Cerebral, cardiac and skeletal muscle stress associated with a series of static and dynamic apnoeas.

PURPOSE: This study sought to explore, for the first time, the effects of repeated maximal static and dynamic apnoeic attempts on the physiological milieu by assessing cerebral, cardiac and striatal muscle stress-related biomarkers in a group of elite breath-hold divers (EBHD). METHODS: Sixteen healthy males were recruited (EBHD = 8; controls = 8). On two separate occasions, EBHD performed two sets of five repeated maximal static apnoeas (STA) or five repeated maximal dynamic apnoeas (DYN). Controls performed a static eupnoeic protocol to negate any effects of water immersion and diurnal variation on haematology (CTL). Venous blood samples were drawn at 30, 90, and 180 min after each protocol to determine S100ß, neuron-specific enolase (NSE), myoglobin, and high sensitivity cardiac troponin T (hscTNT) concentrations. RESULTS: S100ß and myoglobin concentrations were elevated following both apnoeic interventions (p < 0.001; p ≤ 0.028, respectively) but not after CTL (p ≥ 0.348). S100ß increased from baseline (0.024 ± 0.005 µg/L) at 30 (STA, +149%, p < 0.001; DYN, +166%, p < 0.001) and 90 min (STA, +129%, p < 0.001; DYN, +132%, p = 0.008) following the last apnoeic repetition. Myoglobin was higher than baseline (22.3 ± 2.7 ng/ml) at 30 (+42%, p = 0.04), 90 (+64%, p < 0.001) and 180 min (+49%, p = 0.013) post-STA and at 90 min (+63%, p = 0.016) post-DYN. Post-apnoeic S100ß and myoglobin concentrations were higher than CTL (STA, p < 0.001; DYN, p ≤ 0.004). NSE and hscTNT did not change from basal concentrations after the apnoeic (p ≥ 0.146) nor following the eupnoeic (p ≥ 0.553) intervention. CONCLUSIONS: This study suggests that a series of repeated maximal static and dynamic apnoeas transiently disrupt the blood-brain barrier and instigate muscle injury but do not induce neuronal-parenchymal damage or myocardial damage.

Splenic responses to a series of repeated maximal static and dynamic apnoeas with whole-body immersion in water.

NEW FINDINGS: What is the central question of this study? Splenic contractions occur in response to apnoea-induced hypoxia with and without face immersion in water. However, the splenic responses to a series of static or dynamic apnoeas with whole-body water immersion in non-divers and elite breath-hold divers are unknown. What is the main finding and its importance? Static and dynamic apnoeas were equally effective in stimulating splenic contractions across non-divers and elite breath-hold divers. These findings demonstrate that the magnitude of the splenic response is largely dictated by the degree of the hypoxemic stress encountered during voluntary apnoeic epochs. ABSTRACT: Splenic contractions occur in response to apnoea-induced hypoxia with and without facial water immersion. However, the splenic responses to a series of static (STA) or dynamic (DYN) apnoeas with whole-body water immersion in non-divers (NDs) and elite breath-hold divers (EBHDs) are unknown. EBHD (n = 8), ND (n = 10) and control participants (n = 8) were recruited. EBHD and ND performed a series of five maximal DYN or STA on separate occasions. Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on splenic volume and haematology. Heart rate (HR) and peripheral oxygen saturation (SpO2 ) were monitored for 30 s after each apnoea. Pre- and post-apnoeic splenic volumes were quantified ultrasonically, and blood samples were drawn for haematology. For EBHD and ND end-apnoeic HR was higher (P < 0.001) and SpO2 was lower in DYN (P = 0.024) versus STA. EBHD attained lower end-apnoeic SpO2 during DYN and STA than NDs (P < 0.001). Splenic contractions occurred following DYN (EBHD, -47 ± 6%; ND, -37 ± 4%; P < 0.001) and STA (EBHD, -26 ± 4%; ND, -26 ± 8%; P < 0.01). DYN-associated splenic contractions were greater than STA in EBHD only (P = 0.042). Haemoglobin concentrations were higher following DYN only (EBHD, +5 ± 8g/L  , +4 ± 2%; ND, +8 ± 3 g/L , +4.9 ± 3%; P = 0.019). Haematocrit remained unchanged after each protocol. There were no between group differences in post-apnoeic splenic volume or haematology. In both groups, splenic contractions occurred in response to STA and DYN when combined with whole-body immersion. DYN apnoeas, were effective at increasing haemoglobin concentrations but not STA apnoeas. Thus, the magnitude of the splenic response relates to the hypoxemic stress encountered during apnoeic epochs.

Six weeks of dynamic apnoeic training stimulates erythropoiesis but does not increase splenic volume.

