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Article ; Online: The Importance of Fatty Acids as Nutrients during Post-Exercise Recovery.

Lundsgaard, Anne-Marie / Fritzen, Andreas M / Kiens, Bente

2020 Volume 12, Issue 2

Abstract: It is well recognized that whole-body fatty acid (FA) oxidation remains increased for several hours following aerobic endurance exercise, even despite carbohydrate intake. However, the mechanisms involved herein have hitherto not been subject to a ... ...

Abstract	It is well recognized that whole-body fatty acid (FA) oxidation remains increased for several hours following aerobic endurance exercise, even despite carbohydrate intake. However, the mechanisms involved herein have hitherto not been subject to a thorough evaluation. In immediate and early recovery (0-4 h), plasma FA availability is high, which seems mainly to be a result of hormonal factors and increased adipose tissue blood flow. The increased circulating availability of adipose-derived FA, coupled with FA from lipoprotein lipase (LPL)-derived very-low density lipoprotein (VLDL)-triacylglycerol (TG) hydrolysis in skeletal muscle capillaries and hydrolysis of TG within the muscle together act as substrates for the increased mitochondrial FA oxidation post-exercise. Within the skeletal muscle cells, increased reliance on FA oxidation likely results from enhanced FA uptake into the mitochondria through the carnitine palmitoyltransferase (CPT) 1 reaction, and concomitant AMP-activated protein kinase (AMPK)-mediated pyruvate dehydrogenase (PDH) inhibition of glucose oxidation. Together this allows glucose taken up by the skeletal muscles to be directed towards the resynthesis of glycogen. Besides being oxidized, FAs also seem to be crucial signaling molecules for peroxisome proliferator-activated receptor (PPAR) signaling post-exercise, and thus for induction of the exercise-induced FA oxidative gene adaptation program in skeletal muscle following exercise. Collectively, a high FA turnover in recovery seems essential to regain whole-body substrate homeostasis.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adipose Tissue/metabolism ; Biological Availability ; Carnitine O-Palmitoyltransferase/metabolism ; Exercise/physiology ; Fatty Acids/pharmacokinetics ; Glucose/metabolism ; Glycogen/metabolism ; Homeostasis ; Humans ; Hydrolysis/drug effects ; Lipoprotein Lipase/metabolism ; Lipoproteins, VLDL/metabolism ; Muscle, Skeletal/metabolism ; Nutrients/pharmacokinetics ; Oxidation-Reduction/drug effects ; Peroxisome Proliferator-Activated Receptors/metabolism ; Signal Transduction ; Triglycerides/metabolism
Chemical Substances	Fatty Acids ; Lipoproteins, VLDL ; Peroxisome Proliferator-Activated Receptors ; Triglycerides ; Glycogen (9005-79-2) ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Lipoprotein Lipase (EC 3.1.1.34) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-01-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12020280
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Article: The Importance of Fatty Acids as Nutrients during Post-Exercise Recovery

Lundsgaard, Anne-Marie / Fritzen, Andreas M / Kiens, Bente

Nutrients. 2020 Jan. 21, v. 12, no. 2

2020

Abstract	It is well recognized that whole-body fatty acid (FA) oxidation remains increased for several hours following aerobic endurance exercise, even despite carbohydrate intake. However, the mechanisms involved herein have hitherto not been subject to a thorough evaluation. In immediate and early recovery (0–4 h), plasma FA availability is high, which seems mainly to be a result of hormonal factors and increased adipose tissue blood flow. The increased circulating availability of adipose-derived FA, coupled with FA from lipoprotein lipase (LPL)-derived very-low density lipoprotein (VLDL)-triacylglycerol (TG) hydrolysis in skeletal muscle capillaries and hydrolysis of TG within the muscle together act as substrates for the increased mitochondrial FA oxidation post-exercise. Within the skeletal muscle cells, increased reliance on FA oxidation likely results from enhanced FA uptake into the mitochondria through the carnitine palmitoyltransferase (CPT) 1 reaction, and concomitant AMP-activated protein kinase (AMPK)-mediated pyruvate dehydrogenase (PDH) inhibition of glucose oxidation. Together this allows glucose taken up by the skeletal muscles to be directed towards the resynthesis of glycogen. Besides being oxidized, FAs also seem to be crucial signaling molecules for peroxisome proliferator-activated receptor (PPAR) signaling post-exercise, and thus for induction of the exercise-induced FA oxidative gene adaptation program in skeletal muscle following exercise. Collectively, a high FA turnover in recovery seems essential to regain whole-body substrate homeostasis.
Keywords	AMP-activated protein kinase ; adipose tissue ; blood flow ; carbohydrate intake ; carnitine palmitoyltransferase ; exercise ; fatty acids ; genes ; glucose ; glycogen ; homeostasis ; hydrolysis ; lipoprotein lipase ; mitochondria ; muscles ; myocytes ; nutrients ; oxidation ; peroxisome proliferator-activated receptors ; pyruvate dehydrogenase (lipoamide) ; skeletal muscle ; very low density lipoprotein
Language	English
Dates of publication	2020-0121
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-light
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12020280
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Article ; Online: Genetics and diet shape the relationship between islet function and whole-body metabolism.

