Dr Alistair Black

Abstract

There is limited research studying fluid and electrolyte balance in rugby union players, and a paucity of information regarding the test–retest reliability. This study describes the fluid balance of elite rugby union players across multiple squads and the reliability of fluid balance measures between two equivalent training sessions. Sixty‐one elite rugby players completed a single fluid balance testing session during a game simulation training session. A subsample of 21 players completed a second fluid balance testing session during an equivalent training session. Players were weighed in minimal clothing before and after each training session. Each player was provided with their own drinks which were weighed before and after each training session. More players gained body weight (9 (14.8%)) during training than lost greater than 2% of their initial body mass (1 (1.6%)). Pre‐training body mass and rate of fluid loss were significantly associated (r = 0.318, p = .013). There was a significant correlation between rate of fluid loss in sessions 1 (1.74 ± 0.32 L h−1) and 2 (1.10 ± 0.31 L. h−1), (r = 0.470, p = .032). This could be useful for nutritionists working with rugby squads to identify players with high sweat losses.

BACKGROUND: This study aimed to describe the nutrition knowledge, food security risk and eating disorder risk of development male rugby league players. METHODS: Sixty athletes from one Australian professional rugby league club volunteered. A cross sectional online survey questionnaire consisted of three sections (Eating Disorders Inventory (EDI-3), Nutrition Knowledge and Food Security). All athletes completed the online survey without assistance using a personal electronic device. RESULTS: The mean total knowledge score was 65.7±13.1%. There was a positive relationship between age and knowledge score, P=0.050, r

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BACKGROUND: There have been several published studies on the prevalence of low energy availability (LEA) risk amongst North American and European endurance athletes. Yet the prevalence and risk factors amongst rugby league players are less well understood. This study assessed the prevalence of low energy availability risk, eating disorder risk, and food security amongst players from a female National Rugby League squad in Australia. METHODS: Players from one Australian professional rugby league club volunteered to participate in the study. An online questionnaire was conducted to determine the prevalence of low energy availability (Low Energy Availability in Females Questionnaire [LEAF-Q]), eating disorder risk (Eating Disorders Inventory [EDI-3]), and food security. RESULTS: Differences between those “at risk” and “not at risk” based on their total LEAF-Q score were determined. Of the 28 players, 64% (N.=18) were at risk of LEA. Raw scores for the EDI-3 subscales, body dissatisfaction (P=0.043), bulimia (P=0.002), composite score (P=0.038), were significantly higher for those at risk and not at risk of LEA. Forty percent of players had some level of food insecurity. CONCLUSIONS: The results suggest LEA risk is similar to other populations and those at risk of LEA are more likely to have an elevated clinical risk of eating disorders. Food security is also an issue in this population and could contribute to LEA risk for some. Future research is needed amongst team sports athletes to understand interplay between eating disorder risk and food insecurity with LEA risk.

Rugby is a worldwide intermittent team sport. Players tend to be heavier than the majority of similar team sport athletes on whom the dietary guidelines have been developed. Therefore, the aim of the current review was to describe the intakes of rugby union players. Article databases were searched up to February 2017 and were included if they were published in English and reported dietary intakes of male rugby union players. Of the research articles identified, energy intakes were lower than two of three studies that reported intakes and expenditure, which would suggest the players were losing weight that is somewhat supported by the decreases in skinfolds seen during preseason. However, it should also be noted that there are errors in both the measurement of energy intakes and expenditure. Carbohydrate intakes ranged from 2.6 to 6.5 g·kg−1·day−1, which is lower than the current relative to body mass recommendations; however, this would not be classed as a low-carbohydrate diet. The consistently low intakes of carbohydrate suggest that these intake levels maybe sufficient for performance, given the players greater body mass or there are errors in the measurements. However, there is currently no evidence for the carbohydrate needs of rugby union players in terms of performance. The lower intakes than expenditure would suggest the players were losing weight. Previous research shows that rugby union players lose body fat during preseason training.

