2.6 s) and the time at which muscle deoxygenation increased above pre-exercise values was earlier (CON: 9.6 +/- 0.9 vs. GLN: 8.7 +/- 1.1 vs. HYP: 8.5 +/- 0.8 vs. HPG: 8.4 +/- 0.7 s) following glutamine ingestion. In normoxic conditions, plasma lactate concentration was lower following glutamine ingestion compared to placebo. Whilst the results of the present study provide some support for the present hypothesis, the lack of any alteration in the time constant of pulmonary oxygen uptake and muscle deoxygenation kinetics suggest that the normal exercise induced expansion of the TCAi pool size is not limiting to oxidative metabolism at the onset of cycle exercise at 70% VO2max.

The tricarboxylic acid (TCA) cycle is the major final common pathway for oxidation of carbohydrates, lipids and some amino acids, which produces reducing equivalents in the form of nicotinamide adenine dinucleotide and flavin adenine dinucleotide that result in production of large amounts of adenosine triphosphate (ATP) via oxidative phosphorylation. Although regulated primarily by the products of ATP hydrolysis, in particular adenosine diphosphate, the rate of delivery of reducing equivalents to the electron transport chain is also a potential regulatory step of oxidative phosphorylation. The TCA cycle is responsible for the generation of approximately 67% of all reducing equivalents per molecule of glucose, hence factors that influence TCA cycle flux will be of critical importance for oxidative phosphorylation. TCA cycle flux is dependent upon the supply of acetyl units, activation of the three non-equilibrium reactions within the TCA cycle, and it has been suggested that an increase in the total concentration of the TCA cycle intermediates (TCAi) is also necessary to augment and maintain TCA cycle flux during exercise. This article reviews the evidence of the functional importance of the TCAi pool size for oxidative metabolism in exercising human skeletal muscle. In parallel with increased oxidative metabolism and TCA cycle flux during exercise, there is an exercise intensity-dependent 4- to 5-fold increase in the concentration of the TCAi. TCAi concentration reaches a peak after 10-15 minutes of exercise, and thereafter tends to decline. This seems to support the suggestion that the concentration of TCAi may be of functional importance for oxidative phosphorylation. However, researchers have been able to induce dissociations between TCAi pool size and oxidative energy provision using a variety of nutritional, pharmacological and exercise interventions. Brief periods of endurance training (5 days or 7 weeks) have been found to result in reduced TCAi pool expansion at the start of exercise (same absolute work intensity) in parallel with either equivalent or increased oxidative energy provision. Cycloserine inhibits alanine aminotransferase, which catalyses the predominant anaplerotic reaction in exercising human muscle. When infused into contracting rat hindlimb muscle, TCAi pool expansion was reduced by 25% with no significant change in oxidative energy provision or power output. Glutamine supplementation has been shown to enhance TCAi pool expansion at the start of exercise with no increase in oxidative energy provision. In summary, there is a consistent dissociation between the extent of TCAi pool expansion at the onset of exercise and oxidative energy provision. At the other end of the spectrum, the parallel loss of TCAi, glycogen and adenine nucleotides and accumulation of inosine monophosphate during prolonged exercise has led to the suggestion that there is a link between muscle glycogen depletion, reduced TCA cycle flux and the development of fatigue. However, analysis of serial biopsies during prolonged exercise demonstrated dissociation between muscle TCAi content and both muscle glycogen content and muscle oxygen uptake. In addition, the delay in fatigue development achieved through increased carbohydrate availability does not attenuate TCAi reduction during prolonged exercise. Therefore, TCAi concentration in whole muscle homogenate does not seem to be of functional importance. However, TCAi content can currently only be measured in whole muscle homogenate rather than the mitochondrial subfraction where TCA cycle reactions occur. In addition, anaplerotic flux rather than TCAi content per se is likely to be of greater importance in determining TCA cycle flux, since TCAi content is probably merely reflective of anaplerotic substrate concentration. Methodological advances are required to allow researchers to address the questions of whether oxidative phosphorylation is limited by mitochondrial TCAi content and/or anaplerotic flux.

