Pectin-alginate does not further enhance exogenous carbohydrate oxidation in running:Hydrogel and exogenous carbohydrate oxidation

PURPOSE: Maximizing carbohydrate availability is important for many endurance events. Combining pectin and sodium alginate with ingested maltodextrin-fructose (MAL+FRU+PEC+ALG) has been suggested to enhance carbohydrate delivery via hydrogel formation but the influence on exogenous carbohydrate oxidation remains unknown. The primary aim of this study was to assess the effects of MAL+FRU+PEC+ALG on exogenous carbohydrate oxidation during exercise compared to a maltodextrin-fructose mixture (MAL+FRU). MAL+FRU has been well established to increase exogenous carbohydrate oxidation during cycling, compared to glucose-based carbohydrates (MAL+GLU). However, much evidence focuses on cycling, and direct evidence in running is lacking. Therefore, a secondary aim was to compare exogenous carbohydrate oxidation rates with MAL+FRU versus MAL+GLU during running. METHODS: Nine trained runners completed two trials (MAL+FRU and MAL+FRU+PEC+ALG) in a double-blind, randomised crossover design. A subset (n=7) also completed a MAL+GLU trial to address the secondary aim, and a water trial to establish background expired 13CO2 enrichment. Participants ran at 60% \dot{\mathrm{V}}\mathrm{O}_\mathrm{2}peak for 120 min while ingesting either water only, or carbohydrate solutions at a rate of 1.5 g carbohydrate·min-1. RESULTS: At the end of 120 min of exercise, exogenous carbohydrate oxidation rates were 0.9 (SD 0.5) g·min-1 with MAL+GLU ingestion. MAL+FRU ingestion increased exogenous carbohydrate oxidation rates to 1.1 (SD 0.3) g·min-1 (p=0.038), with no further increase with MAL+FRU+PEC+ALG ingestion (1.1 (SD 0.3) g·min-1; p=1.0). No time x treatment interaction effects were observed for plasma glucose, lactate, insulin or non-esterified fatty acids, nor for ratings of perceived exertion or gastrointestinal symptoms (all p>0.05). CONCLUSION: To maximise exogenous carbohydrate oxidation during moderate-intensity running, athletes may benefit from consuming glucose(polymer)-fructose mixtures over glucose-based carbohydrates alone, but the addition of pectin and sodium alginate offers no further benefit

Interrupting Prolonged Sitting with Intermittent Walking Increases Postprandial Gut Hormone Responses

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 &gt; 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.</p

Pectin-alginate does not further enhance exogenous carbohydrate oxidation in running:Hydrogel and exogenous carbohydrate oxidation

PURPOSE: Maximizing carbohydrate availability is important for many endurance events. Combining pectin and sodium alginate with ingested maltodextrin-fructose (MAL+FRU+PEC+ALG) has been suggested to enhance carbohydrate delivery via hydrogel formation but the influence on exogenous carbohydrate oxidation remains unknown. The primary aim of this study was to assess the effects of MAL+FRU+PEC+ALG on exogenous carbohydrate oxidation during exercise compared to a maltodextrin-fructose mixture (MAL+FRU). MAL+FRU has been well established to increase exogenous carbohydrate oxidation during cycling, compared to glucose-based carbohydrates (MAL+GLU). However, much evidence focuses on cycling, and direct evidence in running is lacking. Therefore, a secondary aim was to compare exogenous carbohydrate oxidation rates with MAL+FRU versus MAL+GLU during running. METHODS: Nine trained runners completed two trials (MAL+FRU and MAL+FRU+PEC+ALG) in a double-blind, randomised crossover design. A subset (n=7) also completed a MAL+GLU trial to address the secondary aim, and a water trial to establish background expired 13CO2 enrichment. Participants ran at 60% \dot{\mathrm{V}}\mathrm{O}_\mathrm{2}peak for 120 min while ingesting either water only, or carbohydrate solutions at a rate of 1.5 g carbohydrate·min-1. RESULTS: At the end of 120 min of exercise, exogenous carbohydrate oxidation rates were 0.9 (SD 0.5) g·min-1 with MAL+GLU ingestion. MAL+FRU ingestion increased exogenous carbohydrate oxidation rates to 1.1 (SD 0.3) g·min-1 (p=0.038), with no further increase with MAL+FRU+PEC+ALG ingestion (1.1 (SD 0.3) g·min-1; p=1.0). No time x treatment interaction effects were observed for plasma glucose, lactate, insulin or non-esterified fatty acids, nor for ratings of perceived exertion or gastrointestinal symptoms (all p&gt;0.05). CONCLUSION: To maximise exogenous carbohydrate oxidation during moderate-intensity running, athletes may benefit from consuming glucose(polymer)-fructose mixtures over glucose-based carbohydrates alone, but the addition of pectin and sodium alginate offers no further benefit

Ketone monoester ingestion increases post-exercise serum erythropoietin concentrations in healthy men:Ketones and EPO

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 &lt; 0.01). Serum β-hydroxybutyrate concentrations were also higher, and glucose concentrations lower, with KETONE versus CONTROL (both P &lt; 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 &amp; 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.</p

Ketone monoester ingestion increases post-exercise serum erythropoietin concentrations in healthy men:Ketones and EPO

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 &lt; 0.01). Serum β-hydroxybutyrate concentrations were also higher, and glucose concentrations lower, with KETONE versus CONTROL (both P &lt; 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 &amp; 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.</p