PURPOSE: This study examined the influence of dynamic apnoea training on splenic volume and haematological responses in non-breath-hold divers (BHD). METHODS: Eight non-BHD performed ten maximal dynamic apnoeas, four times a week for  six weeks. Splenic volumes were assessed ultrasonically, and blood samples were drawn for full blood count analysis, erythropoietin, iron, ferritin, albumin, protein and osmolality at baseline, 24 h post the completion of each week's training sessions and seven days post the completion of the training programme. Additionally, blood samples were drawn for haematology at 30, 90, and 180 min post session one, twelve and twenty-four. RESULTS: Erythropoietin was only higher than baseline (6.62 ± 3.03 mlU/mL) post session one, at 90 (9.20 ± 1.88 mlU/mL, p = 0.048) and 180 min (9.04 ± 2.35 mlU/mL, p = 0.046). Iron increased from baseline (18 ± 3 µmol/L) post week five (23 ± 2 µmol/L, p = 0.033) and six (21 ± 6 µmol/L; p = 0.041), whereas ferritin was observed to be lower than baseline (111 ± 82 µg/L) post week five (95 ± 75 µg/L; p = 0.016), six (84 ± 74 µg/L; p = 0.012) and one week post-training (81 ± 63 µg/L; p = 0.008). Reticulocytes increased from baseline (57 ± 12 × 109/L) post week one (72 ± 17 × 109/L, p = 0.037) and six (71 ± 17 × 109/L, p = 0.021) while no changes were recorded in erythrocytes (p = 0.336), haemoglobin (p = 0.124) and splenic volumes (p = 0.357). CONCLUSIONS: Six weeks of dynamic apnoeic training increase reticulocytes without altering mature erythrocyte concentration and splenic volume.

Appetite and energy intake responses to breakfast consumption and carbohydrate supplementation in hypoxia.

PURPOSE: The purpose of experiment one was to determine the appetite, acylated ghrelin and energy intake response to breakfast consumption and omission in hypoxia and normoxia. Experiment two aimed to determine the appetite, acylated ghrelin and energy intake response to carbohydrate supplementation after both breakfast consumption and omission in hypoxia. METHODS: In experiment one, twelve participants rested and exercised once after breakfast consumption and once after omission in normobaric hypoxia (4300 m: FiO2 ~11.7%) and normoxia. In experiment two, eleven participants rested and exercised in normobaric hypoxia (4300 m: FiO2 ~11.7%), twice after consuming a high carbohydrate breakfast and twice after breakfast omission. Participants consumed both a carbohydrate (1.2g·min-1 glucose) and a placebo beverage after breakfast consumption and omission. Measures of appetite perceptions and acylated ghrelin were taken at regular intervals throughout both experiments and an ad-libitum meal was provided post-exercise to quantify energy intake. RESULTS: Breakfast consumption had no significant effect on post exercise energy intake or acylated ghrelin concentrations, despite reductions in appetite perceptions. As such, breakfast consumption increased total trial energy intake compared with breakfast omission in hypoxia (7136 ± 2047 kJ vs. 5412 ± 1652 kJ; p = 0.02) and normoxia (9276 ± 3058 vs. 6654 ± 2091 kJ; p < 0.01). Carbohydrate supplementation had no effect on appetite perceptions or acylated ghrelin concentrations after breakfast consumption or omission. As such, carbohydrate supplementation increased total energy intake after breakfast consumption (10222 ± 2831 kJ vs. 7695 ± 1970 kJ p < 0.01) and omission (8058 ± 2574 kJ vs. 6174 ± 2222 kJ p = 0.02). CONCLUSION: Both breakfast consumption and carbohydrate supplementation provide beneficial dietary interventions for increasing energy intake in hypoxic conditions.

Effects of inorganic nitrate and nitrite consumption on cognitive function and cerebral blood flow: A systematic review and meta-analysis of randomized clinical trials.

We conducted a systematic review and meta-analysis of randomized clinical trials examining the effect of inorganic nitrate or nitrite supplementation on cognitive function (CF) and cerebral blood flow (CBF). Two databases (PubMed, Embase) were searched for articles from inception until May 2017. Inclusion criteria were: randomized clinical trials; participants >18 years old; trials comparing a nitrate/nitrite intervention with a control. Thirteen and nine trials were included in the meta-analysis to assess CF and CBF, respectively. Random-effects models were used and the effect size described as standardized mean differences (SMDs). A total of 297 participants (median of 23 per trial) were included for CF; 163 participants (median of 16 per trial) were included for CBF. Nitrate/nitrite supplementation did not influence CF (SMD +0.06, 95% CI: -0.06, 0.18, P = 0.32) or CBF under resting (SMD +0.14, 95% CI: -0.13, 0.41, P = 0.31), or stimulated conditions (SMD + 0.23, 95% CI: -0.11, 0.56, P = 0.19). The meta-regression showed an inverse association between duration of the intervention and CBF (P = 0.02) but no influence of age, BMI or dose (P < 0.05). Nitrate and nitrite supplementation did not modify CBF or CF. Further trials employing larger samples sizes and interventions with longer duration are warranted.

