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Reliable and valid assessment of sports nutrition knowledge can inform athlete nutrition education to address knowledge gaps. This study aimed to test the reliability and validity of an electronically administered sports nutrition knowledge tool - Platform to Evaluate Athlete Knowledge of Sports Nutrition Questionnaire (PEAKS-NQ). A 94-item PEAKS-NQ was piloted to 149 developmental athletes (DA) in New Zealand, with a subset invited to complete the PEAKS-NQ again to assess reliability. Reliability was evaluated using sign test, intraclass correlation and Cronbach's α. Accredited sports dietitians (ASD; n 255) completed the PEAKS-NQ to establish construct validity via known-groups methodology and provided relevance scores to determine the scale content validity index (S-CVI). Rasch analysis was conducted to identify potentially problematic items and test reliability. Onvansertib nmr Score differences between DA and ASD were analysed using independent t or non-parametric tests. DA (n 88) were 17·8 (sd 1·4) years, 61·4 % female and mostly in high school (94·3 %). ASD (n 45) were 37·8 (sd 7·6) years, 82·2 % female, with >5 years of dietetic experience (59·1 %). ASD scored higher than DA in all sections and overall (91·5 (sd 3·4) v. 67·1 (sd 10·5) %) (P less then 0·001). There were no differences between retests (n 18; P = 0·14). Cronbach's α was 0·86. S-CVI indicated good content validity (0·88). Rasch analysis resulted in a fifty-item PEAKS-NQ with high item (0·91) and person (0·92) reliability. The PEAKS-NQ is reliable and valid for assessing sports nutrition knowledge which could assist practitioners effectively tailor and evaluate nutrition education.Muscle mass may play an important role in the metabolic profile of individuals with or without excess weight. Metabolic phenotypes classify individuals as healthy or unhealthy based on certain metabolic conditions. We investigated the association between skeletal mass indices (SMI) and the metabolically unhealthy phenotype in normal-weight and overweight/obese adults. A total of 660 adults aged 20 to 59 years were assessed by a population-based cross-sectional study. Muscle mass of the limbs or appendicular lean mass (ALM) adjusted for weight (SMIweight) and BMI (SMIBMI) was used to evaluate SMI. Logistic regression was employed to estimate the association between SMIweight, SMIBMI and metabolic phenotypes of normal-weight and overweight/obese individuals. Metabolically unhealthy individuals were older in both sexes. Metabolically unhealthy men had lower SMI values and higher fat percentage than metabolically healthy men. SMIweight was inversely associated with the metabolically unhealthy phenotype, both in normal-weight men (OR 0·49, 95 % CI 0·24, 0·99, P = 0·04) and in overweight/obese men (OR 0·32, 95 % CI 0·16, 0·64, P = 0·001). SMIBMI was inversely associated with the metabolically unhealthy phenotype in overweight/obese men (OR 0·36, 95 % CI 0·18, 0·72, P = 0·004), but not in normal-weight men (OR 0·70, 95 % CI 0·34, 1·43, P = 0·33). Among women, SMI showed no significant association with the phenotypes. In conclusion, the SMI are inversely associated with the metabolically unhealthy phenotype in men, especially among overweight/obese men.We investigated the impact of recent caffeine drinking on glucose and other biomarkers of cardiometabolic function under free-living conditions while also accounting for lifestyle and genetic factors that alter caffeine metabolism and drinking behaviour. Up to 447 794 UK Biobank participants aged 37-73 years in 2006-2010 provided a non-fasting blood sample, for genetic and biomarker measures, and completed questionnaires regarding sociodemographics, medical history and lifestyle. Caffeine drinking (yes/no) about 1 h before blood collection was also recorded. Multivariable regressions were used to examine the association between recent caffeine drinking and serum levels of glycated Hb, glucose, lipids, apo, lipoprotein(a) and C-reactive protein. Men and women reporting recent caffeine drinking had clinically and significantly higher glucose levels than those not recently drinking caffeine (P less then 0·0001). Larger effect sizes were observed among those 55+ years of age and with higher adiposity and longer fasting times (P ≤ 0·02 for interactions). Significant CYP1A2 rs2472297×caffeine and MLXIPL rs7800944 × caffeine interactions on glucose levels were observed among women (P = 0·004), with similar but non-significant interactions in men. Larger effect sizes were observed among women with rs2472297 CC or rs7800944 CC genotypes than among rs2472297 T or rs7800944 T carriers, respectively. In summary, men and women drinking caffeine within about 1 h of blood draw had higher glucose levels than those not drinking caffeine. Findings were modified by age, adiposity, fasting time and genetic factors related to caffeine metabolism and drinking behaviour. Implications for clinical and population studies of caffeine-containing beverages and cardiometabolic health are discussed.Glucagon-like peptide-1 (GLP-1) is postprandially secreted from enteroendocrine L-cells and enhances insulin secretion. Currently, it is still controversial whether postprandial GLP-1 responses are altered in obesity and diabetes. To address the issue and to find out possible factors related, we compared postprandial GLP-1 responses in normal rats and in diabetic rats chronically fed an obesogenic diet. Male Wistar rats and diabetic Goto-Kakizaki (GK) rats were fed either a control diet or a high-fat/high-sucrose (HFS, 30 % fat and 40 % sucrose) diet for 26 weeks. Meal tolerance tests were performed for monitoring postprandial responses after a liquid diet administration (62·76 kJ/kg body weight) every 4 or 8 weeks. Postprandial glucose, GLP-1 and insulin responses in Wistar rats fed the HFS diet (WH) were higher than Wistar rats fed the control diet (WC). Although GK rats fed the HFS diet (GH) had higher glycaemic responses than GK rats fed the control diet (GC), these groups had similar postprandial GLP-1 and insulin responses throughout the study. Jejunal and ileal GLP-1 contents were increased by the HFS diet only in Wistar rats. Furthermore, mRNA expression levels of fatty acid receptors (Ffar1) in the jejunum were mildly (P = 0·053) increased by the HFS diet in Wistar rats, but not in GK rats. These results demonstrate that postprandial GLP-1 responses are enhanced under an obesogenic status in normal rats, but not in diabetic rats. Failure of adaptive enhancement of GLP-1 response in GK rats could be partly responsible for the development of glucose intolerance.
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