Glucose control upon waking is unaffected by hourly sleep fragmentation during the night, but is impaired by morning caffeinated coffee:Sleep fragmentation and caffeinated coffee

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.</p

Muscle Glycogen Utilization during Exercise after Ingestion of Alcohol

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, VO2peak = 4.1 ± 0.2 L·min-1) performed two bouts of fasted cycling exercise at 55% VO2peak 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-1·h-1; 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-1, vs control, 258 [185-331] mmol·kg dm-1; 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-1, vs EtOH, 0.30 [0.21-0.40] mmol·L-1) 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-1, vs EtOH, 1.00 [0.93-1.07] mmol·L-1), 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.</p

The Energy Cost of Sitting versus Standing Naturally in Man

Purpose Prolonged sitting is a major health concern, targeted via government policy and the proliferation of height-adjustable workstations and wearable technologies to encourage standing. Such interventions have the potential to influence energy balance and thus facilitate effective management of body/fat mass. It is therefore remarkable that the energy cost of sitting versus standing naturally remains unknown. Methods Metabolic requirements were quantified via indirect calorimetry from expired gases in 46 healthy men and women (age, 27 ± 12 yr; mass, 79.3 ± 14.7 kg; body mass index, 24.7 ± 3.1 kg·m -2, waist/hip, 0.81 ± 0.06) under basal conditions (i.e., resting metabolic rate) and then, in a randomized and counterbalanced sequence, during lying, sitting and standing. Critically, no restrictions were placed on natural/spontaneous bodily movements (i.e., fidgeting) to reveal the fundamental contrast between sitting and standing in situ while maintaining a comfortable posture. Results The mean (95% confidence interval [CI]) increment in energy expenditure was 0.18 (95% CI, 0.06-0.31 kJ·min -1) from resting metabolic rate to lying was 0.15 (95% CI, 0.03-0.27 kJ·min -1) from lying to sitting and 0.65 (95% CI, 0.53-0.77 kJ·min -1) from sitting to standing. An ancillary observation was that the energy cost of each posture above basal metabolic requirements exhibited marked interindividual variance, which was inversely correlated with resting heart rate for all postures (r = -0.5; -0.7 to -0.1) and positively correlated with self-reported physical activity levels for lying (r = 0.4; 0.1 to 0.7) and standing (r = 0.6; 0.3-0.8). Conclusions Interventions designed to reduce sitting typically encourage 30 to 120 min·d -1 more standing in situ (rather than perambulation), so the 12% difference from sitting to standing reported here does not represent an effective strategy for the treatment of obesity (i.e., weight loss) but could potentially attenuate any continued escalation of the ongoing obesity epidemic at a population level. </p

Physiological responses to maximal eating in men

This study investigated metabolic, endocrine, appetite and mood responses to a maximal eating occasion in fourteen men (mean: age 28 (sd 5) years, body mass 77·2 (sd 6·6) kg and BMI 24·2 (sd 2·2) kg/m2) who completed two trials in a randomised crossover design. On each occasion, participants ate a homogenous mixed-macronutrient meal (pizza). On one occasion, they ate until 'comfortably full' (ad libitum) and on the other, until they 'could not eat another bite' (maximal). Mean energy intake was double in the maximal (13 024 (95 % CI 10 964, 15 084) kJ; 3113 (95 % CI 2620, 3605) kcal) compared with the ad libitum trial (6627 (95 % CI 5708, 7547) kJ; 1584 (95 % CI 1364, 1804) kcal). Serum insulin incremental AUC (iAUC) increased approximately 1·5-fold in the maximal compared with ad libitum trial (mean: ad libitum 43·8 (95 % CI 28·3, 59·3) nmol/l × 240 min and maximal 67·7 (95 % CI 47·0, 88·5) nmol/l × 240 min, P &lt; 0·01), but glucose iAUC did not differ between trials (ad libitum 94·3 (95 % CI 30·3, 158·2) mmol/l × 240 min and maximal 126·5 (95 % CI 76·9, 176·0) mmol/l × 240 min, P = 0·19). TAG iAUC was approximately 1·5-fold greater in the maximal v. ad libitum trial (ad libitum 98·6 (95 % CI 69·9, 127·2) mmol/l × 240 min and maximal 146·4 (95 % CI 88·6, 204·1) mmol/l × 240 min, P &lt; 0·01). Total glucagon-like peptide-1, glucose-dependent insulinotropic peptide and peptide tyrosine-tyrosine iAUC were greater in the maximal compared with ad libitum trial (P &lt; 0·05). Total ghrelin concentrations decreased to a similar extent, but AUC was slightly lower in the maximal v. ad libitum trial (P = 0·02). There were marked differences on appetite and mood between trials, most notably maximal eating caused a prolonged increase in lethargy. Healthy men have the capacity to eat twice the energy content required to achieve comfortable fullness at a single meal. Postprandial glycaemia is well regulated following initial overeating, with elevated postprandial insulinaemia probably contributing.</p

Muscle Glycogen Utilization during Exercise after Ingestion of Alcohol

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, VO2peak = 4.1 ± 0.2 L·min-1) performed two bouts of fasted cycling exercise at 55% VO2peak 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-1·h-1; 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-1, vs control, 258 [185-331] mmol·kg dm-1; 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-1, vs EtOH, 0.30 [0.21-0.40] mmol·L-1) 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-1, vs EtOH, 1.00 [0.93-1.07] mmol·L-1), 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.</p