Substrate oxidation and the influence of breakfast in normobaric hypoxia and normoxia.

PURPOSE: Previous research has reported inconsistent effects of hypoxia on substrate oxidation, which may be due to differences in methodological design, such as pre-exercise nutritional status and exercise intensity. This study investigated the effect of breakfast consumption on substrate oxidation at varying exercise intensities in normobaric hypoxia compared with normoxia. METHODS: Twelve participants rested and exercised once after breakfast consumption and once after omission in normobaric hypoxia (4300 m: FiO2 ~ 11.7%) and normoxia. Exercise consisted of walking for 20 min at 40%, 50% and 60% of altitude-specific [Formula: see text]O2max at 10-15% gradient with a 10 kg backpack. Indirect calorimetry was used to calculate carbohydrate and fat oxidation. RESULTS: The relative contribution of carbohydrate oxidation to energy expenditure was significantly reduced in hypoxia compared with normoxia during exercise after breakfast omission at 40% (22.4 ± 17.5% vs. 38.5 ± 15.5%, p = 0.03) and 60% [Formula: see text]O2max (35.4 ± 12.4 vs. 50.1 ± 17.6%, p = 0.03), with a trend observed at 50% [Formula: see text]O2max (23.6 ± 17.9% vs. 38.1 ± 17.0%, p = 0.07). The relative contribution of carbohydrate oxidation to energy expenditure was not significantly different in hypoxia compared with normoxia during exercise after breakfast consumption at 40% (42.4 ± 15.7% vs. 48.5 ± 13.3%, p = 0.99), 50% (43.1 ± 11.7% vs. 47.1 ± 14.0%, p = 0.99) and 60% [Formula: see text]O2max (54.6 ± 17.8% vs. 55.1 ± 15.0%, p = 0.99). CONCLUSIONS: Relative carbohydrate oxidation was significantly reduced in hypoxia compared with normoxia during exercise after breakfast omission but not during exercise after breakfast consumption. This response remained consistent with increasing exercise intensities. These findings may explain some of the disparity in the literature.

Erythropoietic responses to a series of repeated maximal dynamic and static apnoeas in elite and non-breath-hold divers.

PURPOSE: Serum erythropoietin (EPO) concentration is increased following static apnoea-induced hypoxia. However, the acute erythropoietic responses to a series of dynamic apnoeas in non-divers (ND) or elite breath-hold divers (EBHD) are unknown. METHODS: Participants were stratified into EBHD (n = 8), ND (n = 10) and control (n = 8) groups. On two separate occasions, EBHD and ND performed a series of five maximal dynamic apnoeas (DYN) or two sets of five maximal static apnoeas (STA). Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on EPO. Peripheral oxygen saturation (SpO2) levels were monitored up to 30 s post each maximal effort. Blood samples were collected at 30, 90, and 180 min after each protocol for EPO, haemoglobin and haematocrit concentrations. RESULTS: No between group differences were observed at baseline (p > 0.05). For EBHD and ND, mean end-apnoea SpO2 was lower in DYN (EBHD, 62 ± 10%, p = 0.024; ND, 85 ± 6%; p = 0.020) than STA (EBHD, 76 ± 7%; ND, 96 ± 1%) and control (98 ± 1%) protocols. EBHD attained lower end-apnoeic SpO2 during DYN and STA than ND (p < 0.001). Serum EPO increased from baseline following the DYN protocol in EBHD only (EBHD, p < 0.001; ND, p = 0.622). EBHD EPO increased from baseline (6.85 ± 0.9mlU/mL) by 60% at 30 min (10.82 ± 2.5mlU/mL, p = 0.017) and 63% at 180 min (10.87 ± 2.1mlU/mL, p = 0.024). Serum EPO did not change after the STA (EBHD, p = 0.534; ND, p = 0.850) and STE (p = 0.056) protocols. There was a significant negative correlation (r = - 0.49, p = 0.003) between end-apnoeic SpO2 and peak post-apnoeic serum EPO concentrations. CONCLUSIONS: The novel findings demonstrate that circulating EPO is only increased after DYN in EBHD. This may relate to the greater hypoxemia achieved by EBHD during the DYN.

