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OBJECTIVE: The objective of this study was to explore how dietary macronutrient composition influences postprandial appetite hormone responses and subsequent energy intake. METHODS: A total of 20 adults (mean [SEM], age 30 [1] years, BMI 27.8 [1.3] kg/m2, n = 8 with normal weight, n = 6 with overweight, n = 6 with obesity) consumed a low-fat (LF) diet (10% fat, 75% carbohydrate) and a low-carbohydrate (LC) diet (10% carbohydrate, 75% fat) for 2 weeks each in an inpatient randomized crossover design. At the end of each diet, participants consumed isocaloric macronutrient-representative breakfast test meals, and 6-h postprandial responses were measured. Ad libitum energy intake was measured for the rest of the day. RESULTS: The LC meal resulted in greater mean postprandial plasma active glucagon-like peptide-1 (GLP-1; LC: 6.44 [0.78] pg/mL, LF: 2.46 [0.26] pg/mL; p < 0.0001), total glucose-dependent insulinotropic polypeptide (GIP; LC: 578 [60] pg/mL, LF: 319 [37] pg/mL; p = 0.0004), and peptide YY (PYY; LC: 65.6 [5.6] pg/mL, LF: 50.7 [3.8] pg/mL; p = 0.02), whereas total ghrelin (LC: 184 [25] pg/mL, LF: 261 [47] pg/mL; p = 0.0009), active ghrelin (LC: 91 [9] pg/mL, LF: 232 [28] pg/mL; p < 0.0001), and leptin (LC: 26.9 [6.5] ng/mL, LF: 35.2 [7.5] ng/mL; p = 0.01) were lower compared with LF. Participants ate more during LC at lunch (244 [85] kcal; p = 0.01) and dinner (193 [86] kcal; p = 0.04), increasing total subsequent energy intake for the day compared with LF (551 [103] kcal; p < 0.0001). CONCLUSIONS: In the short term, endogenous gut-derived appetite hormones do not necessarily determine ad libitum energy intake.
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Restricted sugar and ketogenic diets can alter energy balance/metabolism, but decreased energy intake may be compensated by reduced expenditure. In healthy adults, randomization to restricting free sugars or overall carbohydrates (ketogenic diet) for 12 weeks reduces fat mass without changing energy expenditure versus control. Free-sugar restriction minimally affects metabolism or gut microbiome but decreases low-density lipoprotein cholesterol (LDL-C). In contrast, a ketogenic diet decreases glucose tolerance, increases skeletal muscle PDK4, and reduces AMPK and GLUT4 levels. By week 4, the ketogenic diet reduces fasting glucose and increases apolipoprotein B, C-reactive protein, and postprandial glycerol concentrations. However, despite sustained ketosis, these effects are no longer apparent by week 12, when gut microbial beta diversity is altered, possibly reflective of longer-term adjustments to the ketogenic diet and/or energy balance. These data demonstrate that restricting free sugars or overall carbohydrates reduces energy intake without altering physical activity, but with divergent effects on glucose tolerance, lipoprotein profiles, and gut microbiome.
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Dieta Cetogênica , Microbioma Gastrointestinal , Metabolismo dos Lipídeos , Humanos , Microbioma Gastrointestinal/fisiologia , Metabolismo dos Lipídeos/fisiologia , Masculino , Adulto , Feminino , Fenótipo , Metabolismo Energético/fisiologia , Glicemia/metabolismo , Pessoa de Meia-IdadeRESUMO
BACKGROUND: Crossover studies can induce order effects, especially when they lack a wash-out period. OBJECTIVE: We performed a secondary analyses comparing groups of subjects randomized to different diet orders in two inpatient crossover studies originally designed to compare within subject differences in ad libitum energy intake. One study compared minimally processed low carbohydrate (LC) versus low fat (LF) diets and the other matched macronutrients and compared minimally processed food (MPF) versus ultra-processed food (UPF) diets. METHODS: Diet order group comparisons of changes in body weight and body composition, and differences in energy expenditure, food intake were assessed over four weeks in 20 adults randomized to either the LC followed immediately by the LF diet (LCâLF) or the opposite order (LFâLC) as well as 20 adults randomized to either the MPF followed by UPF (MPFâUPF) diets or the opposite order (UPFâMPF). RESULTS: Subjects randomized to LCâLF lost 2.9 ± 1.1 kg more body weight (p < 0.001) and 1.5 ± 0.6 kg more body fat (p = 0.03) than the LFâLC group, likely because the LCâLF group consumed 921 ± 304 kcal/d less than the LFâLC group (p = 0.003). These energy intake differences were driven by the last two weeks (-1610 ± 312 kcal/d; p < 0.0001), perhaps due to carryover effects of gut adaptations during the first two weeks arising from large differences in the mass of food (1296 ± 215 g/d; p < 0.00001) and fiber consumed (58 ± 6 g/d; p < 0.00001). There were no significant diet order effects on energy intake, body weight, or body composition changes between UPFâMPF versus MPFâUPF groups. CONCLUSIONS: Diet order significantly affected energy intake, body weight, and body fat in a 4-week crossover inpatient diet study varying in macronutrients, but not in a similarly structured study varying in ultra-processed foods. CLINICAL TRIAL REGISTRATION: NCT03407053 and NCT03878108.