Yau, Belinda / Madsen, Søren / Healy, Marin E / Cooke, Kristen C / Fritzen, Andreas M / Thorius, Ida H / Stöckli, Jacqueline / James, David E / Kebede, Melkam A

American journal of physiology. Endocrinology and metabolism

2024

Abstract: Despite the fact that genes and the environment are known to play a central role in islet function, our knowledge of how these parameters interact to modulate insulin secretory function remains relatively poor. Presently, we ... ...

Abstract	Despite the fact that genes and the environment are known to play a central role in islet function, our knowledge of how these parameters interact to modulate insulin secretory function remains relatively poor. Presently, we performed
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00060.2024
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Article ; Online: Pharmacological activation of PDC flux reverses lipid-induced inhibition of insulin action in muscle during recovery from exercise.

Carl, Christian S / Jensen, Marie M / Sjøberg, Kim A / Constantin-Teodosiu, Dumitru / Hill, Ian R / Kjøbsted, Rasmus / Greenhaff, Paul L / Wojtaszewski, Jørgen F P / Richter, Erik A / Fritzen, Andreas M / Kiens, Bente

Diabetes

2024

Abstract: Insulin resistance is a risk factor for type 2 diabetes and exercise can improve insulin sensitivity. However, following exercise high circulating fatty acid (FA) levels might counteract this. We hypothesized that such inhibition would be reduced by ... ...

Abstract	Insulin resistance is a risk factor for type 2 diabetes and exercise can improve insulin sensitivity. However, following exercise high circulating fatty acid (FA) levels might counteract this. We hypothesized that such inhibition would be reduced by forcibly increasing carbohydrate oxidation through pharmacological activation of the pyruvate dehydrogenase complex (PDC). Insulin-stimulated glucose uptake was examined with a cross-over design in healthy young men (n = 8) in a previously exercised and a rested leg during a hyperinsulinemiceuglycemic clamp five hours after one-legged exercise with: 1) infusion of saline, 2) infusion of intralipid imitating circulating FA levels during recovery from whole-body exercise, and 3) infusion of intralipid + oral PDC-activator, dichloroacetate (DCA). Intralipid infusion reduced insulin-stimulated glucose uptake by 19% in the previously exercised leg, which was not observed in the contralateral rested leg. Interestingly, this effect of intralipid in the exercised leg was abolished by DCA, which increased muscle PDC activity (130%) and flux (acetylcarnitine 130%) and decreased inhibitory phosphorylation of PDC on Ser293 (∼40%) and Ser300 (∼80%). Novel insight is provided into the regulatory interaction between glucose and lipid metabolism during exercise recovery. Coupling exercise and PDC flux activation upregulated the capacity for both glucose transport (exercise) and oxidation (DCA), which seems necessary to fully stimulate insulin-stimulated glucose uptake during recovery.
Language	English
Publishing date	2024-04-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db23-0879
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Article ; Online: Small Amounts of Dietary Medium-Chain Fatty Acids Protect Against Insulin Resistance During Caloric Excess in Humans.