Skeletal muscle, haematological and splenic volume characteristics of elite breath-hold divers.

PURPOSE: The aim of the study was to provide an evaluation of the oxygen transport, exchange and storage capacity of elite breath-hold divers (EBHD) compared with non-divers (ND). METHODS: Twenty-one healthy males' (11 EBHD; 10 ND) resting splenic volumes were assessed by ultrasound and venous blood drawn for full blood count analysis. Percutaneous skeletal muscle biopsies were obtained from the m. vastus lateralis to measure capillarisation, and fibre type-specific localisation and distribution of myoglobin and mitochondrial content using quantitative immunofluorescence microscopy. RESULTS: Splenic volume was not different between groups. Reticulocytes, red blood cells and haemoglobin concentrations were higher (+ 24%, p < 0.05; + 9%, p < 0.05; + 3%, p < 0.05; respectively) and mean cell volume was lower (- 6.5%, p < 0.05) in the EBHD compared with ND. Haematocrit was not different between groups. Capillary density was greater (+ 19%; p < 0.05) in the EBHD. The diffusion distance (R95) was lower in type I versus type II fibres for both groups (EBHD, p < 0.01; ND, p < 0.001), with a lower R95 for type I fibres in the EBHD versus ND (- 13%, p < 0.05). Myoglobin content was higher in type I than type II fibres in EBHD (+ 27%; p < 0.01) and higher in the type I fibres of EBHD than ND (+ 27%; p < 0.05). No fibre type differences in myoglobin content were observed in ND. Mitochondrial content was higher in type I than type II fibres in EBHD (+ 35%; p < 0.05), with no fibre type differences in ND or between groups. CONCLUSIONS: In conclusion, EBDH demonstrate enhanced oxygen storage in both blood and skeletal muscle and a more efficient oxygen exchange capacity between blood and skeletal muscle versus ND.

Liver and muscle glycogen oxidation and performance with dose variation of glucose-fructose ingestion during prolonged (3 h) exercise.

PURPOSE: This study investigated the effect of small manipulations in carbohydrate (CHO) dose on exogenous and endogenous (liver and muscle) fuel selection during exercise. METHOD: Eleven trained males cycled in a double-blind randomised order on 4 occasions at 60% [Formula: see text] for 3 h, followed by a 30-min time-trial whilst ingesting either 80 g h-1 or 90 g h-1 or 100 g h-1 13C-glucose-13C-fructose [2:1] or placebo. CHO doses met, were marginally lower, or above previously reported intestinal saturation for glucose-fructose (90 g h-1). Indirect calorimetry and stable mass isotope [13C] techniques were utilised to determine fuel use. RESULT: Time-trial performance was 86.5 to 93%, 'likely, probable' improved with 90 g h-1 compared 80 and 100 g h-1. Exogenous CHO oxidation in the final hour was 9.8-10.0% higher with 100 g h-1 compared with 80 and 90 g h-1 (ES = 0.64-0.70, 95% CI 9.6, 1.4 to 17.7 and 8.2, 2.1 to 18.6). However, increasing CHO dose (100 g h-1) increased muscle glycogen use (101.6 ± 16.6 g, ES = 0.60, 16.1, 0.9 to 31.4) and its relative contribution to energy expenditure (5.6 ± 8.4%, ES = 0.72, 5.6, 1.5 to 9.8 g) compared with 90 g h-1. Absolute and relative muscle glycogen oxidation between 80 and 90 g h-1 were similar (ES = 0.23 and 0.38) though a small absolute (85.4 ± 29.3 g, 6.2, - 23.5 to 11.1) and relative (34.9 ± 9.1 g, - 3.5, - 9.6 to 2.6) reduction was seen in 90 g h-1 compared with 100 g h-1. Liver glycogen oxidation was not significantly different between conditions (ES < 0.42). Total fat oxidation during the 3-h ride was similar in CHO conditions (ES < 0.28) but suppressed compared with placebo (ES = 1.05-1.51). CONCLUSION: 'Overdosing' intestinal transport for glucose-fructose appears to increase muscle glycogen reliance and negatively impact subsequent TT performance.

The availability of water associated with glycogen during dehydration: a reservoir or raindrop?