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The aim of this study was to assess whether adding Ca2+ to aggregate or native forms of ß-lactoglobulin alters gut hormone secretion, gastric emptying rates and energy intake in healthy men and women. Fifteen healthy adults (mean ± sd: 9M/6F, age: 24 ± 5 years) completed four trials in a randomised, double-blind, crossover design. Participants consumed test drinks consisting of 30 g of ß-lactoglobulin in a native form with (NATIVE + MINERALS) and without (NATIVE) a Ca2+-rich mineral supplement and in an aggregated form both with (AGGREG + MINERALS) and without the mineral supplement (AGGREG). Arterialised blood was sampled for 120 min postprandially to determine gut hormone concentrations. Gastric emptying was determined using 13C-acetate and 13C-octanoate, and energy intake was assessed with an ad libitum meal at 120 min. A protein × mineral interaction effect was observed for total glucagon-like peptide-1 (GLP-1TOTAL) incremental AUC (iAUC; P < 0·01), whereby MINERALS + AGGREG increased GLP-1TOTAL iAUC to a greater extent than AGGREG (1882 ± 603 v. 1550 ± 456 pmol·l-1·120 min, P < 0·01), but MINERALS + NATIVE did not meaningfully alter the GLP-1 iAUC compared with NATIVE (1669 ± 547 v. 1844 ± 550 pmol·l-1·120 min, P = 0·09). A protein × minerals interaction effect was also observed for gastric emptying half-life (P < 0·01) whereby MINERALS + NATIVE increased gastric emptying half-life compared with NATIVE (83 ± 14 v. 71 ± 8 min, P < 0·01), whereas no meaningful differences were observed between MINERALS + AGGREG v. AGGREG (P = 0·70). These did not result in any meaningful changes in energy intake (protein × minerals interaction, P = 0·06). These data suggest that the potential for Ca2+ to stimulate GLP-1 secretion at moderate protein doses may depend on protein form. This study was registered at clinicaltrials.gov (NCT04659902).
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Cálcio da Dieta , Estudos Cross-Over , Ingestão de Energia , Esvaziamento Gástrico , Peptídeo 1 Semelhante ao Glucagon , Lactoglobulinas , Humanos , Peptídeo 1 Semelhante ao Glucagon/sangue , Peptídeo 1 Semelhante ao Glucagon/metabolismo , Masculino , Feminino , Adulto , Método Duplo-Cego , Adulto Jovem , Lactoglobulinas/metabolismo , Cálcio da Dieta/administração & dosagem , Suplementos Nutricionais , Período Pós-Prandial , Cálcio/metabolismoAssuntos
Resistência à Insulina , Insulina , Humanos , Obesidade , Carboidratos , Insulina Regular Humana , Carboidratos da Dieta , GlicemiaRESUMO
BACKGROUND: Crossover studies can induce order effects, especially when they lack a wash-out period. OBJECTIVE: To explore diet order effects on energy balance and food intake between randomized diet order groups in two inpatient crossover studies originally designed to compare within-subject differences in ad libitum energy intake between either minimally processed low carbohydrate (LC) versus low fat (LF) diets or macronutrient-matched diets composed of mostly minimally processed food (MPF) or ultra-processed food (UPF). METHODS: Diet order group comparisons of changes in body weight, body composition, and differences in energy expenditure, and food intake were assessed over four weeks in 20 adults randomized to either the LC followed immediately by the LF diet (LCâLF) or the opposite order (LFâLC) as well as 20 adults randomized to either the MPF followed by UPF (MPFâUPF) diets or the opposite order (UPFâMPF). RESULTS: Subjects randomized to LCâLF lost 2.9 ± 1.1 kg more body weight (p < 0.001) and 1.5 ± 0.6 kg more body fat (p = 0.03) than the LFâLC group likely because the LCâLF group consumed 922 ± 304 kcal/d less than the LFâLC group (p = 0.0024). Reduced energy intake in LCâLF vs LFâLC was driven by the last two weeks (-1610 ± 306 kcal/d; p<0.00001) perhaps due to carryover effects of gut adaptations over the first two weeks arising from large differences in the mass of food (1295 ± 209 g/d; p<0.00001) and fiber intake (58 ± 5 g/d; p<0.00001). There were no diet order effects on ad libitum energy intake, body weight, or body composition change between UPFâMPF versus MPFâUPF groups. CONCLUSIONS: Diet order influences daily ad libitum energy intake, body weight change, and fat change within the context of a 4-week crossover inpatient diet study varying in macronutrients, but not varying in extent and purpose of processing. Funding sources: Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. Clinical Trial Registration: NCT03407053 and NCT03878108.