Lundsgaard, Anne-Marie / Fritzen, Andreas M / Sjøberg, Kim A / Kleinert, Maximilian / Richter, Erik A / Kiens, Bente

Diabetes

2020 Volume 70, Issue 1, Page(s) 91–98

Abstract: Medium-chain fatty acids (MCFAs) have in rodents been shown to have protective effects on glucose homeostasis during high-fat overfeeding. In this study, we investigated whether dietary MCFAs protect against insulin resistance induced by a hypercaloric ... ...

Abstract	Medium-chain fatty acids (MCFAs) have in rodents been shown to have protective effects on glucose homeostasis during high-fat overfeeding. In this study, we investigated whether dietary MCFAs protect against insulin resistance induced by a hypercaloric high-fat diet in humans. Healthy, lean men ingested a eucaloric control diet and a 3-day hypercaloric high-fat diet (increase of 75% in energy, 81-83% energy [E%] from fat) in randomized order. For one group (
MeSH term(s)	Adult ; Blood Glucose/metabolism ; Diet, High-Fat ; Dietary Fats/administration & dosage ; Energy Intake/physiology ; Energy Metabolism/physiology ; Fatty Acids/administration & dosage ; Humans ; Insulin/blood ; Insulin Resistance/physiology ; Male ; Triglycerides/blood ; Young Adult
Chemical Substances	Blood Glucose ; Dietary Fats ; Fatty Acids ; Insulin ; Triglycerides
Language	English
Publishing date	2020-10-29
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db20-0582
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Article ; Online: Salt-inducible kinases are required for glucose uptake and insulin signaling in human adipocytes.

Säll, Johanna / Lindahl, Maria / Fritzen, Andreas M / Fryklund, Claes / Kopietz, Franziska / Nyberg, Emma / Warvsten, Anna / Morén, Björn / Foretz, Marc / Kiens, Bente / Stenkula, Karin G / Göransson, Olga

Obesity (Silver Spring, Md.)

2023 Volume 31, Issue 10, Page(s) 2515–2529

Abstract: Objective: Salt-inducible kinase 2 (SIK2) is abundantly expressed in adipocytes and downregulated in adipose tissue from individuals with obesity or insulin resistance. The main aims of this work were to investigate the involvement of SIKs in the ... ...

Abstract	Objective: Salt-inducible kinase 2 (SIK2) is abundantly expressed in adipocytes and downregulated in adipose tissue from individuals with obesity or insulin resistance. The main aims of this work were to investigate the involvement of SIKs in the regulation of glucose uptake in primary mature human adipocytes and to identify mechanisms underlying this regulation. Methods: Primary mature adipocytes were isolated from human, rat, or mouse adipose tissue and treated with pan-SIK inhibitors. Adipocytes isolated from wild type, ob/ob, and SIK2 knockout mice were also used. Glucose uptake was examined by glucose tracer assay. The insulin signaling pathway was monitored by Western blotting, co-immunoprecipitation, and total internal reflection fluorescence microscopy. Results: This study demonstrates that SIK2 is downregulated in obese ob/ob mice and that SIK activity is required for intact glucose uptake in primary human and mouse adipocytes. The underlying mechanism involves direct effects on the insulin signaling pathway, likely at the level of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) generation or breakdown. Moreover, lack of SIK2 alone is sufficient to attenuate glucose uptake in mouse adipocytes. Conclusions: SIK2 is required for insulin action in human adipocytes, and the mechanism includes direct effects on the insulin signaling pathway.
MeSH term(s)	Animals ; Humans ; Mice ; Rats ; Adipocytes ; Adipose Tissue ; Glucose ; Insulin ; Mice, Knockout ; Obesity ; Protein Serine-Threonine Kinases/genetics ; Signal Transduction
Chemical Substances	Glucose (IY9XDZ35W2) ; Insulin ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; SIK2 protein, rat (EC 2.7.11.1) ; salt-inducible kinase-2, human (EC 2.7.1.-)
Language	English
Publishing date	2023-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.23858
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Article ; Online: Dietary medium-chain fatty acids reduce food intake via the GDF15-GFRAL axis in mice.