PURPOSE: This study evaluated whether glycogen-associated water is a protected entity not subject to normal osmotic homeostasis. An investigation into practical and theoretical aspects of the functionality of this water as a determinant of osmolality, dehydration, and glycogen concentration was undertaken. METHODS: In vitro experiments were conducted to determine the intrinsic osmolality of glycogen-potassium phosphate mixtures as would be found intra-cellularly at glycogen concentrations of 2% for muscle and 5 and 10% for liver. Protected water would not be available to ionic and osmotic considerations, whereas free water would obey normal osmotic constraints. In addition, the impact of 2 L of sweat loss in situations of muscle glycogen repletion and depletion was computed to establish whether water associated with glycogen is of practical benefit (e.g., to increase "available total body water"). RESULTS: The osmolality of glycogen-potassium phosphate mixtures is predictable at 2% glycogen concentration (predicted 267, measured 265.0 ± 4.7 mOsmol kg-1) indicating that glycogen-associated water is completely available to all ions and is likely part of the greater osmotic system of the body. At higher glycogen concentrations (5 and 10%), there was a small amount of glycogen water (~ 10-20%) that could be considered protected. However, the majority of the glycogen-associated water behaved to normal osmotic considerations. The theoretical exercise of selective dehydration (2 L) indicated a marginal advantage to components of total body water such as plasma volume (1.57% or 55 mL) when starting exercise glycogen replete. CONCLUSION: Glycogen-associated water does not appear to be a separate reservoir and is not able to uniquely replete water loss during dehydration.

Three-Compartment Body Composition Changes in Professional Rugby Union Players Over One Competitive Season: A Team and Individualized Approach.

The purpose of this study was to investigate the longitudinal body composition of professional rugby union players over one competitive season. Given the potential for variability in changes, and as the first to do so, we conducted individual analysis in addition to analysis of group means. Thirty-five professional rugby union players from one English Premiership team (forwards: n = 20, age: 25.5 ± 4.7 yr; backs: n = 15, age: 26.1 ± 4.5 yr) received one total-body dual-energy X-ray absorptiometry scan at preseason (August), midseason (January), and endseason (May), enabling quantification of body mass, total and regional fat mass, lean mass, percentage tissue fat mass (%TFM), and bone mineral content (BMC). Individual analysis was conducted by applying least significant change (LSC), derived from our previously published precision data and in accordance with International Society for Clinical Densitometry guidelines. Mean body mass remained stable throughout the season (p > 0.05), but total fat mass and %TFM increased from pre- to endseason, and from mid- to endseason (p <0.05). There were also statistically significant increases in total-body BMC across the season (p <0.05). In both groups, there was a loss of lean mass between mid- and endseason (p <0.018). Individual evaluation using LSC and Bland-Altman analysis revealed a meaningful loss of lean mass in 17 players and a gain of fat mass in 21 players from pre- to endseason. Twelve players had no change and there were no differences by playing position. There were individual gains or no net changes in BMC across the season for 10 and 24 players, respectively. This study highlights the advantages of an individualized approach to dual-energy X-ray absorptiometry body composition monitoring and this can be achieved through application of derived LSC.

Effect of Galactose Ingestion Before and During Exercise on Substrate Oxidation, Postexercise Satiety, and Subsequent Energy Intake in Females.

OBJECTIVE: To examine the effects of consuming a galactose carbohydrate (CHO) drink on substrate oxidation, postexercise satiety, and subsequent energy intake. METHODS: Nine recreationally active eumenorrheic females undertook 3 trials, each consisting of running for 60 minutes at 65% VO(2peak) followed immediately by a 90-minute rest period. Prior to (300 ml) and at 15-minute intervals during exercise (150 ml), participants consumed either a glucose (GLU: GI 89) or galactose (GAL: GI 20) drink, each of which contained 45 g of CHO, or an artificially sweetened placebo (PLA). Following the rest period, participants were provided with an ad libitum test lunch and asked to record food intake for the remainder of the day. RESULTS: Plasma glucose was significantly greater throughout exercise and rest following the GLU trial compared with the GAL and PLA trials (P < 0.05); however there were no differences in CHO oxidation. Hunger was significantly lower (P < 0.05) throughout the GAL compared to the GLU and PLA trials. There were no significant differences between trials for energy intake during the postexercise meal. Overall net energy balance for the 24 hours was negative in both the GAL (-162 ± 115 kcal; P < 0.05 vs GLU) and PLA trials (-49 ± 160 kcal). CONCLUSIONS: Results demonstrate that ingesting a solution containing GAL before and during exercise can positively impact postexercise satiety and energy balance throughout the day, compared to a more readily available and widely consumed form of CHO. Despite this, there appears to be no apparent benefit in consuming a CHO beverage on fuel utilization for this moderate exercise intensity and duration.

The effect of pre-exercise galactose and glucose ingestion on high-intensity endurance cycling.