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Gut-derived hormones affect appetite and are thought to play an important role in body weight regulation. Dietary macronutrient composition can influence gut-derived appetite hormone concentrations, thereby providing theoretical basis for why some diets might facilitate weight loss better than others. We investigated postprandial gut-derived appetite hormones in 20 inpatient adults after 2 weeks of eating either a low carbohydrate (LC) or a low fat (LF) diet followed by the alternate diet in random order. A LC meal resulted in significantly greater postprandial GLP-1, GIP, and PYY but lower ghrelin compared to an isocaloric LF meal (all p≤0.02). However, differences in gut-derived appetite hormones were incommensurate with subsequent ad libitum energy intake over the rest of the day, which was 551±103 kcal (p<0.0001) greater with the LC as compared to the LF diet. The effects of gut-derived appetite hormones on ad libitum energy intake can be dominated by other diet-related factors, at least in the short-term.
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Background: Continuous glucose monitors (CGMs) are being used to characterize postprandial glycemic responses and thereby provide personalized dietary advice to minimize glycemic excursions. However, the efficacy of such advice depends on reliable CGM responses. Objective: To explore within-subject variability of CGM responses to duplicate meals in an inpatient setting. Methods: CGM data were collected in two controlled feeding studies (NCT03407053 and NCT03878108) in 30 participants without diabetes capturing 1056 meal responses in duplicate ~1 week apart from four dietary patterns. One study used two different CGMs (Abbott Freestyle Libre Pro and Dexcom G4 Platinum) whereas the other study used only Dexcom. We calculated the incremental area under the curve (iAUC) for each 2-h post-meal period and compared within-subject iAUCs using the same CGM for the duplicate meals using linear correlations, intra-class correlation coefficients (ICC), Bland-Altman analyses, and compared individual variability of glycemic responses to duplicate meals versus different meals using standard deviations (SDs). Results: There were weak to moderate positive linear correlations between within- subject iAUCs for duplicate meals (Abbott r=0.47, p<0.0001, Dexcom r=0.43, p<0.0001), with low within-participant reliability indicated by ICC (Abbott 0.31, Dexcom 0.14). Bland-Altman analyses indicated wide limits of agreement (Abbott -31.3 to 31.5 mg/dL, Dexcom -30.8 to 30.4 mg/dL) but no significant bias of mean iAUCs for duplicate meals (Abbott 0.1 mg/dL, Dexcom -0.2 mg/dL). Individual variability of glycemic responses to duplicate meals was similar to that of different meals evaluated each diet week for both Abbott (SDduplicate = 10.7 mg/dL , SDweek 1 =12.4 mg/dL, SDweek 2 =11.6 mg/dL, p=0.38) and Dexcom (SDduplicate = 11.1 mg/dL, SDweek 1 = 11.5 mg/dL, SDweek 2 =11.9 mg/dL, p=0.60). Conclusions: Individual postprandial CGM responses to duplicate meals were unreliable in adults without diabetes. Personalized diet advice based on CGM measurements in adults without diabetes requires more reliable methods involving aggregated repeated measurements.