Kanta, Josephine M / Deisen, Luisa / Johann, Kornelia / Holm, Stephanie / Lundsgaard, Annemarie / Lund, Jens / Jähnert, Markus / Schürmann, Annette / Clemmensen, Christoffer / Kiens, Bente / Fritzen, Andreas M / Kleinert, Maximilian

Molecular metabolism

2023 Volume 74, Page(s) 101760

Abstract: Objective: Medium chain fatty acids (MCFAs), which are fatty acids with chain lengths of 8-12 carbon atoms, have been shown to reduce food intake in rodents and humans, but the underlying mechanisms are unknown. Unlike most other fatty acids, MCFAs are ... ...

Abstract	Objective: Medium chain fatty acids (MCFAs), which are fatty acids with chain lengths of 8-12 carbon atoms, have been shown to reduce food intake in rodents and humans, but the underlying mechanisms are unknown. Unlike most other fatty acids, MCFAs are absorbed from the intestine into the portal vein and enter first the liver. We thus hypothesized that MCFAs trigger the release of hepatic factors that reduce appetite. Methods: The liver transcriptome in mice that were orally administered MCFAs as C8:0 triacylglycerol (TG) was analyzed. Circulating growth/differentiation factor 15 (GDF15), tissue Gdf15 mRNA and food intake were investigated after acute oral gavage of MCFAs as C8:0 or C10:0 TG in mice. Effects of acute and subchronic administration of MCFAs as C8:0 TG on food intake and body weight were determined in mice lacking either the receptor for GDF15, GDNF Family Receptor Alpha Like (GFRAL), or GDF15. Results: Hepatic and small intestinal expression of Gdf15 and circulating GDF15 increased after ingestion of MCFAs, while intake of typical dietary long-chain fatty acids (LCFAs) had no effect. Plasma GDF15 levels also increased in the portal vein with MCFA intake, indicating that in addition to the liver, the small intestine contributes to the rise in circulating GDF15. Acute oral provision of MCFAs decreased food intake over 24 h compared with a LCFA-containing bolus, and this anorectic effect required the GDF15 receptor, GFRAL. Moreover, subchronic oral administration of MCFAs reduced body weight over 7 days, an effect that was blunted in mice lacking either GDF15 or GFRAL. Conclusions: We have identified ingestion of MCFAs as a novel nutritional approach that increases circulating GDF15 in mice and have revealed that the GDF15-GFRAL axis is required for the full anorectic effect of MCFAs.
MeSH term(s)	Humans ; Mice ; Animals ; Appetite Depressants/pharmacology ; Glial Cell Line-Derived Neurotrophic Factor/pharmacology ; Body Weight ; Fatty Acids/metabolism ; Diet, High-Fat ; Triglycerides ; Eating ; Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism
Chemical Substances	Appetite Depressants ; Glial Cell Line-Derived Neurotrophic Factor ; Fatty Acids ; Triglycerides ; GDF15 protein, human ; Growth Differentiation Factor 15
Language	English
Publishing date	2023-06-24
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2023.101760
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Article ; Online: Skeletal muscle proteins involved in fatty acid transport influence fatty acid oxidation rates observed during exercise.

Maunder, Ed / Rothschild, Jeffrey A / Fritzen, Andreas M / Jordy, Andreas B / Kiens, Bente / Brick, Matthew J / Leigh, Warren B / Chang, Wee-Leong / Kilding, Andrew E

Pflugers Archiv : European journal of physiology

2023 Volume 475, Issue 9, Page(s) 1061–1072

Abstract: Several proteins are implicated in transmembrane fatty acid transport. The purpose of this study was to quantify the variation in fatty acid oxidation rates during exercise explained by skeletal muscle proteins involved in fatty acid transport. Seventeen ...