This study evaluated the effects of the pre-exercise (30 minutes) ingestion of galactose (Gal) or glucose (Glu) on endurance capacity as well as glycemic and insulinemic responses. Ten trained male cyclists completed 3 randomized high-intensity cycling endurance tests. Thirty minutes before each trial, cyclists ingested 1 L of either 40 g of glucose, 40 g of galactose, or a placebo in a double-blind manner. The protocol comprised 20 minutes of progressive incremental exercise (70-85% maximal power output [Wmax]); ten 90-second bouts at 90% Wmax, separated by 180 seconds at 55% Wmax; and 90% Wmax until exhaustion. Blood samples were drawn throughout the protocol. Times to exhaustion were longer with Gal (68.7 ± 10.2 minutes, p = 0.005) compared with Glu (58.5 ± 24.9 minutes), with neither being different to placebo (63.9 ± 16.2 minutes). Twenty-eight minutes after Glu consumption, plasma glucose and serum insulin concentrations were higher than with Gal and placebo (p < 0.001). After the initial 20 minutes of exercise, plasma glucose concentrations increased to a relative hyperglycemia during the Gal and placebo, compared with Glu condition. Higher plasma glucose concentrations during exercise, and the attenuated serum insulin response at rest, may explain the significantly longer times to exhaustion produced by Gal compared with Glu. However, neither carbohydrate treatment produced significantly longer times to exhaustion than placebo, suggesting that the pre-exercise ingestion of galactose and glucose alone is not sufficient to support this type of endurance performance.

Liver and muscle glycogen repletion using 13C magnetic resonance spectroscopy following ingestion of maltodextrin, galactose, protein and amino acids.

The present study evaluated whether the inclusion of protein (PRO) and amino acids (AA) within a maltodextrin (MD) and galactose (GAL) recovery drink enhanced post-exercise liver and muscle glycogen repletion. A total of seven trained male cyclists completed two trials, separated by 7 d. Each trial involved 2 h of standardised intermittent cycling, followed by 4 h recovery. During recovery, one of two isoenergetic formulations, MD-GAL (0.9 g MD/kg body mass (BM) per h and 0.3 g GAL/kg BM per h) or MD-GAL-PRO+AA (0.5 g MD/kg BM per h, 0.3 g GAL/kg BM per h, 0.4 g whey PRO hydrolysate plus l-leucine and l-phenylalanine/kg BM per h) was ingested at every 30 min. Liver and muscle glycogen were measured after depletion exercise and at the end of recovery using 1H-13C-magnetic resonance spectroscopy. Despite higher postprandial insulin concentations for MD-GAL-PRO+AA compared with MD-GAL (61.3 (se 6.2) v. 29.6 (se 3.0) mU/l, (425.8 (se 43.1) v. 205.6 (se 20.8) pmol/l) P= 0.03), there were no significant differences in post-recovery liver (195.3 (se 2.6) v. 213.8 (se 18.0) mmol/l) or muscle glycogen concentrations (49.7 (se 4.0) v. 51.1 (se 7.9) mmol/l). The rate of muscle glycogen repletion was significantly higher for MD-GAL compared with MD-GAL-PRO+AA (5.8 (se 0.7) v. 3.7 (se 0.6) mmol/l per h, P= 0.04), while there were no significant differences in the rate of liver glycogen repletion (15.0 (se 2.5) v. 13.0 (se 2.7) mmol/l per h). PRO and AA within a MD-GAL recovery drink, compared with an isoenergetic mix of MD-GAL, did not enhance but matched liver and muscle glycogen recovery. This suggests that the increased postprandial insulinaemia only compensated for the lower MD content in the MD-GAL-PRO+AA treatment.

Glucose and Fructose Hydrogel Enhances Running Performance, Exogenous Carbohydrate Oxidation, and Gastrointestinal Tolerance.

PURPOSE: Beneficial effects of carbohydrate (CHO) ingestion on exogenous CHO oxidation and endurance performance require a well-functioning gastrointestinal (GI) tract. However, GI complaints are common during endurance running. This study investigated the effect of a CHO solution-containing sodium alginate and pectin (hydrogel) on endurance running performance, exogenous and endogenous CHO oxidation, and GI symptoms. METHODS: Eleven trained male runners, using a randomized, double-blind design, completed three 120-min steady-state runs at 68% V˙O2max, followed by a 5-km time-trial. Participants ingested 90 g·h-1 of 2:1 glucose-fructose (13C enriched) as a CHO hydrogel, a standard CHO solution (nonhydrogel), or a CHO-free placebo during the 120 min. Fat oxidation, total and exogenous CHO oxidation, plasma glucose oxidation, and endogenous glucose oxidation from liver and muscle glycogen were calculated using indirect calorimetry and isotope ratio mass spectrometry. GI symptoms were recorded throughout the trial. RESULTS: Time-trial performance was 7.6% and 5.6% faster after hydrogel ([min:s] 19:29 ± 2:24, P < 0.001) and nonhydrogel (19:54 ± 2:23, P = 0.002), respectively, versus placebo (21:05 ± 2:34). Time-trial performance after hydrogel was 2.1% faster (P = 0.033) than nonhydrogel. Absolute and relative exogenous CHO oxidation was greater with hydrogel (68.6 ± 10.8 g, 31.9% ± 2.7%; P = 0.01) versus nonhydrogel (63.4 ± 8.1 g, 29.3% ± 2.0%; P = 0.003). Absolute and relative endogenous CHO oxidation was lower in both CHO conditions compared with placebo (P < 0.001), with no difference between CHO conditions. Absolute and relative liver glucose oxidation and muscle glycogen oxidation were not different between CHO conditions. Total GI symptoms were not different between hydrogel and placebo, but GI symptoms were higher in nonhydrogel compared with placebo and hydrogel (P < 0.001). CONCLUSION: The ingestion of glucose and fructose in hydrogel form during running benefited endurance performance, exogenous CHO oxidation, and GI symptoms compared with a standard CHO solution.