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Intravenous ketone body infusion can increase erythropoietin (EPO) concentrations, but responses to ketone monoester ingestion postexercise are currently unknown. The purpose of this study was to assess the effect of ketone monoester ingestion on postexercise erythropoietin (EPO) concentrations. Nine healthy men completed two trials in a randomized, crossover design (1-wk washout). During trials, participants performed 1 h of cycling (initially alternating between 50% and 90% of maximal aerobic capacity for 2 min each interval, and then 50% and 80%, and 50% and 70% when the higher intensity was unsustainable). Participants ingested 0.8 g·kg-1 sucrose with 0.4 g·kg-1 protein immediately after exercise, and at 1, 2, and 3 h postexercise. During the control trial (CONTROL), no further nutrition was provided, whereas on the ketone monoester trial (KETONE), participants also ingested 0.29 g·kg-1 of the ketone monoester (R)-3-hydroxybutyl (R)-3-hydroxybutyrate immediately postexercise and at 1 and 2 h postexercise. Blood was sampled immediately postexercise, every 15 min in the first hour and hourly thereafter for 4 h. Serum EPO concentrations increased to a greater extent in KETONE than in CONTROL (time × condition interaction: P = 0.046). Peak serum EPO concentrations were higher with KETONE (means ± SD: 9.0 ± 2.3 IU·L-1) compared with CONTROL (7.5 ± 1.5 IU·L-1, P < 0.01). Serum ß-hydroxybutyrate concentrations were also higher, and glucose concentrations lower, with KETONE versus CONTROL (both P < 0.01). In conclusion, ketone monoester ingestion increases postexercise erythropoietin concentrations, revealing a new avenue for orally ingestible ketone monoesters to potentially alter hemoglobin mass.NEW & NOTEWORTHY To our knowledge, this study was the first to assess the effects of ketone monoester ingestion on erythropoietin concentrations after exercise. We demonstrated that ingestion of a ketone monoester postexercise increased serum erythropoietin concentrations and reduced serum glucose concentrations in healthy men. These data reveal the possibility for ketone monoesters to alter hemoglobin mass.
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Eritropoetina , Cetonas , Masculino , Humanos , Ácido 3-Hidroxibutírico , Glucose , Ingestão de AlimentosRESUMO
PURPOSE: To determine the effects of dietary sugar or carbohydrate restriction on physical activity energy expenditure, energy intake, and physiological outcomes across 24 h. METHODS: In a randomized, open-label crossover design, twenty-five healthy men (n = 10) and women (n = 15) consumed three diets over a 24-h period: moderate carbohydrate and sugar content (MODSUG = 50% carbohydrate [20% sugars], 15% protein, 35% fat); low sugar content (LOWSUG = 50% carbohydrate [< 5% sugars], 15% protein, 35% fat); and low carbohydrate content (LOWCHO = 8% carbohydrate [< 5% sugars], 15% protein, 77% fat). Postprandial metabolic responses to a prescribed breakfast (20% EI) were monitored under laboratory conditions before an ad libitum test lunch, with subsequent diet and physical activity monitoring under free-living conditions until blood sample collection the following morning. RESULTS: The MODSUG, LOWSUG and LOWCHO diets resulted in similar mean [95%CI] rates of both physical activity energy expenditure (771 [624, 919] vs. 677 [565, 789] vs. 802 [614, 991] kcal·d-1; p = 0.29] and energy intake (2071 [1794, 2347] vs. 2195 [1918, 2473] vs. 2194 [1890, 2498] kcal·d-1; P = 0.34), respectively. The LOWCHO condition elicited the lowest glycaemic and insulinaemic responses to breakfast (P < 0.01) but the highest 24-h increase in LDL-cholesterol concentrations (P < 0.001), with no differences between the MODSUG and LOWSUG treatments. Leptin concentrations decreased over 24-h of consuming LOWCHO relative to LOWSUG (p < 0.01). CONCLUSION: When energy density is controlled for, restricting either sugar or total dietary carbohydrate does not modulate physical activity level or energy intake over a 24-h period (~ 19-h free-living) despite substantial metabolic changes. CLINICAL TRIALS REGISTRATION ID: NCT03509610, https://clinicaltrials.gov/show/NCT03509610.
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Ingestão de Energia , Açúcares , Masculino , Humanos , Feminino , Estudos Cross-Over , Dieta , Carboidratos da Dieta , Metabolismo Energético , Exercício FísicoRESUMO
INTRODUCTION: Continuous exercise can increase postprandial gut hormone such as glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) responses, but it is unknown whether interrupting prolonged sitting with intermittent walking elicits this effect. METHOD: Ten participants with central overweight/obesity (7 men and 3 postmenopausal women, 51 ± 5 yr; mean ± SD) completed a randomized crossover study in which they consumed breakfast and lunch in the laboratory while either sitting continuously for the entire 5.5-h period (SIT) or the prolonged sitting interrupted every 20 min by walking briskly (6.4 km·h-1) for 2 min (BREAKS). Blood samples were collected at regular intervals to examine postprandial plasma GLP-1, PYY, and glucose-dependent insulinotropic polypeptide concentrations. Adipose tissue samples were collected at baseline and at the end of the trials to examine changes in net dipeptidyl peptidase 4 secretion from primary explants. RESULTS: Mean (95% confidence interval) postprandial GLP-1 and PYY incremental area under curve values were elevated by 26% and 31% in the BREAKS trial versus SIT (8.4 [0.7, 16.1] vs 6.7 [-0.8, 14.2], P = 0.001, and 26.9 [8.1, 45.6] vs 20.4 [5.1, 35.8] nmol·330 min·L-1, P = 0.024, respectively) but without any such effect on glucose-dependent insulinotropic polypeptide (P = 0.076) or net adipose tissue dipeptidyl peptidase 4 secretion (P > 0.05). CONCLUSIONS: Interrupting prolonged sitting with regular short bouts of brisk walking increases postprandial GLP-1 and PYY concentrations in healthy middle-age men and women with central adiposity.