Abstract	Several proteins are implicated in transmembrane fatty acid transport. The purpose of this study was to quantify the variation in fatty acid oxidation rates during exercise explained by skeletal muscle proteins involved in fatty acid transport. Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to estimate peak whole-body fatty acid oxidation rate (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 2 h of fed-state, moderate-intensity cycling to estimate whole-body fatty acid oxidation during fed-state exercise (FO). Bivariate correlations and stepwise linear regression models of PFO and FO during 0-30 min (early FO) and 90-120 min (late FO) of continuous cycling were constructed using muscle data. To assess the causal role of transmembrane fatty acid transport in fatty acid oxidation rates during exercise, we measured fatty acid oxidation during in vivo exercise and ex vivo contractions in wild-type and CD36 knock-out mice. We observed a novel, positive association between vastus lateralis FATP1 and PFO and replicated work reporting a positive association between FABPpm and PFO. The stepwise linear regression model of PFO retained CD36, FATP1, FATP4, and FABPpm, explaining ~87% of the variation. Models of early and late FO explained ~61 and ~65% of the variation, respectively. FATP1 and FATP4 emerged as contributors to models of PFO and FO. Mice lacking CD36 had impaired whole-body and muscle fatty acid oxidation during exercise and muscle contractions, respectively. These data suggest that substantial variation in fatty acid oxidation rates during exercise can be explained by skeletal muscle proteins involved in fatty acid transport.
MeSH term(s)	Male ; Mice ; Animals ; Fatty Acid Transport Proteins/metabolism ; Muscle Proteins/metabolism ; Muscle, Skeletal/metabolism ; CD36 Antigens/metabolism ; Fatty Acids/metabolism ; Oxidation-Reduction
Chemical Substances	Fatty Acid Transport Proteins ; Muscle Proteins ; CD36 Antigens ; Fatty Acids
Language	English
Publishing date	2023-07-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-023-02843-7
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Article ; Online: The GDF15-GFRAL pathway is dispensable for the effects of metformin on energy balance.

Klein, Anders B / Nicolaisen, Trine S / Johann, Kornelia / Fritzen, Andreas M / Mathiesen, Cecilie V / Gil, Cláudia / Pilmark, Nanna S / Karstoft, Kristian / Blond, Martin B / Quist, Jonas S / Seeley, Randy J / Færch, Kristine / Lund, Jens / Kleinert, Maximilian / Clemmensen, Christoffer

Cell reports

2022 Volume 40, Issue 8, Page(s) 111258

Abstract: Metformin is a blood-glucose-lowering medication with physiological effects that extend beyond its anti-diabetic indication. Recently, it was reported that metformin lowers body weight via induction of growth differentiation factor 15 (GDF15), which ... ...

Abstract	Metformin is a blood-glucose-lowering medication with physiological effects that extend beyond its anti-diabetic indication. Recently, it was reported that metformin lowers body weight via induction of growth differentiation factor 15 (GDF15), which suppresses food intake by binding to the GDNF family receptor α-like (GFRAL) in the hindbrain. Here, we corroborate that metformin increases circulating GDF15 in mice and humans, but we fail to confirm previous reports that the GDF15-GFRAL pathway is necessary for the weight-lowering effects of metformin. Instead, our studies in wild-type, GDF15 knockout, and GFRAL knockout mice suggest that the GDF15-GFRAL pathway is dispensable for the effects of metformin on energy balance. The data presented here question whether metformin is a sufficiently strong stimulator of GDF15 to drive anorexia and weight loss and emphasize that additional work is needed to untangle the relationship among metformin, GDF15, and energy balance.
MeSH term(s)	Animals ; Glial Cell Line-Derived Neurotrophic Factor Receptors/metabolism ; Growth Differentiation Factor 15/metabolism ; Humans ; Metformin/pharmacology ; Metformin/therapeutic use ; Mice ; Obesity/metabolism ; Weight Loss
Chemical Substances	GDF15 protein, human ; GFRAL protein, mouse ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Growth Differentiation Factor 15 ; Metformin (9100L32L2N)
Language	English
Publishing date	2022-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111258
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Article ; Online: Nutritional optimization for female elite football players-topical review.

de Sousa, Maysa V / Lundsgaard, Anne-Marie / Christensen, Peter M / Christensen, Lars / Randers, Morten B / Mohr, Magni / Nybo, Lars / Kiens, Bente / Fritzen, Andreas M

Scandinavian journal of medicine & science in sports

2021 Volume 32 Suppl 1, Page(s) 81–104

Abstract: 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 ...

Abstract	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.
MeSH term(s)	Athletes ; Carbohydrates ; Energy Intake ; Female ; Humans ; Micronutrients ; Soccer ; Sports Nutritional Physiological Phenomena
Chemical Substances	Carbohydrates ; Micronutrients
Language	English
Publishing date	2021-12-05
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1077418-x
ISSN	1600-0838 ; 0905-7188
ISSN (online)	1600-0838
ISSN	0905-7188
DOI	10.1111/sms.14102
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