Relative changes in brain and kidney biomarkers with Exertional Heat Illness during a cool weather marathon.

BACKGROUND: Medical personnel may find it challenging to distinguish severe Exertional Heat Illness (EHI), with attendant risks of organ-injury and longer-term sequalae, from lesser forms of incapacity associated with strenuous physical exertion. Early evidence for injury at point-of-incapacity could aid the development and application of targeted interventions to improve outcomes. We aimed to investigate whether biomarker surrogates for end-organ damage sampled at point-of-care (POC) could discriminate EHI versus successful marathon performance. METHODS: Eight runners diagnosed as EHI cases upon reception to medical treatment facilities and 30 successful finishers of the same cool weather marathon (ambient temperature 8 rising to 12 ºC) were recruited. Emerging clinical markers associated with injury affecting the brain (neuron specific enolase, NSE; S100 calcium-binding protein B, S100ß) and renal system (cystatin C, cysC; kidney-injury molecule-1, KIM-1; neutrophil gelatinase-associated lipocalin, NGAL), plus copeptin as a surrogate for fluid-regulatory stress, were sampled in blood upon marathon collapse/completion, as well as beforehand at rest (successful finishers only). RESULTS: Versus successful finishers, EHI showed significantly higher NSE (10.33 [6.37, 20.00] vs. 3.17 [2.71, 3.92] ug.L-1, P<0.0001), cysC (1.48 [1.10, 1.67] vs. 1.10 [0.95, 1.21] mg.L-1, P = 0.0092) and copeptin (339.4 [77.0, 943] vs. 18.7 [7.1, 67.9] pmol.L-1, P = 0.0050). Discrimination of EHI by ROC (Area-Under-the-Curve) showed performance that was outstanding for NSE (0.97, P<0.0001) and excellent for copeptin (AUC = 0.83, P = 0.0066). CONCLUSIONS: As novel biomarker candidates for EHI outcomes in cool-weather endurance exercise, early elevations in NSE and copeptin provided sufficient discrimination to suggest utility at point-of-incapacity. Further investigation is warranted in patients exposed to greater thermal insult, followed up over a more extended period.

Quantitation of plasma 13C-galactose and 13C-glucose during exercise by liquid chromatography/isotope ratio mass spectrometry.

The utilisation of carbohydrate sources under exercise conditions is of considerable importance in performance sports. Incorporation of optimal profiles of macronutrients can improve endurance performance in athletes. However, gaining an understanding of the metabolic partitioning under sustained exercise can be problematical and isotope labelling approaches can help quantify substrate utilisation. The utilisation of oral galactose was investigated using (13)C-galactose and measurement of plasma galactose and glucose enrichment by liquid chromatography/isotope ratio mass spectrometry (LC/IRMS). As little as 100 µL plasma could readily be analysed with only minimal sample processing. Fucose was used as a chemical and isotopic internal standard for the quantitation of plasma galactose and glucose concentrations, and isotopic enrichment. The close elution of galactose and glucose required a correction routine to be implemented to allow the measurement, and correction, of plasma glucose δ(13)C, even in the presence of very highly enriched galactose. A Bland-Altman plot of glucose concentration measured by LC/IRMS against glucose measured by an enzymatic method showed good agreement between the methods. Data from seven trained cyclists, undergoing galactose supplementation before exercise, demonstrate that galactose is converted into glucose and is available for subsequent energy metabolism.

Three-compartment body composition changes in elite rugby league players during a super league season, measured by dual-energy X-ray absorptiometry.

