BackgroundLow-carbohydrate, high-fat and ketogenic diets are increasingly adopted by athletes for body composition and sports performance enhancements. However, as yet, there is no consensus on their efficacy in improving performance. There is also no comprehensive literature on athletes’ experiences while undertaking this diet. The purpose of this pilot work was two-fold: i. to examine the effects of a non-calorie controlled ketogenic diet on body composition and performance outcomes of endurance athletes, and ii. to evaluate the athletes’ experiences of the ketogenic diet during the 10-week intervention.MethodsUsing a case study design, five New Zealand endurance athletes (4 females, 1 male) underwent a 10-week ketogenic dietary intervention. Body composition (sum of 8 skinfolds), performance indicators (time to exhaustion, VO2 max, peak power and ventilatory threshold), and gas exchange thresholds were measured at baseline and at 10 weeks. Mean change scores were calculated, and analysed using t-tests; Cohen’s effect sizes and 90% confidence limits were applied to quantify change. Individual interviews conducted at 5 weeks and a focus group at 10 weeks assessed athletes’ ketogenic diet experiences. Data was transcribed and analysed using thematic analysis.ResultsAll athletes increased their ability to utilise fat as a fuel source, including at higher exercise intensities. Mean body weight was reduced by 4 kg ± SD 3.1 (p = 0.046; effect size (ES):0.62), and sum of 8 skinfolds by 25.9 mm ± SD 6.9; ES: 1.27; p = 0.001). Mean time to exhaustion dropped by ~2 min (±SD 0.7; p = 0.004; ES: 0.53). Other performance outcomes showed mean reductions, with some increases or unchanged results in two individuals (VO2 Max: −1.69 ml.kg.min ± SD 3.4 (p = 0.63); peak power: -18 W ± SD 16.4 (p = 0.07), and VT2: -6 W ± SD 44.5 (p = 0.77). Athletes reported experiencing reduced energy levels initially, followed by a return of high levels thereafter, especially during exercise, but an inability to easily undertake high intense bouts. Each athlete reported experiencing enhanced well-being, included improved recovery, improvements in skin conditions and reduced inflammation.ConclusionsDespite performance decrements and some negative experiences, athletes were keen to pursue a modified low-carbohydrate, high-fat eating style moving forward due to the unexpected health benefits they experienced.Trial registrationACTRN: ACTRN12617000613303. Registered 28 April 2017, retrospectively registered.

Implementation of a breast milk/nutrition change package by an 11-site collaborative resulted in an increase in breast milk feeding and decrease in NEC that was sustained over an 18-month period.

The SeaQuest spectrometer at Fermilab was designed to detect oppositely-charged pairs of muons

To quantify the effects of adaptation to acutely intermittent hypoxia on running performance, we randomized 29 trained male hockey and soccer players in double-blind fashion to altitude or placebo groups for 15 days of daily use of a functional or placebo hypoxic re-breathing device. Each day's exposure consisted of alternately breathing stale and fresh air for 6 and 4 min respectively over 1 h. Oxygen saturation was monitored with pulse oximeters and progressively reduced in the hypoxia group (90% on Day 1, 77% on Day 15; equivalent to altitudes of Â/3600 Á6000 m above sea level). Performance tests were an incremental run to maximum speed followed by six maximal-effort running sprints; tests were performed 1 day before, 3 days after, and 12 days after the 15-day treatment. Relative to placebo, at 3 days post treatment the hypoxia group showed a mean increase in maximum speed of 2.0% (90% confidence limits, 9/0.5%); sprint speed was relatively faster by 1.5% (9/1.7%) in the first sprint through 7.0% (9/1.5%) in the last; there were also substantial reductions in exercise lactate concentration and resting and exercise heart rate. Substantial effects on performance were still present 9 days later. Thus, adaptation to acutely intermittent hypoxia substantially improves high-intensity running performance.

The mechanisms for stress-induced changes in hematocrit and blood viscosity are unclear. Twenty-two males completed experimental (30 min baseline, 10 min mental stress, 30 min recovery) and no-stress control conditions (70 min). Hemostatic and hemodynamic activity were measured throughout. Hematocrit, colloid osmotic pressure, and blood viscosity displayed parallel patterns: a progressive increase with stress, followed by a gradual recovery. Correlational and covariance analyses indicated that the increase in hematocrit may be mediated by arterial pressure whereas recovery may be mediated by colloid osmotic pressure. Analyses also indicated that acute changes in blood viscosity may depend on hematocrit. These data suggest that stress disturbs hematocrit, colloid osmotic pressure, and blood viscosity through arterial pressure. Poststress, elevated colloid osmotic pressure may drive its own recovery and that of hematocrit and blood viscosity.