Nutritional optimization for female elite football players-topical review.

Women's football is an intermittent sport characterized by frequent intense actions throughout the match. The high number of matches with limited recovery time played across a long competitive season underlines the importance of nutritional strategies to meet these large physical demands. In order to maximize sport performance and maintain good health, energy intake must be optimal. However, a considerable proportion of female elite football players does not have sufficient energy intake to match the energy expenditure, resulting in low energy availability that might have detrimental physiologic consequences and impair performance. Carbohydrates appear to be the primary fuel covering the total energy supply during match-play, and female elite football players should aim to consume sufficient carbohydrates to meet the requirements of their training program and to optimize the replenishment of muscle glycogen stores between training bouts and matches. However, several macro- and micronutrients are important for ensuring sufficient energy and nutrients for performance optimization and for overall health status in female elite football players. The inadequacy of macro-and micronutrients in the diet of these athletes may impair performance and training adaptations, and increase the risk of health disorders, compromising the player's professional career. In this topical review, we present knowledge and relevant nutritional recommendations for elite female football players for the benefit of sports nutritionists, dietitians, sports scientists, healthcare specialists, and applied researchers. We focus on dietary intake and cover the most pertinent topics in sports nutrition for the relevant physical demands in female elite football players as follows: energy intake, macronutrient and micronutrient requirements and optimal composition of the everyday diet, nutritional and hydration strategies to optimize performance and recovery, potential ergogenic effects of authorized relevant supplements, and future research considerations.

Mechanisms Preserving Insulin Action during High Dietary Fat Intake.

Prolonged intervention studies investigating molecular metabolism are necessary for a deeper understanding of dietary effects on health. Here we provide mechanistic information about metabolic adaptation to fat-rich diets. Healthy, slightly overweight men ingested saturated or polyunsaturated fat-rich diets for 6 weeks during weight maintenance. Hyperinsulinemic clamps combined with leg balance technique revealed unchanged peripheral insulin sensitivity, independent of fatty acid type. Both diets increased fat oxidation potential in muscle. Hepatic insulin clearance increased, while glucose production, de novo lipogenesis, and plasma triacylglycerol decreased. High fat intake changed the plasma proteome in the immune-supporting direction and the gut microbiome displayed changes at taxonomical and functional level with polyunsaturated fatty acid (PUFA). In mice, eucaloric feeding of human PUFA and saturated fatty acid diets lowered hepatic triacylglycerol content compared with low-fat-fed control mice, and induced adaptations in the liver supportive of decreased gluconeogenesis and lipogenesis. Intake of fat-rich diets thus induces extensive metabolic adaptations enabling disposition of dietary fat without metabolic complications.

Circulating FGF21 in humans is potently induced by short term overfeeding of carbohydrates.

OBJECTIVE: Fibroblast-growth factor 21 (FGF21) is thought to be important in metabolic regulation. Recently, low protein diets have been shown to increase circulating FGF21 levels. However, when energy contribution from dietary protein is lowered, other macronutrients, such as carbohydrates, must be increased to meet eucaloric balance. This raises the possibility that intake of a diet rich in carbohydrates may induce an increase in plasma FGF21 levels per se. Here we studied the role of dietary carbohydrates on the levels of circulating FGF21 and concomitant physiologic effects by feeding healthy men a carbohydrate rich diet without reducing protein intake. METHODS: A diet enriched in carbohydrates (80 E% carbohydrate; CHO) and a eucaloric control diet (CON) were provided to nine healthy men for three days. The energy intake during the CHO diet was increased (+75% energy) to ensure similar dietary protein intake in CHO and CON. To control for the effect of caloric surplus, we similarly overfed (+75% energy) the same subjects for three days with a fat-rich diet (78 E% fat; FAT), consisting of primarily unsaturated fatty acids. The three diets were provided in random order. RESULTS: After CHO, plasma FGF21 concentration increased 8-fold compared to CON (329 ± 99 vs. 39 ± 9 pg ml-1, p < 0.05). In contrast, after FAT only a non-significant tendency (p = 0.073) to an increase in plasma FGF21 concentration was found. The increase in FGF21 concentration after CHO correlated closely (r = 0.88, p < 0.01) with increased leg glucose uptake (62%, p < 0.05) and increased hepatic glucose production (17%, p < 0.01), indicating increased glucose turnover. Plasma fatty acid (FA) concentration was decreased by 68% (p < 0.01), supported by reduced subcutaneous adipose tissue HSL Ser660 phosphorylation (p < 0.01) and perilipin 1 protein content (p < 0.01), pointing to a suppression of adipose tissue lipolysis. Concomitantly, a 146% increase in the plasma marker of hepatic de novo lipogenesis C16:1 n-7 FA (p < 0.01) was observed together with 101% increased plasma TG concentration (p < 0.001) in association with CHO intake and increased plasma FGF21 concentration. CONCLUSION: Excess dietary carbohydrate, but not fat, led to markedly increased FGF21 secretion in humans, notably without protein restriction, and affected glucose and lipid homeostais.