PURPOSE: This study was conducted to test whether a low-frequency vibration-like stimulus (rapid variable resistance) applied during a single session of knee extension exercise would alter muscle performance. METHODS: Torque, knee joint angle, EMG activity of rectus femoris (RF) and vastus lateralis (VL) muscles, and VL muscle oxygenation status (near-infrared spectroscopy) were recorded during metronome-guided knee extension exercise. Nine healthy adults completed four trials exercising at contraction intensities of 35% (L) or 70% (H) of one-repetition maximum (1RM) in control (no vibration, Vb-) or vibrated condition (superimposed 10-Hz vibration-like stimulus, Vb+). Maximum voluntary contraction and 1RM were tested pre- and postexercise. RESULTS: During 1RM tests, muscle dynamic strength (P=0.02) and power (P=0.05) were significantly higher during vibrated rather than nonvibrated trials, and strength was significantly higher post- than preexercise (P=0.002), except during LVb- trial. Median spectral frequency of VL and RF EMG activity was significantly higher during postexercise than preexercise 1RM test in the vibration trials but unchanged in the control trials (P

PURPOSE: the aim of the present study was to test the applicability and sensitivity of new electromyography (EMG) spectral indices in assessing peripheral muscle fatigue during dynamic knee-extension exercise. METHODS: Seven subjects completed 10 sets of 15 repetitions of right knee-extension exercise lifting 50% of their one-repetition maximum. Torque (T), knee-joint angle, and the interference EMG of rectus femoris muscle were recorded simultaneously. Maximal voluntary isometric contraction (MVC) was tested before and after exercise. Median spectral frequency (Fmed) and new spectral indices of muscle fatigue (FInsmk) were calculated for each repetition. RESULTS: the rate and range of FInsmk- and Fmed-relative changes against the first repetition of the corresponding set increased gradually across successive repetitions within the set, reflecting accumulation of peripheral muscle fatigue. The maximal change of FInsmk observed in the present experiment was approximately eightfold, whereas that of Fmed was only 32%. Significant between-subject variability in the range of FInsmk changes (P < 0.0001) was found, so a hierarchical cluster analysis of muscle fatigue indices was conducted. Three distinct subgroups of subjects were identified: high (N = 1, FInsmk change > 400%), medium (N = 4, 200% < FInsmk change < 400%), and low (N = 2, FInsmk change < 200%) muscle fatigability. The changes in muscle performance during (last vs first repetition peak T, P = 0.03) and after (post- vs preexercise MVC, P = 0.012) exercise were significantly different between clusters (one-way ANOVA). The rate of fatigue development was also significantly different between clusters (linear regression analysis of Fmed and FInsmk changes). CONCLUSIONS: the new spectral indices are a valid and reliable tool for assessment of muscle fatigability irrespective of EMG signal variability caused by dynamic muscle contractions, and these indices are more sensitive than those traditionally used.

There is an up to four-fold increase in the concentration of the tricarboxylic acid (TCA) cycle intermediates at the start of exercise. The rate of TCA cycle flux and, hence, oxidative metabolism may be limited by the concentration of the intermediates in the cycle. The dramatic decline in intramuscular glutamate at the start of exercise, in tandem with increased intramuscular alanine, suggests that glutamate is an important anaplerotic precursor. We hypothesized that oral glutamine might enhance the exercise-induced TCA cycle intermediate pool expansion. Indeed, a greater increase in the sum of muscle citrate, malate, fumarate, and succinate concentrations (approximately 85% total TCA intermediate pool) occurred at the start of exercise after ingestion of glutamine rather than of placebo or ornithine alpha-ketoglutarate. However, neither endurance capacity nor the degree of phosphocreatine depletion or lactate accumulation was altered. This suggests that TCA cycle intermediates do not limit flux through the cycle or that more intense exercise is required to show the limitation.