This study investigated the acute changes in body composition that occur over the course of a competitive season in elite rugby league players. Twenty elite senior players from an English Super League rugby league team underwent a total-body dual-energy X-ray absorptiometry scan at 3 phases of a competitive season: preseason (February), midseason (June), and postseason (September). Body mass (BM), fat mass (FM), lean mass, percentage body fat, and bone mineral content (BMC) were reported at each phase. Between the start and midpoint of the season, BM, lean mass, FM, and body fat percentage showed no significant change (p > 0.05); however, BMC was significantly increased (+0.71%; 30.70 ± 38.00 g; p < 0.05). Between the midseason and postseason phase, BM and BMC showed no significant change (p > 0.05); however, significant changes were observed in lean mass (-1.54%; 1.19 ± 1.43 kg), FM (+4.09%; 0.57 ± 1.10 kg), and body fat percentage (+4.98%; 0.78 ± 1.09%; p < 0.05). The significant changes in body composition seen over the latter stages of the competitive season may have implications for performance capabilities at this important stage of competition. An increase in FM and decrease in lean mass may have a negative effect on the power/BM ratio, and therefore may be a cause for concern for playing, coaching, and medical staff. Coaching and strength and conditioning staff should aim to prescribe appropriate training and nutritional practices with the aim of maintaining the players' optimal body composition until the conclusion of the competitive season, in order that performance capabilities are maximized over the entire competition period.

Carbohydrate Supplementation and the Influence of Breakfast on Fuel Use in Hypoxia.

PURPOSE: This study investigated the effect of carbohydrate supplementation on substrate oxidation during exercise in hypoxia after preexercise breakfast consumption and omission. METHODS: Eleven men walked in normobaric hypoxia (FiO2 ~11.7%) for 90 min at 50% of hypoxic V˙O2max. Participants were supplemented with a carbohydrate beverage (1.2 g·min-1 glucose) and a placebo beverage (both enriched with U-13C6 D-glucose) after breakfast consumption and after omission. Indirect calorimetry and isotope ratio mass spectrometry were used to calculate carbohydrate (exogenous and endogenous [muscle and liver]) and fat oxidation. RESULTS: In the first 60 min of exercise, there was no significant change in relative substrate oxidation in the carbohydrate compared with placebo trial after breakfast consumption or omission (both P = 0.99). In the last 30 min of exercise, increased relative carbohydrate oxidation occurred in the carbohydrate compared with placebo trial after breakfast omission (44.0 ± 8.8 vs 28.0 ± 12.3, P < 0.01) but not consumption (51.7 ± 12.3 vs 44.2 ± 10.4, P = 0.38). In the same period, a reduction in relative liver (but not muscle) glucose oxidation was observed in the carbohydrate compared with placebo trials after breakfast consumption (liver, 7.7% ± 1.6% vs 14.8% ± 2.3%, P < 0.01; muscle, 25.4% ± 9.4% vs 29.4% ± 11.1%, P = 0.99) and omission (liver, 3.8% ± 0.8% vs 8.7% ± 2.8%, P < 0.01; muscle, 19.4% ± 7.5% vs 19.2% ± 12.2%, P = 0.99). No significant difference in relative exogenous carbohydrate oxidation was observed between breakfast consumption and omission trials (P = 0.14). CONCLUSION: In acute normobaric hypoxia, carbohydrate supplementation increased relative carbohydrate oxidation during exercise (>60 min) after breakfast omission, but not consumption.

Response: Commentary on the effects of hypoxia on energy substrate use during exercise.

BACKGROUND: A recent commentary has been published on our meta-analysis, which investigated substrate oxidation during exercise matched for relative intensities in hypoxia compared with normoxia. Within this commentary, the authors proposed that exercise matched for absolute intensities in hypoxia compared with normoxia, should have been included within the analysis, as this model provides a more suitable experimental design when considering nutritional interventions in hypoxia. MAIN BODY: Within this response, we provide a rationale for the use of exercise matched for relative intensities in hypoxia compared with normoxia. Specifically, we argue that this model provides a physiological stimulus replicable of real world situations, by reducing the absolute workload undertaken in hypoxia. Further, the use of exercise matched for relative intensities isolates the metabolic response to hypoxia, rather than the increased relative exercise intensity experienced in hypoxia when utilising exercise matched for absolute intensities. In addition, we also report previously unpublished data analysed at the time of the original meta-analysis, assessing substrate oxidation during exercise matched for absolute intensities in hypoxia compared with normoxia. CONCLUSION: An increased reliance on carbohydrate oxidation was observed during exercise matched for absolute intensities in hypoxia compared with normoxia. These data now provide a comparable dataset for the use of researchers and practitioners alike in the design of nutritional interventions for relevant populations.