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Glicemia , Dipeptidil Peptidase 4 , Estudos Cross-Over , Feminino , Peptídeo 1 Semelhante ao Glucagon , Humanos , Insulina , Masculino , Pessoa de Meia-Idade , Obesidade , Obesidade Abdominal , Peptídeo YY , Período Pós-Prandial , Caminhada/fisiologiaRESUMO
Caffeine is a psycho-active stimulant that can improve physical and cognitive performance. We systematically reviewed the evidence on the effects of acute caffeine ingestion on physiological parameters, physical and technical-skill performance during high-performance team-sport match-play. Following PRISMA guidelines, studies were identified using scientific databases (PubMed, Web-of-Science, Scopus, and SPORTDiscus) in February 2021. Of 281 results, 13 studies met inclusion, totalling 213 participants. Included studies adopted the randomised double-blinded cross-over design, involving caffeine and control conditions. In studies reporting physiological variables, responses to caffeine included higher peak (n=6/ 8 [n/ total studies measuring the variable]) and mean (n=7/ 9) heart rates, increased blood glucose (n=2/ 2) and lactate (n=2/ 2) concentrations. Improvements in physical performance were widely documented with caffeine, including greater distance coverage (n=7/ 7), high-speed distance coverage (n=5/ 7) and impact frequencies (n=6/ 8). From three studies that assessed technical-skills, it appears caffeine may benefit gross-skill performance, but have no effect, or negatively confound finer technical-skill outcomes. There is compelling evidence that ingesting moderate caffeine doses (~3 to 6 mg·kg-1) ~60 minutes before exercise may improve physical performance in team-sports, whereas evidence is presently too scarce to draw confident conclusions regarding sport-specific skill performance.
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Desempenho Atlético , Estimulantes do Sistema Nervoso Central , Substâncias para Melhoria do Desempenho , Desempenho Atlético/fisiologia , Cafeína , Estudos Cross-Over , Suplementos Nutricionais , Humanos , Substâncias para Melhoria do Desempenho/farmacologiaRESUMO
A high dose of whey protein hydrolysate fed with milk minerals rich in calcium (Capolac®) results in enhanced glucagon-like peptide-1 (GLP-1) concentrations in lean individuals; however, the effect of different calcium doses ingested alongside protein is unknown. The present study assessed the dose response of calcium fed alongside 25 g whey protein hydrolysate on GLP-1 concentrations in individuals with overweight/obesity. Eighteen adults (mean ± sd: 8M/10F, 34 ± 18 years, 28·2 ± 2·9 kgm-2) completed four trials in a randomised, double-blind, crossover design. Participants consumed test solutions consisting of 25 g whey protein hydrolysate (CON), supplemented with 3179 mg (LOW), 6363 mg (MED) or 9547 mg (HIGH) Capolac® on different occasions, separated by at least 48 h. The calcium content of test solutions equated to 65, 892, 1719 and 2547 mg, respectively. Arterialised-venous blood was sampled over 180 min to determine plasma concentrations of GLP-1TOTAL, GLP-17-36amide, insulin, glucose, NEFA, and serum concentrations of calcium and albumin. Ad libitum energy intake was measured at 180 min. Time-averaged incremental AUC (iAUC) for GLP-1TOTAL (pmol·l-1·min-1) did not differ between CON (23 ± 4), LOW (25 ± 6), MED (24 ± 5) and HIGH (24 ± 6). Energy intake (kcal) did not differ between CON (940 ± 387), LOW (884 ± 345), MED (920 ± 334) and HIGH (973 ± 390). Co-ingestion of whey protein hydrolysate with Capolac® does not potentiate GLP-1 release in comparison with whey protein hydrolysate alone. The study was registered at clinical trials (NCT03819972).