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine α-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at ∼70% maximal O2 uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine α-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (ΣTCAI; citrate, malate, fumarate, and succinate, ∼85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, ΣTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 ± 0.61) than in the CON condition (3.74 ± 0.38, P < 0.05) and the OKG condition (3.85 ± 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of α-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at approximately 70% maximal O2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (SigmaTCAI; citrate, malate, fumarate, and succinate, approximately 85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, SigmaTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 +/- 0.61) than in the CON condition (3.74 +/- 0.38, P < 0.05) and the OKG condition (3.85 +/- 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.

After exhaustive exercise, intravenous or oral glutamine promoted skeletal muscle glycogen storage. However, when glutamine was ingested with glucose polymer, whole-body carbohydrate storage was elevated, the most likely site being liver and not muscle, possibly due to increased glucosamine formation. The rate of tricarboxylic acid (TCA) cycle flux and hence oxidative metabolism may be limited by the availability of TCA intermediates. There is some evidence that intramuscular glutamate normally provides alpha-ketoglutarate to the mitochondrion. We hypothesized that glutamine might be a more efficient anaplerotic precursor than endogenous glutamate alone. Indeed, a greater expansion of the sum of muscle citrate, malate, fumarate and succinate concentrations was observed at the start of exercise (70% VO2(max)) after oral glutamine than when placebo or ornithine alpha-ketoglutarate was given. However, neither endurance time nor the extent of phosphocreatine depletion or lactate accumulation during the exercise was altered, suggesting either that TCA intermediates were not limiting for energy production or that the severity of exercise was insufficient for the limitation to be operational. We have also shown that in the perfused working rat heart, there is a substantial fall in intramuscular glutamine and alpha-ketoglutarate, especially after ischemia. Glutamine (but not glutamate, alpha-ketoglutarate or aspartate) was able to rescue the performance of the postischemic heart. This ability appears to be connected to the ability to sustain intracardiac ATP, phosphocreatine and glutathione.

Seven untrained male subjects participated in a double-blind, crossover study conducted to determine the efficacy of different carbohydrate drinks in promoting carbohydrate storage in the whole body and skeletal muscle during recovery from exhaustive exercise. The postabsorptive subjects first completed an exercise protocol designed to deplete muscle fibers of glycogen, then consumed 330 ml of one of three carbohydrate drinks (18.5% glucose polymer, 18.5% sucrose, or 12% sucrose; wt/vol) and also received a primed constant infusion of [1-(13)C]glucose for 2 h. Nonoxidative glucose disposal (3.51 +/- 0.28, 18.5% glucose polymer; 2.96 +/- 0.32, 18.5% sucrose; 2.97 +/- 0.16, 12% sucrose; all mmol. kg(-1). h(-1)) and storage of muscle glycogen (5.31 +/- 1.11, 18.5% glucose polymer; 4.07 +/- 1.05, 18.5% sucrose; 3.45 +/- 0.85, 12% sucrose; all mmol. kg wet wt(-1). h(-1); P < 0.05) were greater after consumption of the glucose polymer drink than after either sucrose drink. The results suggest that the consumption of a glucose polymer drink (containing 61 g carbohydrate) promotes a more rapid storage of carbohydrate in the whole body, skeletal muscle in particular, than an isoenergetic sucrose drink.

The aim of this study was to determine the effect of glucose supplementation on leucine turnover during and after exercise and whether variation in the previous dietary protein content modulated this effect. Postabsorptive subjects received a primed constant [1-13C, 15N]leucine infusion for 6 h, after previous consumption of a high (1.8 g kg-1 day-1, HP, n = 16) or low (0.7 g kg-1 day-1, LP, n = 16) protein diet for 7 days. The subjects were studied at rest; during 2 h of exercise, during which half of the subjects from each dietary protocol received 0.75 g kg-1 h-1 glucose (HP + G, LP + G) and the other half received water (HP + W, LP + W); then again for 2 h of rest. Glucose supplementation suppressed leucine oxidation (P < 0.01) by 20% in subjects consuming the high protein diet (58.2 +/- 2.8 micromol kg-1 h-1, HP + G; 72.4 +/- 3.9 micromol kg-1 h-1, HP + W) but not the low protein diet (51.1 +/- 5.9 micromol kg-1 h-1, LP + G; 51.7 +/- 5.5 micromol kg-1 h-1, LP + W), with no difference in skeletal muscle branched-chain 2-oxo acid dehydrogenase (BCOADH) activity between groups. Glucose supplementation did not alter the rate of whole-body protein synthesis or breakdown. The sparing effect of glucose on leucine oxidation appears only to occur if previous protein intake was high. It was not mediated by a suppression of BCOADH fractional activity but may be due to reduced substrate availability.

