This study aimed to assess nutritional intake, sports nutrition knowledge and risk of Low Energy Availability (LEA) in female Australian rules football players. Victorian Football League Women’s competition (VFLW) players (n = 30) aged 18–35 (weight: 64.5 kg ± 8.0; height: 168.2 cm ± 7.6) were recruited from Victoria, Australia. Nutritional intake was quantified on training days using the Automated 24 h Dietary Assessment Tool (ASA24-Australia), and sports nutrition knowledge was measured by the 88-item Sports Nutrition Knowledge Questionnaire (SNKQ). The risk of LEA was assessed using the Low Energy Availability in Females Questionnaire (LEAF-Q). Daily mean carbohydrate intake in the current investigation was 3 g⋅kg−1⋅d−1, therefore, below the minimum carbohydrate recommendation for moderate exercise of approximately one hour per day (5–7 g⋅kg−1⋅d−1) and for moderate to intense exercise for 1–3 h per day (6–10 g⋅kg−1⋅d−1) for 96.3% and 100% of players, respectively. Daily mean protein intake was 1.5 g⋅kg−1⋅d−1, therefore, consistent with recommendations (1.2–2.0 g⋅kg−1⋅d−1) for 77.8% of players. Daily mean calcium intake was 924.8 mg⋅d−1, therefore, below recommendations (1000 mg⋅d−1) for 65.5% of players, while mean iron intake was 12.2 mg⋅d−1, also below recommendations (18 mg⋅d−1) for 100% of players. Players answered 54.5% of SNKQ questions correctly, with the lowest scores observed in the section on supplements. Risk of LEA was evident in 30% of players, with no differences in carbohydrate (p = 0.238), protein (p = 0.296), fat (p = 0.490) or energy (p = 0.971) intakes between players at risk of LEA and those not at risk. The results suggest that female Australian rules football players have an inadequate intake of carbohydrate and calcium and low sports nutrition knowledge. Further investigation to assess the risk of LEA using direct measures is required.

The short term benefit of higher protein diets appears to persist to a small degree long term. Benefits are greater with better compliance to the diet.

There are limited and inconsistent data suggesting that mild iodine deficiency in pregnancy might be associated with poorer developmental outcomes in children. Between 2011 and 2015, we conducted a prospective cohort study in Australia examining the relationship between maternal iodine intake in pregnancy and childhood neurodevelopment, assessed using Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III), in 699 children at 18 months. Maternal iodine intake and urinary iodine concentration (UIC) were assessed at study entry (<20 weeks’ gestation) and at 28 weeks’ gestation. Maternal iodine intake in the lowest (<220 μg/day) or highest (≥391 μg/day) quartile was associated with lower cognitive, language, and motor scores (mean differences ranged from 2.4 (95% confidence interval (CI): 0.01, 4.8) to 7.0 (95% CI: 2.8, 11.1) points lower) and higher odds (odds ratios ranged from 2.7 (95% CI: 1.3, 5.6) to 2.8 (95% CI: 1.3, 5.7)) of cognitive developmental delay (Bayley-III score <1 standard deviation) compared with mothers with an iodine intake in the middle quartiles. There was no association between UIC in pregnancy and Bayley-III outcomes regardless of whether UIC and the outcomes were analyzed as continuous or categorical variables. Both low and high iodine intakes in pregnancy were associated with poorer childhood neurodevelopment in this iodine-sufficient population.

Mandatory iodine fortification of bread was introduced in 2009 in Australia in response to the reemergence of iodine deficiency. The aim of this study was to assess iodine intake, urinary iodine concentration (UIC) and their correlation in pregnant women (n = 783) recruited from South Australia 2 years following mandatory iodine fortification. Total iodine intake (food and supplements) and UIC were assessed at study entry (<20 weeks') and at 28 weeks' gestation. Mean (±SD) total iodine intake at study entry and 28 weeks' gestation was 307 ± 128 μg/day and 300 ± 127 μg/day, respectively. Overall, 85.9% of women met the estimated average intake (≥160 μg/day) for iodine in pregnancy, but only 44.5% met the estimated average intake from food alone. The main food sources of iodine were dairy foods and iodine-fortified bread. Median (interquartile range) UIC at study entry and 28 weeks' gestation was 189 μg/L and 172 μg/L, respectively. At study entry, median UIC was higher in women taking supplements containing iodine ≥150 μg/day compared with those containing iodine <150 μg/day (221 μg/L vs. 163 μg/L, p = .003) and those not taking supplements containing iodine (221 μg/L vs. 159 μg/L, p < .001). At 28 weeks' gestation, the median UIC for the groups was 187, 152 and 141 μg/L, respectively (each of the two comparisons yielded p < .001). Total iodine intake (food and supplements) from all women was positively, though weakly, correlated with UIC (r = .23, p < .001). In conclusion, pregnant women in South Australia are iodine sufficient postmandatory iodine fortification of bread. However, without iodine supplementation, it may be difficult to achieve a UIC >150 μg/L.