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It is unclear whether neuromuscular electrical stimulation (NMES) has meaningful metabolic effects when users have the opportunity to self-select the intensity to one that can be comfortably tolerated. Nine healthy men aged 28 ± 9 y (mean ± SD) with a body mass index 22.3 ± 2.3 kg/m2 completed 3 trials involving a 2-h oral glucose tolerance test whilst, in a randomised counterbalanced order, (1) sitting motionless (SIT), (2) standing motionless (STAND); and (3) sitting motionless with NMES of quadriceps and calves at a self-selected tolerable intensity. The mean (95% confidence interval [CI]) total energy expenditure was greater in the NMES trial (221 [180-262] kcal/2 h) and STAND trial (178 [164-191] kcal/2 h) than during SIT (159 [150-167] kcal/2 h) (both, p < 0.05). This was primarily driven by an increase in carbohydrate oxidation in the NMES and STAND trials compared with the SIT trial (p < 0.05). Postprandial insulin iAUC was lower in both NMES and STAND compared with SIT (16.4 [7.7-25.1], 17 [7-27] and 22.6 [10.8-34.4] nmol·120 min/L, respectively; both, p < 0.05). Compared with sitting, both NMES and STAND increased energy expenditure and whole-body carbohydrate oxidation and reduced postprandial insulin concentrations in healthy men, with more pronounced effects seen with NMES. Self-selected NMES is a potential strategy for improving metabolic health. This trial is registered at ClinicalTrials.gov (ID: NCT04389736). Novelty: NMES at a comfortable intensity enhances energy expenditure and carbohydrate oxidation, and reduces postprandial insulinemia. Thus, self-selected NMES represents a potential strategy to improve metabolic health.
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Intermittent fasting may impart metabolic benefits independent of energy balance by initiating fasting-mediated mechanisms. This randomized controlled trial examined 24-hour fasting with 150% energy intake on alternate days for 3 weeks in lean, healthy individuals (0:150; n = 12). Control groups involved a matched degree of energy restriction applied continuously without fasting (75% energy intake daily; 75:75; n = 12) or a matched pattern of fasting without net energy restriction (200% energy intake on alternate days; 0:200; n = 12). Primary outcomes were body composition, components of energy balance, and postprandial metabolism. Daily energy restriction (75:75) reduced body mass (-1.91 ± 0.99 kilograms) almost entirely due to fat loss (-1.75 ± 0.79 kilograms). Restricting energy intake via fasting (0:150) also decreased body mass (-1.60 ± 1.06 kilograms; P = 0.46 versus 75:75) but with attenuated reductions in body fat (-0.74 ± 1.32 kilograms; P = 0.01 versus 75:75), whereas fasting without energy restriction (0:200) did not significantly reduce either body mass (-0.52 ± 1.09 kilograms; P ≤ 0.04 versus 75:75 and 0:150) or fat mass (-0.12 ± 0.68 kilograms; P ≤ 0.05 versus 75:75 and 0:150). Postprandial indices of cardiometabolic health and gut hormones, along with the expression of key genes in subcutaneous adipose tissue, were not statistically different between groups (P > 0.05). Alternate-day fasting less effectively reduces body fat mass than a matched degree of daily energy restriction and without evidence of fasting-specific effects on metabolic regulation or cardiovascular health.
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Jejum , Redução de Peso , Adulto , Composição Corporal , Peso Corporal , Restrição Calórica , Ingestão de Energia , Metabolismo Energético , Humanos , ObesidadeRESUMO
This study investigated whether carbohydrate-energy replacement immediately after prolonged endurance exercise attenuates insulin sensitivity the following morning, and whether exercise improves insulin sensitivity the following morning independent of an exercise-induced carbohydrate deficit. Oral glucose tolerance and whole-body insulin sensitivity were compared the morning after 3 evening conditions, involving (1) treadmill exercise followed by a carbohydrate replacement drink (200 or 150 g maltodextrin for males and females, respectively; CHO-replace); (2) treadmill exercise followed by a non-caloric, taste-matched placebo (CHO-deficit); or (3) seated rest with no drink provided (Rest). Treadmill exercise involved 90 minutes at â¼80% age-predicted maximum heart rate. Seven males and 2 females (aged 23 ± 1 years; body mass index 24.0 ± 2.7 kg·m-2) completed all conditions in a randomised order. Matsuda index improved by 22% (2.2 [0.3, 4.0] au, p = 0.03) and HOMA2-IR improved by 10% (-0.04 [-0.08, 0.00] au, p = 0.04) in CHO-deficit versus CHO-replace, without corresponding changes in postprandial glycaemia. Outcomes were similar between Rest and other conditions. These data suggest that improvements to insulin sensitivity in healthy populations following acute moderate/vigorous intensity endurance exercise may be dependent on the presence of a carbohydrate-energy deficit. Novelty: Restoration of carbohydrate balance following acute endurance exercise attenuated whole-body insulin sensitivity. Exercise per se failed to enhance whole-body insulin sensitivity. Maximising or prolonging the post-exercise carbohydrate deficit may enhance acute benefits to insulin sensitivity.