The ergogenic benefits of carbohydrate (CHO) ingestion in cycling and running have been widely reported. Studies directly comparing the effect of CHO ingestion on CHO oxidation rates in cycling and running suggest no difference in exogenous CHO oxidation between these exercise modes. Potential differences in endogenous fuel use between cycling and running when ingesting CHO may lead to a greater benefit in cycling rather than running time trial (TT) performance. Direct comparisons of the effect of CHO ingestion during endurance exercise on subsequent cycling or running TT performance are limited. This study tested the hypothesis that ingesting CHO during 120 min of constant intensity exercise would benefit subsequent TT performance more in cycling than running. Methods: In a randomised, placebo controlled, double blind crossover trial, 10 male triathletes (VO2 max cycle 51.65±5.53, run 59.07±6.14 mL kg min ) completed 4 separate exercise trials. Each trial consisted of cycling or running at 70% of mode specific VO2max for 120min whilst ingesting either a CHO drink (2:1 glucose: fructose, 90g h ) or an equal volume of taste matched 0% CHO placebo (PLA) (750mL h ). After 10min recovery, participants completed a TT in the same mode of exercise, running 6km or cycling 16km. The CHO drink was enriched with uniformly labelled C glucose and C fructose isotopes to quantify exogenous and endogenous CHO oxidation. Due to limitations of the tracer methods used in the first hour, only data for the final 60min of exercise are presented. Total CHO and fat oxidation rates were calculated from expired air using stoichiometric equations. Data were analysed using ANOVA, values are means±SD. Results: From 60 120 min of exercise mean fat oxidation rates did not differ between exercise modes (PLA cycle 0.52±0.17, run 0.56±0.22g min p=0.86; CHO cycle 0.37±0.12 run 0.40±0.17g min , p=0.82). CHO ingestion reduced fat oxidation within cycling (p<0.01) and running trials (p=0.02) compared to PLA. Mean total CHO oxidation rates did not differ between trials (PLA cycle 2.52±0.74, run 2.21±0.46g min , p=0.23, CHO cycle 2.95±0.40, run 2.77±0.55g min , p=0.47). Mean exogenous CHO oxidation did not differ with CHO ingestion (cycle 0.87±0.22 run 0.75±0.31g min , p=0.31). CHO ingestion reduced endogenous CHO oxidation in cycling (PLA 2.52±0.74, CHO 2.10±0.41g min , p=0.03) but not running (PLA 2.21±0.46, CHO 2.00±0.61g min , p=0.44). TT performance improved 10% in cycling and 3% in running after CHO ingestion (p<0.01). TT performance improvement was greater in cycling than running (p=0.04, ES=1.45). Conclusions: This study demonstrates a greater improvement in cycling versus running TT performance after CHO ingestion. This may relate to the greater sparing of endogenous CHO in cycling versus running during the previous exercise period when CHO is ingested.

We investigated the effects of ingesting a leucine-enriched essential amino acid (EAA) gel alone or combined with resistance exercise (RE) versus RE alone (control) on plasma aminoacidemia and intramyocellular anabolic signalling in healthy younger (28 ± 4 years) and older (71 ± 3 years) adults. Blood samples were obtained throughout the three trials, while muscle biopsies were collected in the postabsorptive state and 2 h following RE; following the consumption of two 50 mL EAA gels (40% leucine, 15 g total EAA); and following RE with EAA (combination; COM). Protein content and the phosphorylation status of key anabolic signalling proteins were determined via immunoblotting. Irrespective of age, during EAA and COM peak leucinemia (younger: 454 ± 32 µM and 537 ± 111 µM; older: 417 ± 99 µM and 553 ± 136 µM) occurred ~60 – 120 min post-ingestion (younger: 66 ± 6 min and 120 ± 60 min; older: 90 ± 13 min and 78 ± 12 min). In the pooled sample, area under the curve for plasma leucine and the sum of branched-chain amino acids was significantly greater in EAA and COM compared with RE. For intramyocellular signalling, significant main effects were found for condition (mTOR (Ser2481), rpS6 (Ser235/236)) and age (S6K1 (Thr421/Ser424), 4E-BP1 (Thr37/46)) in age group analyses. The phosphorylation of rpS6 was of similar magnitude (~8-fold) in pooled and age group data 2 h following COM. Our findings suggest that a gel-based, leucine-enriched EAA supplement is associated with aminoacidemia and a muscle anabolic signalling response, thus representing an effective means of stimulating muscle protein anabolism in younger and older adults following EAA and COM.

Purpose: This study compared the co-ingestion of glucose and fructose on exogenous and endogenous substrate oxidation during prolonged exercise at terrestrial high altitude (HA) versus sea level, in women. Method: Five women completed two bouts of cycling at the same relative workload (55% Wmax) for 120 minutes on acute exposure to HA (3375m) and at sea level (~113m). In each trial, participants ingested 1.2 g.min-1 of glucose (enriched with 13C glucose) and 0.6 g.min-1 of fructose (enriched with 13C fructose) before and every 15 minutes during exercise. Indirect calorimetry and isotope ratio mass spectrometry were used to calculate fat oxidation, total and exogenous carbohydrate oxidation, plasma glucose oxidation and endogenous glucose oxidation derived from liver and muscle glycogen. Results: The rates and absolute contribution of exogenous carbohydrate oxidation was significantly lower at HA compared with sea level (ES>0.99, P<0.024), with the relative exogenous carbohydrate contribution approaching significance (32.6±6.1 vs. 36.0±6.1%, ES=0.56, P=0.059) during the second hour of exercise. In comparison, no significant differences were observed between HA and sea level for the relative and absolute contributions of liver glucose (3.2±1.2 vs. 3.1±0.8%, ES=0.09, P=0.635 and 5.1±1.8 vs. 5.4±1.7 grams, ES=0.19, P=0.217), and muscle glycogen (14.4±12.2% vs. 15.8±9.3%, ES=0.11, P=0.934 and 23.1±19.0 vs. 28.7±17.8 grams, ES=0.30, P=0.367). Furthermore, there was no significant difference in total fat oxidation between HA and sea level (66.3±21.4 vs. 59.6±7.7 grams, ES=0.32, P=0.557). Conclusion: In women, acute exposure to HA reduces the reliance on exogenous carbohydrate oxidation during cycling at the same relative exercise intensity.