The purpose of this study was to determine the efficacy of glutamine in promoting whole body carbohydrate storage and muscle glycogen resynthesis during recovery from exhaustive exercise. Postabsorptive subjects completed a glycogen-depleting exercise protocol, then consumed 330 ml of one of three drinks, 18.5% (wt/vol) glucose polymer solution, 8 g glutamine in 330 ml glucose polymer solution, or 8 g glutamine in 330 ml placebo, and also received a primed constant infusion of [1-13C]glucose for 2 h. Plasma glutamine concentration was increased after consumption of the glutamine drinks (0.7-1.1 mM, P < 0.05). In the second hour of recovery, whole body nonoxidative glucose disposal was increased by 25% after consumption of glutamine in addition to the glucose polymer (4.48 +/- 0.61 vs. 3.59 +/- 0.18 mmol/kg, P < 0.05). Oral glutamine alone promoted storage of muscle glycogen to an extent similar to oral glucose polymer. Ingestion of glutamine and glucose polymer together promoted the storage of carbohydrate outside of skeletal muscle, the most feasible site being the liver.

The aim of this study was to investigate dietary protein-induced changes in whole body leucine turnover and oxidation and in skeletal muscle branched chain 2-oxo acid dehydrogenase (BCOADH) activity, at rest and during exercise. Postabsorptive subjects received a primed constant infusion of L-[1-13C,15N]leucine for 6 h, after previous consumption of a high- (HP; 1.8 g. kg-1. day-1, n = 8) or a low-protein diet (LP; 0.7 g. kg-1. day-1, n = 8) for 7 days. The subjects were studied at rest for 2 h, during 2-h exercise at 60% maximum oxygen consumption, then again for 2 h at rest. Exercise induced a doubling of both leucine oxidation from 20 micromol. kg-1. h-1 and BCOADH percent activation from 7% in all subjects. Leucine oxidation was greater before (+46%) and during (+40%, P < 0.05) the first hour of exercise in subjects consuming the HP rather than the LP diet, but there was no additional change in muscle BCOADH activity. The results suggest that leucine oxidation was increased by previous ingestion of an HP diet, attributable to an increase in leucine availability rather than to a stimulation of the skeletal muscle BCOADH activity.

In an attempt to measure gastric emptying of carbohydrate solutions after exercise, we used the 13C acetate breath test to differentiate the gastric emptying of three approximately isoenergetic carbohydrate solutions (i.e. glucose, glucose polymer and sucrose) from each other and from water. On four separate occasions, six post-absorptive subjects walked on an inclined treadmill at 70% maximum oxygen uptake for 1 h and were then given 330 ml of one of the solutions in which 150 mg of sodium 1-[13C] acetate had been dissolved. Breath samples were collected at regular (2-30 min) intervals over the next 3.5 h for analysis of expired 13CO2 by isotope ratio mass spectrometry. When water was given, all subjects reached peak breath enrichment after 30 min, and had a mean (SE) gastric emptying time of 33.2 (1.6) min. Peak breath enrichment occurred later for sucrose and glucose polymer at 54.3 (3.1) min and 59.0 (2.1) min respectively (P < 0.01), and for glucose this was even later, at 62.3 (1.0) min (P < 0.05). Calculated gastric emptying times for sucrose and glucose polymer were almost identical [66.5 (2.5) and 69.8 (2.9) min respectively], whereas that for glucose was significantly slower [76.8 (3.2) min; P < 0.02], probably reflecting the effects of increased osmolality. The gastric emptying of all carbohydrates were significantly longer than for water (P < 0.01). These results show that in the post-exercise state the 13C acetate breath test can be used to differentiate the gastric emptying rates of water and carbohydrate solutions of different properties.