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Carboidratos da Dieta/administração & dosagem , Exercício Físico , Resistência à Insulina , Adulto , Glicemia , Treino Aeróbico , Feminino , Teste de Tolerância a Glucose , Humanos , Masculino , Resistência Física , Adulto JovemRESUMO
This study explored lifestyle and biological determinants of peak fat oxidation (PFO) during cycle ergometry, using duplicate measures to account for day-to-day variation. Seventy-three healthy adults (age range: 19-63 years; peak oxygen consumption [VËO2peak]: 42.4 [10.1] ml·kg BM-1·min-1; n = 32 women]) completed trials 7-28 days apart that assessed resting metabolic rate, a resting venous blood sample, and PFO by indirect calorimetry during an incremental cycling test. Habitual physical activity (combined heart rate accelerometer) and dietary intake (weighed record) were assessed before the first trial. Body composition was assessed 2-7 days after the second identical trial by dual-energy X-ray absorptiometry scan. Multiple linear regressions were performed to identify determinants of PFO (mean of two cycle tests). A total variance of 79% in absolute PFO (g·min-1) was explained with positive coefficients for VËO2peak (strongest predictor), FATmax (i.e the % of VËO2peak that PFO occurred at), and resting fat oxidation rate (g·min-1), and negative coefficients for body fat mass (kg) and habitual physical activity level. When expressed relative to fat-free mass, 64% of variance in PFO was explained: positive coefficients for FATmax (strongest predictor), VËO2peak, and resting fat oxidation rate, and negative coefficients for male sex and fat mass. This duplicate design revealed that biological and lifestyle factors explain a large proportion of variance in PFO during incremental cycling. After accounting for day-to-day variation in PFO, VËO2peak and FATmax were strong and consistent predictors of PFO.
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Ciclismo/psicologia , Gorduras/metabolismo , Adulto , Testes Respiratórios , Calorimetria Indireta , Estudos Transversais , Registros de Dieta , Exercício Físico , Teste de Esforço , Feminino , Humanos , Modelos Lineares , Lipídeos , Masculino , Pessoa de Meia-Idade , Oxirredução , Fatores Sexuais , Adulto JovemRESUMO
PURPOSE: Ingested ethanol (EtOH) is metabolized gastrically and hepatically, which may influence resting and exercise metabolism. Previous exercise studies have provided EtOH intravenously rather than orally, altering the metabolic effects of EtOH. No studies to date have investigated the effects of EtOH ingestion on systemic and peripheral (e.g., skeletal muscle) exercise metabolism. METHODS: Eight men (mean ± SD; age = 24 ± 5 yr, body mass = 76.7 ± 5.6 kg, height = 1.80 ± 0.04 m, VËO2peak = 4.1 ± 0.2 L·min) performed two bouts of fasted cycling exercise at 55% VËO2peak for 2 h, with (EtOH) and without (control) prior ingestion of EtOH 1 h and immediately before exercise (total dose = 0.1 g·kg lean body mass·h; 30.2 ± 1.1 g 40% ABV Vodka; fed in two equal boluses) in a randomized order, separated by 7-10 d. RESULTS: Muscle glycogen use during exercise was not different between conditions (mean [normalized 95% confidence interval]; EtOH, 229 [156-302] mmol·kg dm, vs control, 258 [185-331] mmol·kg dm; P = 0.67). Mean plasma glucose concentrations during exercise were similar (control, 5.26 [5.22-5.30], vs EtOH, 5.34 [5.30-5.38]; P = 0.06). EtOH ingestion resulted in similar plasma nonesterified fatty acid concentrations compared with rest (control, 0.43 [0.31-0.55] mmol·L, vs EtOH, 0.30 [0.21-0.40] mmol·L) and during exercise. Plasma lactate concentration was higher during the first 30 min of rest after EtOH consumption (mean concentration; control, 0.83 [0.77-0.90] mmol·L, vs EtOH, 1.00 [0.93-1.07] mmol·L), but the response during exercise was similar between conditions. CONCLUSIONS: Muscle glycogen utilization was similar during exercise with or without prior EtOH ingestion, reflected in similar total whole-body carbohydrate oxidation rates observed.