Adequate iodine is important during pregnancy to ensure optimal growth and development of the offspring. We validated an iodinespecific FFQ (I-FFQ) for use in Australian pregnant women. A forty-four-item I-FFQ was developed to assess iodine intake from food and was administered to 122 pregnant women at 28 weeks gestation. Iodine supplement use was captured separately at 28 weeks gestation. Correlation between iodine intake from food estimated using the I-FFQ and a 4 d weighed food record as well as correlation between total iodine intake and 24 h urinary iodine excretion (UIE), 24 h urinary iodine concentration (UIC), spot UIC and thyroid function were assessed at 28 weeks gestation. A moderate correlation between the two dietary methods was shown (r 0·349, P,0·001), and it was strengthened with the addition of iodine supplements (r 0·876, P,0·001). There was a fair agreement (k ¼ 0·28, P,0·001) between the two dietary measures in the classification of women as receiving adequate ($ 160 mg/d) or inadequate (,160 mg/d) iodine intake from food, but the limits of agreement from the Bland-Altman plot were large. Total iodine intake was associated with 24 h UIE (b ¼ 0·488, P, 0·001) but not with spot UIC. Iodine intake from food using the I-FFQ was assessed at study entry (, 20 weeks gestation) in addition to 28 weeks gestation, and there was a strong correlation in iodine intake at the two time points (r 0·622, P, 0·001), which indicated good reproducibility. In conclusion, the I-FFQ provides a valid tool for estimating iodine intake in pregnant women and can be used to screen women who are at risk of inadequate intake.

This study compared the energy, macronutrient, and micronutrient intake in elite and sub-elite Australian football players and compared nutritional intake to current recommendations. Sports nutrition knowledge was also quantified and compared between elite and sub-elite players. Nutritional intake was quantified in elite (n = 35) and sub-elite (n = 31) players using the Automated Self-Administered 24-Hour Dietary Assessment Tool. The 88-item Sports Nutrition Knowledge Questionnaire was used to quantify knowledge related to general nutrition concepts, fluid, recovery, weight control, and supplements. Elite players had a higher nutritional intake (mean ± SD) for energy (14,140 ± 5,887 kJ [elite players] vs 10,412 ± 3,316 kJ [sub-elite players]; P = .002) and fat (40% ± 6% [elite players] vs 34% ± 6% [sub-elite players]; P < .001). Protein intake exceeded the recommended intake in 77% of elite players and 68% of sub-elite players, and carbohydrate intake was below the recommended intake for 91% of elite players and 97% of sub-elite players. Sodium intake recommendations were exceeded by 100% of elite and sub-elite players. Both elite and sub-elite players answered 51% of the Sports Nutrition Knowledge Questionnaire questions correctly. The percentage of correctly answered questions specific to supplements was 27% for elite players and 18% for sub-elite players. The results of the current investigation suggest that Australian football players' nutritional intake is inconsistent with current recommendations for macronutrients and some micronutrients. Furthermore, players may benefit from additional knowledge of the risks and benefits of supplement use.

Acute and chronic sleep loss are linked with a range of negative physiological and psychological outcomes (Kecklund & Axelsson, 2016). While complete sleep deprivation rapidly impedes simple and complex cognitive functions, sleep restriction impairs whole-body homeostasis, leading to undesirable metabolic consequences in the short-and longer-term (Reutrakul & Van Cauter, 2018). Most metabolic tissues including liver (Shigiyama et al., 2018), adipose tissue (Wilms et al., 2019), and skeletal muscle are at risk of developing sleep loss-associated adverse outcomes.Skeletal muscle is a primary regulator of human metabolism. Sleep deprivation (Cedernaes et al., 2015(Cedernaes et al., , 2018 and restriction (Harfmann et al., 2015) have the potential to profoundly affect muscle health by altering gene regulation and substrate metabolism. Even relatively short periods of sleep restriction (less than a week) can compromise

To compare the effect of 500 mg·kg−1 body mass (BM) sodium citrate ingested in solution or capsules on induced alkalosis, gastrointestinal symptoms and palatability. Twenty‐four healthy and active participants completed two testing sessions, ingesting 500 mg·kg−1 BM sodium citrate within solution or capsules. Capillary blood samples were collected pre‐ingestion, and every 30‐min for 240‐min post‐ingestion; samples were analyzed for blood pH and [HCO3−]. A validated questionnaire was used to quantify gastrointestinal symptoms at the same 30‐min intervals. Palatability was quantified immediately after ingestion using a validated scale. There was a greater peak and change from baseline for capsules versus solution for blood pH (P < 0.001) and [HCO3−] (P = 0.013). Blood pH and [HCO3−] time to peak was 199 and 204 min, respectively, after capsule ingestion, both significantly later than after solution (P = 0.034, P = 0.001). Gastrointestinal symptoms were significantly elevated above baseline for both ingestion modes at each time point between 30 and 120 min after ingestion (P = 0.003), with no differences between modes at any time point (P = 0.644). Capsules were significantly more palatable than solution (P < 0.001). We recommend 500 mg·kg−1 BM sodium citrate ingestion in capsules, at least 200 min before exercise, to achieve greater alkalosis, minimize gastrointestinal symptoms, and maximize.