Assuntos
Consumo de Bebidas Alcoólicas/metabolismo , Exercício Físico/fisiologia , Glicogênio/metabolismo , Músculo Esquelético/metabolismo , Adulto , Bebidas Alcoólicas , Glicemia/metabolismo , Estudos Cross-Over , Etanol/sangue , Ácidos Graxos não Esterificados/sangue , Humanos , Ácido Láctico/sangue , Masculino , Adulto JovemRESUMO
This study assessed the effects of glucose-fructose co-ingestion during recovery from high-intensity rugby training on subsequent performance. Nine professional, senior academy Rugby Union players performed two trials in a double-blind, randomized, crossover design. Identical rugby training sessions were separated by a 3-hour recovery period, during which participants ingested protein (0.3 g×kg BM×h-1) and carbohydrate-containing (0.8 g×kg BM×h-1) recovery drinks, comprised of glucose polymers (GLUCOSE ONLY) or a glucose-fructose mixture (GLUCOSE+FRUCTOSE). Performance outcomes were determined from global positioning systems combined with accelerometry and heart rate monitoring. Mean speed during sessions 1 (am) and 2 (pm) of GLUCOSE ONLY was (mean±SD) 118±6 and 117±4 m×min-1, respectively. During GLUCOSE+FRUCTOSE, mean speed during session 1 and 2 was 117±4 and 116±5 m×min-1, respectively (time x trial interaction, p = 0.61). Blood lactate concentrations were higher throughout recovery in GLUCOSE+FRUCTOSE (mean ±SD: 1-h 3.2 ±2.0 mmol×L-1; 3-h 2.1 ±1.2 mmol×L-1) compared to GLUCOSE ONLY (1-h 2.0 ±1.0 mmol×L-1; 3-h 1.4 ±1.0 mmol×L-1; trial effect p = 0.05). Gastrointestinal discomfort low in both conditions. These data suggest glucose-fructose mixtures consumed as protein-carbohydrate recovery drinks following rugby training do not enhance subsequent performance compared to glucose-based recovery drinks.
Assuntos
Desempenho Atlético/fisiologia , Sacarose Alimentar/administração & dosagem , Futebol Americano/fisiologia , Frutose/administração & dosagem , Condicionamento Físico Humano/fisiologia , Bebidas Adoçadas com Açúcar , Acelerometria/métodos , Estudos Cross-Over , Sacarose Alimentar/efeitos adversos , Método Duplo-Cego , Dispepsia/induzido quimicamente , Frutose/efeitos adversos , Sistemas de Informação Geográfica , Frequência Cardíaca , Humanos , Ácido Láctico/sangue , Masculino , Percepção/fisiologia , Esforço Físico/fisiologia , Bebidas Adoçadas com Açúcar/efeitos adversosRESUMO
Morning coffee is a common remedy following disrupted sleep, yet each factor can independently impair glucose tolerance and insulin sensitivity in healthy adults. Remarkably, the combined effects of sleep fragmentation and coffee on glucose control upon waking per se have never been investigated. In a randomised crossover design, twenty-nine adults (mean age: 21 (sd 1) years, BMI: 24·4 (sd 3·3) kg/m2) underwent three oral glucose tolerance tests (OGTT). One following a habitual night of sleep (Control; in bed, lights-off trying to sleep approximately 23.00-07.00 hours), the others following a night of sleep fragmentation (as Control but waking hourly for 5 min), with and without morning coffee approximately 1 h after waking (approximately 300 mg caffeine as black coffee 30 min prior to OGTT). Individualised peak plasma glucose and insulin concentrations were unaffected by sleep quality but were higher following coffee consumption (mean (normalised CI) for Control, Fragmented and Fragmented + Coffee, respectively; glucose: 8·20 (normalised CI 7·93, 8·47) mmol/l v. 8·23 (normalised CI 7·96, 8·50) mmol/l v. 8·96 (normalised CI 8·70, 9·22) mmol/l; insulin: 265 (normalised CI 247, 283) pmol/l; and 235 (normalised CI 218, 253) pmol/l; and 310 (normalised CI 284, 337) pmol/l). Likewise, incremental AUC for plasma glucose was higher in the Fragmented + Coffee trial compared with Fragmented. Whilst sleep fragmentation did not alter glycaemic or insulinaemic responses to morning glucose ingestion, if a strong caffeinated coffee is consumed, then a reduction in glucose tolerance can be expected.